CRISPR Technology Industry 2020 Market Research Report A new report added by DeepResearchReports.com to its research database. CRISPR Technology Market is segmented by Regions/Countries. All the key market aspects that influence the CRISPR Technology market currently and will have an impact on it have been assessed and propounded in the CRISPR Technology market research status and development trends reviewed in the new report.

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The economical unrest across the globe due to Covid19 pandemic has affected different industries. Several businesses have gone through revenue hassles. It has impacted many product launches and marketing strategies to an extent that numerous industries and global businesses were compelled to either cease, halt or even shut their operations. Now, when businesses are trying to refurbish their existence across the globe, a ready referral guide in the form of market research report can help in providing a direction with the useful information about the market dynamics.

Next, learn how to build the strategy and business case to implement. Learn about CRISPR Technology market and how it can provide value to your business. In this market, you will find the competitive scenario of the major market players focusing on their sales revenue, customer demands, company profile, import/export scenario, business strategies that will help the emerging market segments in making major business decisions. This report also studies the global market competition landscape, market drivers and trends, opportunities and challenges, risks and entry barriers, sales channels, distributors and Porters Five Forces Analysis.

About the report:

The new tactics of CRISPR Technology market report offers a comprehensive market breakdown on the basis of value, volume, CAGR, and Y-o-Y growth. For business robust expansion, the report suggests new tools and technology development will drive to boom in the near future by 2026. The CRISPR Technology market report provides a comprehensive outline of Invention, Industry Requirement, technology and production analysis considering major factors such as revenue, investments and business growth.

This report for CRISPR Technology Market discovers diverse topics such as regional market scope, product-market various applications, market size according to a specific product, CRISPR Technology sales and revenue by region, manufacturing cost analysis, industrial chain, market effect factors Analysis, and more.

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Table of Contents

Chapter 1 CRISPR Technology Market OverviewChapter 2 Global CRISPR Technology Competition by Players/Suppliers, Type and ApplicationChapter 3 United States CRISPR Technology (Volume, Value and Sales Price)Chapter 4 China CRISPR Technology (Volume, Value and Sales Price)Chapter 5- Europe CRISPR Technology (Volume, Value and Sales Price)Chapter 6 Japan CRISPR Technology (Volume, Value and Sales Price)Chapter 7 Southeast Asia CRISPR Technology (Volume, Value and Sales Price)Chapter 8 India CRISPR Technology (Volume, Value and Sales Price)Chapter 9 Global CRISPR Technology Players/Suppliers Profiles and Sales DataChapter 10 CRISPR Technology Manufacturing Cost AnalysisChapter 11 Industrial Chain, Sourcing Strategy and Downstream BuyersChapter 12 Marketing Strategy Analysis, Distributors/TradersChapter 13 Market Effect Factors AnalysisChapter 14 Global CRISPR Technology Market Forecast (2020-2026)Chapter 15 Research Findings and ConclusionChapter 16 Appendix

Key Questions Answered in this Report:

What is the market size of the CRISPR Technologyindustry?This report covers the historical market size of the industry (2013-2019), and forecasts for 2020 and the next 5 years. Market size includes the total revenues of companies.

What is the outlook for the CRISPR Technologyindustry?This report has over a dozen market forecasts (2020 and the next 5 years) on the industry, including total sales, a number of companies, attractive investment opportunities, operating expenses, and others.

What industry analysis/data exists for the CRISPR Technologyindustry?This report covers key segments and sub-segments, key drivers, restraints, opportunities, and challenges in the market and how they are expected to impact the CRISPR Technologyindustry. Take a look at the table of contents below to see the scope of analysis and data on the industry.

How many companies are in the CRISPR Technologyindustry?This report analyzes the historical and forecasted number of companies, locations in the industry, and breaks them down by company size over time. The report also provides company rank against its competitors with respect to revenue, profit comparison, operational efficiency, cost competitiveness, and market capitalization.

What are the financial metrics for the industry?This report covers many financial metrics for the industry including profitability, Market value- chain, and key trends impacting every node with reference to the companys growth, revenue, return on sales, etc.

What are the most important benchmarks for the CRISPR Technologyindustry?Some of the most important benchmarks for the industry include sales growth, productivity (revenue), operating expense breakdown, span of control, organizational make-up. All of which youll find in this market report.

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Deep Research Reports is digital database of syndicated market reports for global and China industries. These reports offer competitive intelligence data for companies in varied market segments and for decision makers at multiple levels in these organizations. We provide 24/7 online and offline support to our customers.

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Covid-19 Impact on CRISPR Technology Market to Witness Huge Growth by 2026: Future Development and Top Manufacturers Analysis - Verdant News

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Key Developments in the Market:

In March 2018, Kaneka Corporation announced that they have acquired a patent in the Japan for the creation of the method to mass-culture pluripotent stem cells including iPS cells and ES cells. This will help the company to use the technology to produce high quality pluripotent stem cells which can be used in the drug and cell therapy.

In March 2015, Fujifilm announced that they have acquired Cellular Dynamics International. The main aim of the acquisition is to expand their business in the iPS cell-based drug discovery support service with the use of CDS technology. It will help them to product high- quality automatic human cells with the help of the induced pluripotent stem cells. This will help the company to be more competitive in the drug discovery and regenerative medicine.

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Global Induced Pluripotent Stem Cells (iPSCs) Market Scope and Market Size

Induced pluripotent stem cells (iPSCs) market is segmented of the basis of derived cell type, application and end- user. The growth amongst these segments will help you analyse meagre growth segments in the industries, and provide the users with valuable market overview and market insights to help them in making strategic decisions for identification of core market applications.

Global Induced Pluripotent Stem Cells (iPSCs) Market Drivers:

Increasing R&D investment activities is expected to create new opportunity for the market.

Increasing demand for personalized regenerative cell therapies among medical researchers & healthcare is expected to enhance the market growth. Some of the other factors such as increasing cases of chronic diseases, growing awareness among patient, rising funding by government & private sectors and rising number ofclinical trialsis expected to drive the induced pluripotent stem cells (iPSCs) market in the forecast period of 2020 to 2027.

High cost of the induced pluripotent stem cells (iPSCs) and increasing ethical issues & lengthy processes is expected to hamper the market growth in the mentioned forecast period.

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Global Induced Pluripotent Stem Cells (iPSCs) Market 2020 Manufacturer Analysis, Technology Advancements, Industry Scope and Forecast to 2027||Fate...

Recommendation and review posted by Bethany Smith

Its uncontroversial among biologists that many species have two, distinct biological sexes. Theyre distinguished by the way that they package their DNA into gametes, the sex cells that merge to make a new organism. Males produce small gametes, and females produce large gametes. Male and female gametes are very different in structure, as well as in size. This is familiar from human sperm and eggs, and the same is true in worms, flies, fish, molluscs, trees, grasses and so forth.

Different species, though, manifest the two sexes in different ways. The nematode worm Caenorhabditis elegans, a common laboratory organism, has two forms not male and female, but male and hermaphrodite. Hermaphroditic individuals are male as larvae, when they make and store sperm. Later they become female, losing the ability to make sperm but acquiring the ability to make eggs, which they can fertilise with the stored sperm.

This biological definition of sex has been swept up into debates over the status of transgender people in society. Some philosophers and gender theorists define a woman as a biologically female human being. Others strongly disagree. Im addressing those who reject the very idea that there are two biological sexes. Instead, they argue, there are many biological sexes, or a continuum of biological sexes.

Theres no need to reject how biologists define the sexes to defend the view that trans women are women. When we look across the diversity of life, sex takes stranger forms than anyone has dreamt of for humans. The biological definition of sex takes all this in its stride. It does so despite the fact that there are no more than two biological sexes in any species youre likely to have heard of. To many people, that might seem to have conservative implications, or to fly in the face of the diversity we see in actual human beings. I will make clear why it does not.

I call this the biological definition of sex because its the one biologists use when studying sex that is, the process by which organisms use their DNA to make offspring. Many philosophers and gender theorists will protest at making the creation of offspring foundational to how we define sex or distinguish different sexes. Theyre surely right that sex as a social phenomenon is much richer than that. But the use of DNA to make offspring is a central topic in biology, and understanding and explaining the diversity of reproductive systems is an important scientific task. Gender theorists are understandably worried about how the biology of sex will be applied or misapplied to humans. What they might not appreciate is why biologists use this definition when classifying the mind-stretching forms of reproduction observed in limpets, worms, fish, lizards, voles and other organisms and they might not understand the difficulties that arise if you try to use another definition.

Many people assume that if there are only two sexes, that means everyone must fall into one of them. But the biological definition of sex doesnt imply that at all. As well as simultaneous hermaphrodites, which are both male and female, sequential hermaphrodites are first one sex and then the other. There are also individual organisms that are neither male nor female. The biological definition of sex is not based on an essential quality that every organism is born with, but on two distinct strategies that organisms use to propagate their genes. They are not born with the ability to use these strategies they acquire that ability as they grow up, a process which produces endless variation between individuals. The biology of sex tries to classify and explain these many systems for combining DNA to make new organisms. That can be done without assigning every individual to a sex, and we will see that trying to do so quickly leads to asking questions that have no biological meaning.

While the biological definition of sex is needed to understand the diversity of life, that doesnt mean its the best definition for ensuring fair competition in sport or adequate access to healthcare. We cant expect sporting codes, medical systems and family law to adopt a definition simply because biologists find it useful. Conversely, most institutional definitions of sex break down immediately in biology, because other species contradict human assumptions about sex. The United States National Institutes of Health (NIH) uses a chromosomal definition of sex XY for males and XX for females. Many reptiles, such as the terrifying saltwater crocodiles of northern Australia, dont have any sex chromosomes, but a male saltie has no trouble telling if the crocodile that has entered his territory is a male. Even among mammals, at least five species are known that dont have male sex chromosomes, but they develop into males just fine. Gender theorists have extensively criticised the chromosomal definition of human sexes. But however well or badly that definition works for humans, its an abject failure when you look at sex across the diversity of life.

The same is true of phenotypic sex, the familiar idea that sex is defined by the typical physical characteristics (phenotypes) of males and females. Obviously, this approach will produce completely different definitions of male and female for humans, for worms, for trees and so forth. Incubating eggs inside your body, for example, is a female characteristic in humans but a male one in seahorses. That doesnt mean that human institutions cant use the phenotypic definition. But it isnt useful when studying the common patterns in the genetics, evolution and so forth of female humans, female seahorses and female worms.

Understanding the complex ways in which chromosomes and phenotypes relate to biological sex will make clear why the biological definition of sex shouldnt be the battleground for philosophers and gender theorists who disagree about the definition of woman. There might be very good reasons not to define woman in this way, but not because the definition itself is poor biology.

Why did sexes evolve in the first place? Biologists define sex as a step towards answering this question. Not all species have biological sexes, and biology seeks to explain why some do and others dont. The fact that no species has evolved more than two biological sexes is also a puzzle. It would be quite straightforward to engineer a species that has three, but none has evolved naturally.

Many species reproduce asexually, with each individual using its own DNA to create offspring. But other species, including our own, combine DNA from more than one organism. Thats sexual reproduction, where two sex cells gametes merge to make a new individual. In some species, these two gametes are identical; many species of yeast, for example, make new individuals from two, identical gametes. They reproduce sexually, but they have no sexes, or, if you prefer, they have only one sex. But in species that make two different kinds of gamete and where one gamete of each kind is needed to make a new organism there are two sexes. Each sex makes one of the two kinds of gamete.

In complex multicellular organisms, such as plants and animals, these two kinds of gamete are very different. One is a large, complex cell, what wed typically call an egg. Its similar to the eggs produced by asexual species, which can develop into a new organism all on their own. Many species of insect and some lizards, snakes and sharks can reproduce using just an egg cell. The other kind of gamete is a much smaller cell that contains very little beyond some DNA and some machinery to get that DNA to the larger gamete. We are familiar with these two kinds of gametes from human eggs and sperm.

Theres no obvious reason why complex multicellular organisms need to have two kinds of gamete, or why these two kinds are so different in size and structure. Its perfectly possible to make three or more different kinds of gamete, or gametes that vary continuously, just as people vary continuously in height. One question that biologists seek to answer, then, is why those forms of sexual reproduction arent observed in complex organisms such as animals and plants.

Earthworms are hermaphrodites: one part of the worm produces sperm and another part produces eggs

When a species produces two different kinds of gamete, biologists call this anisogamy, meaning not-equal-gametes. Some anisogamic species have separate sexes, like humans do, where each individual can produce only one kind of gamete. Other anisogamic species are hermaphrodites, where each individual produces both kinds of gamete. Because they produce two kinds of gametes, hermaphroditic species still have two biological sexes they simply combine them in one organism. When a biologist tells you that earthworms are hermaphrodites, they mean that one part of the worm produces sperm and another part produces eggs.

Some single-celled and very simple multicellular organisms have evolved something called mating types. These are gametes that are identical in size and structure, but in which the genome of each gamete contains genetic markers that affect which other gametes it can combine with. Typically, gametes with the same genetic marker cant recombine with one another. Some species have many hundreds of these mating types, and newspapers often report research into this phenomenon under headlines such as: Scientists discover species with hundreds of sexes! But, formally, biologists refer to these as mating types, and reserve the term sexes for gametes that are different in size and structure.

Why distinguish between these two phenomena? One reason is that the evolution of anisogamy gametes that differ in size and structure explains the later evolution of sex chromosomes, sex-associated physical characteristics and much more. But the existence of mating types doesnt have these dramatic knock-on evolutionary effects. Another reason to keep the distinction is that anisogamy and mating types are thought to have evolved via different evolutionary processes. One theory is that anisogamy appeared when mating-type genome markers somehow became linked to genes that controlled the size of the gamete, or mutated in some way that affected gamete size. These differences in gamete size would then kickstart the evolution of sexes.

The evolution of sex seems to be strongly associated with multicellularity, so the obvious place to look for a shift from mating types to sexes is in organisms that sit at the multicellular boundary such as algae, which sometimes exist as single-celled organisms, and sometimes as colonies of cells. And indeed, there are species of algae where gametes are just a little bit anisogamous, blurring the distinction between mating types and sexes. Theres much we dont know about how sex evolved, and how it might have evolved differently across species. But the point is that sexes and mating types are very different phenomena, with different causes and consequences.

The fact that sex evolved in some species but not others tells us something important about how biologists think about sex. Many cultures take the difference between male and female to be something fundamental, and label other natural phenomena such as the Sun and the Moon as male or female. But for biologists, the separation between male and female is no more fundamental or universal than photosynthesis or being warm-blooded. Some species have evolved these things, and some havent. They exist when they do only because of the local advantages they afforded in evolutionary competition.

So why did some species evolve two, distinct sexes? To answer this question, we need to forget about creatures with complex sex organs and mating behaviours. These evolved later. Instead, think of an organism that releases its gametes into the sea, such as coral, or into the air, such as fungal spores. Next, consider that there are two goals that any gamete must achieve if its to reproduce sexually. The first is finding and recombining with another gamete. The second is producing a new individual with enough resources to survive. One widely accepted idea, then, is that the evolution of sexes reflects a trade-off between these goals. Because no organism has infinite resources, organisms can either produce many small gametes, making it more likely that some of them will find a partner, or produce fewer but larger gametes, making it more likely that the resulting individual will have what it needs to survive and thrive.

Since the 1970s, this idea has been used to model how anisogamic species might have evolved from species with only one kind of gamete. As mutations introduce differences in gamete size, two winning strategies emerge. One is to produce a large number of small gametes too small to create viable offspring unless they recombine with a larger, well-provisioned gamete. The other winning strategy is to produce a few, large, well-resourced gametes that can create viable offspring, no matter how small the recombinant they end up merging with. Intermediate approaches, such as producing a moderate number of moderately well-provisioned gametes, dont do well. Organisms that try to follow the middle way end up with gametes less likely to find a partner than smaller gametes, and more likely to have insufficient resources than larger gametes. When the two successful complementary strategies have evolved, fresh evolutionary pressures make the gametes even more distinct from one another. For example, it can be advantageous for the small gametes to become more mobile, or for the large, immobile gametes to send signals to the mobile ones.

Once anisogamy has evolved, it shapes many other aspects of reproductive biology. Most species of limpet shellfish that you see on rocks at the beach are sequential hermaphrodites. When young and small they are male, and when mature and large they become female. This is believed to be because small limpets dont have sufficient resources to produce large female gametes, but theyre capable of producing the smaller male ones. In some other species, successful males can arrest their growth and remain small (and male) for their entire life.

Chromosomes arent male or female because these bits of DNA define biological sex. Its the other way around

Sequential hermaphroditism occurs in the opposite direction too. Australian snorkellers love to spot the large blue males of the eastern blue groper, but its rare to see more than one. Most groper are smaller, brown females. They are all born female and become sexually mature after a few years, when 20 or 30 cm in length. At around 50 cm, they change sex and acquire other male characteristics, such as being blue. Unlike the limpet, the main problem facing a male groper is controlling a territory on the reef, so becoming male when youre small is a losing strategy.

Biology aims to understand the extraordinary diversity of ways in which organisms reproduce themselves, as well as to identify common patterns, and to explain why they occur. In general, organisms become sexually mature when they reach an optimal size for reproduction. This optimal size is often different for the two sexes, because the two sexes represent divergent strategies for reproduction. The limpet and the groper are two of many examples. In constructing these explanations, biological sex is defined as the production of one type of viable anisogamous gamete. If we defined sex in some other way, it would be hard to see the common patterns across the diversity of life, and hard to explain them.

So-called sex chromosomes, such as the XX and XY chromosome pairs seen in humans, are often brandished as something thats fundamental to sex. Its partly the inadequacy of this definition that drives scepticism about the existence of two, discrete biological sexes. Molecular genetics is likely to require a shift from binary sex to quantum sex, with a dozen or more genes each conferring a small percentage likelihood of male or female sex that is still further dependent on micro- and macroenvironmental interactions, writes the gender scholar Vernon Rosario.

But any biologist already knows that theres more to sex determination than chromosomes and genes, and that male and female sex chromosomes are neither necessary nor sufficient to make organisms male and female. Several species of mammal, all rodents of one kind or another, have completely lost the male Y chromosome, but these rats and voles all produce perfectly normal, fertile males. Other groups of species, such as crocodiles and many fish, have neither sex chromosomes nor any other genes that determine sex. Yet they still have two, discrete biological sexes. The Australian saltwater crocodile, whom we met before, lays eggs that are very likely to develop into gigantic, highly territorial males if incubated between 30 and 33 degrees Celsius. At other temperatures, genetically identical eggs develop into much smaller females.

The reality is that chromosomes arent called male or female because these bits of DNA define biological sex. Its the other way around in some species that reproduce using two discrete sexes, those sexes are associated with different bits of DNA. But in other species this association is either absent or unreliable. Medical institutions use a chromosomal definition of sex because they judge, rightly or wrongly, that this is a reliable way of categorising humans. But humans really arent the best place to start when trying to understand sex across the diversity of life.

So much for genes. But perhaps sex could be defined by the physical characteristics that organisms develop, which then add up to constitute an organisms sex? An organism with more female than male characteristics would be more female than male and vice-versa. Thats a reasonable way to think about sex, and this idea of phenotypic sex is widely used. But if we apply the biological definition of sex, some of the individuals who are in the middle as far as sex-associated characteristics go are bona fide members of one biological sex. Others are not clearly members of either biological sex.

Nothing in the biological definition of sex requires that every organism be a member of one sex or the other. That might seem surprising, but it follows naturally from defining each sex by the ability to do one thing: to make eggs or to make sperm. Some organisms can do both, while some cant do either. Consider the sex-switching species described above: what sex are they when theyre halfway through switching? What sex are they if something goes wrong, perhaps due to hormone-mimicking chemicals from decaying plastic waste? Once we see the development of sex as a process and one that can be disrupted it is inevitable that there will be many individual organisms that arent clearly of either sex. But that doesnt mean that there are many biological sexes, or that biological sex is a continuum. There remain just two, distinct ways in which organisms contribute genetic material to their offspring.

Whats more, the physical characteristics of an organism can be labelled as male or female only if there is already a definition of sex. Whats so male about a groper being blue as opposed to brown? Many male organisms are brown. Whats so female about incubating eggs in a womb? After all, in many pipefish and seahorse species the male incubates the eggs in his brood pouch. What makes this part of the hermaphroditic earthworm male and that part female? Gender studies scholars have noticed this logical discrepancy, and some have gone on to argue that the sexes must therefore be defined in terms of gender. But from a biological perspective, what makes an observable physical characteristic male or female is not its association with gender, but its association with something more tangible: the production of one or other of the two kinds of gamete.

This explains why the existence of individuals with combinations of male and female characteristics doesnt show that biological sex is a continuum. These organisms have a combination of characteristics associated with one biological sex and characteristics associated with the other biological sex. They do not have some part of the ability to make small gametes combined with some part of the ability to make large gametes. Their phenotypic sex might be intermediate, but their biological sex is not. Being fully biologically male and fully biologically female hermaphroditic can be an effective evolutionary strategy, and we have encountered several hermaphroditic species already. But making both kinds of gametes incompletely would be an evolutionary dead-end.

Like phenotypic characteristics, sex chromosomes can be more or less reliably associated with biological sex. The eastern three-lined skink, an Australian lizard, has sex chromosomes, and under some circumstances XY skinks become male and XX skinks become female, just as in humans. But in cold nests, every skink becomes male, whatever their chromosomes. By becomes male, biologists mean that they grow up to produce small gametes sperm.

No animal is conceived with the ability to make sperm or eggs (or both). This ability has to grow

This effect of temperature on sex is not surprising, as many reptile species produce genetically identical offspring whose sex is determined by incubation temperature. Whats more surprising is that varying the size of the egg yolk in this species of skink can produce both sexes with the wrong sex chromosomes: XX males and XY females. The skink seems to have three mechanisms for determining sex chromosomes, temperature and hormones in the yolk. This is not a mere quirk of nature. The skink is one of many species that actively control the sex of their offspring, responding to environmental cues that predict whether male or female offspring have better chances of surviving and reproducing.

If all species were like the skink, we probably wouldnt label sex chromosomes as male or female. After all, we dont think of extreme nest temperatures as female and intermediate temperatures as male, merely because they produce male and female crocodiles or male and female geckos. We think of sex chromosomes as male or female because we focus on species where they are reliably associated with the production of male or female gametes.

Sex chromosomes play much the same role in sex determination as nest temperatures and hormones. Theyre simply mechanisms that organisms use to turn genes on and off in offspring so that they develop a biological sex. No animal is conceived with the ability to make sperm or eggs (or both). This ability has to grow, through a cascade of interactions between genes and environments. In some species, once an individual acquires a sex, it remains that sex for the rest of its life. In others, individuals can switch sex one or more times. But in every case, the underlying mechanisms are designed to grow organisms that make either male or female gametes (or both). The other changes the body undergoes as it becomes male, female or hermaphroditic are designed to fit the reproductive strategies that this species has evolved.

These mechanisms by which organisms develop or switch biological sex are complex, and many factors can interfere with them. So they produce a lot of phenotypic diversity. Sometimes, organisms grow up able to make fertile gametes, but otherwise atypical for their biological sex. Sometimes, they grow up unable to make fertile gametes of either kind. This is usually an accident, but sometimes by design. In bees, eggs that arent fertilised develop into males, so male bees have half as many chromosomes as female bees. Meanwhile, all fertilised eggs start to develop into females, but most of them never complete their sexual development. The queen sends chemical signals that block the development of the worker bees ovaries at an early stage. So worker bees are female in the extended sense that they would develop into fertile females if they werent actively prevented from doing so. Occasionally, worker bees manage to evade these controls and lay their own eggs. They are not popular with beekeepers, who select against these mutant strains.

The diversity of outcomes in individual sexual development doesnt mean that there are many biological sexes or that biological sex is a continuum. Whatever the merits of those views for chromosomal sex or phenotypic sex, they are not true of biological sex. A good way to grasp this is to imagine a species that really does have three biological sexes. Biotechnologists have proposed curing mitochondrial diseases by removing the nucleus from an egg with healthy mitochondrial DNA, and inserting a new nucleus containing the nuclear DNA from an unhealthy egg and the nuclear DNA from a sperm. The resulting child would have three genetic parents.

Now imagine if there was a whole species like this, where three different kinds of gametes combined to make a new individual a sperm, an egg and a third, mitochondrial gamete. This species would have three biological sexes. Something like this has actually been observed in slime moulds, an amoeba that can, but need not, get its mitochondria from a third parent. The novelist Kurt Vonnegut imagined an even more complex system in Slaughterhouse-Five (1969): There were five sexes on Tralfamadore, each of them performing a step necessary in the creation of a new individual. But the first question a biologist would ask is: why havent these organisms been replaced by mutants that dispense with some of the sexes? Having even two sexes imposes many extra costs the simplest is just finding a mate and these costs increase as the number of sexes required for mating rises. Mutants with fewer sexes would leave more offspring and would rapidly replace the existing Tralfamadorians. Something like this likely explains why two-sex systems predominate on Earth.

We can also imagine a species where biological sex really does form a continuum. Recall that some algae have slightly anisogamous gametes, much closer together than sperm and eggs. We can imagine a more complex organism using this system, with some slightly smaller gametes and some slightly larger ones. Successful reproduction might require two gametes that, when added together, are big enough but not too big. But the sexually reproducing plants and animals that actually exist all have just two, very different kinds of gamete male and female. Theyre not merely different in size, theyre fundamentally different in structure. This is the result of competition between organisms to leave the greatest number of genetic descendants. In complex multicellular organisms such as plants and animals, we know of only three successful reproductive strategies: two biological sexes in different individuals, two biological sexes combined in hermaphroditic individuals, and asexual reproduction. Some species use one of these strategies, some use more than one.

Human beings have come up with many ways to classify the diversity of individual outcomes from human sexual development. People who want to apply the biological definition of sex to humans should recognise that its ill-suited to do what many human institutions want, which is to sort every individual into one category or another. What sex are worker bees? They are sterile workers whose genome was designed by natural selection to terminate ovary development on receipt of a signal from the queen bee. They share much of the biology of fertile female bees but if someone wants to know Are worker bees really female?, theyre asking a question that biology simply cant answer.

Nor is being a sterile worker a third biological sex alongside male and female. This is easier to see in ants, where there is more than one sterile caste. Workers, soldiers, queens and male flying ants each have specialised bodies and behaviour, but there are not four biological sexes of ant. Workers and soldiers are both female in an extended sense, but not in the full-blown sense that queen ants are female. There is a human imperative to give everything a sex, as mentioned above, but biology doesnt share it.

The biological definition of sex wasnt designed to ensure fair sporting competition, or settle healthcare disputes

Juvenile organisms and postmenopausal human females also cant produce either kind of gamete. Juveniles are assigned to the sex they have started to grow into. But once again, this is more complicated than it seems when we focus only on humans. In almost all mammals, sexual differentiation is initiated by a region of the Y chromosome, so a mammalian egg can become either male or female. In birds, its the other way around the egg carries the sex-determining W chromosome, so sperm can become either male or female. After fertilisation, therefore, we can say that an individual mammal or bird has a sex in the sense that it has started to grow the ability to produce either male or female gametes. With a crocodile or a turtle, though, wed have to wait until nest temperature had its sex-determining effect. But that doesnt mean that we need to create a third biological sex for crocodile eggs!

More importantly, nothing guarantees that any of these organisms, including those with sex chromosomes, will continue to grow to the point where they can actually produce male or female gametes. Any number of things can interfere. From a biological point of view, there is nothing mysterious about the fact that organisms have to grow into a biological sex, that it takes them a while to get there, and that some individuals develop in unusual or idiosyncratic ways. This is a problem only if a definition of sex must sort every individual organism into one sex or another. Biology doesnt need to do that.

In human populations, there are plenty of individuals whose sex is hard to determine. Biologists arent blind to this. The definition of biological sex is designed to classify the human reproductive system and all the others in a way that helps us to understand and explain the diversity of life. Its not designed to exhaustively classify every human being, or every living thing. Trying to do so quickly leads to questions that have no biological meaning.

Human societies cant delegate to biology the job of defining sex as a social institution. The biological definition of sex wasnt designed to ensure fair sporting competition, or to settle disputes about access to healthcare. Theorists who want to use the biological definition of sex in those ways need to show that it will do a good job at the Olympics or in Medicare. The fact that its needed in biology isnt good enough. On the other hand, whatever its shortcomings as an institutional definition, the concept of biological sex remains essential to understand the diversity of life. It shouldnt be discarded or distorted because of arguments about its use in law, sport or medicine. That would be a tragic mistake.

The authors research is supported by the Australian Research Council and the John Templeton Foundation. He would also like to thank Nicole Vincent, Jussi Lehtonen, Stefan Gawronski and Joshua Christie for their feedback on earlier drafts.

More:
Sex is real - aeon.co

Recommendation and review posted by Bethany Smith

Twenty-two research projects led by researchers from the Faculty of Medicine and affiliated health authority research centres were awarded $15 million from the Canadian Institute of Health Research Project Grant Spring 2020 competition.

The Project Grant program supports researchers in building and conducting health-related research and knowledge translation projects, covering all areas of health.

In addition to the Project Grant Spring 2020 competition, one Faculty of Medicine project was awarded a priority announcement bridge grant of $100,000.

Pilot RCT for cognitive-behavioural & mindfulness-based online programs for female sexual dysfunctionUBC Principal Investigator: Dr. Lori Brotto, department of obstetrics & gynaecology

Identification of HOXB13 inhibitors to treat castrate-resistant prostate cancerUBC Principal Investigators: Dr. Martin Gleave, department of urologic sciences, Nathan Lack, department of urologic sciences

Predicting and Evaluating Anal Cancer in HIV with novel biomarkers: The PEACH StudyUBC Principal Investigators: Dr. Jonathan (Troy) Grennan, department of medicine

A randomized trial of doxycycline chemoprophylaxis for the prevention of sexually transmitted infections in gay, bisexual and other men who have sex with men (gbMSM)UBC Principal Investigators: Dr. Jonathan (Troy) Grennan, department of medicine, Mark Hull, department of medicine

Chronic diseases in mothers and risks of neuro-developmental disorders in offspring: an international comparisonUBC Principal Investigator: Dr. K. S. Joseph, School of Population and Public Health

Novel endothelial engineering and localized immunosuppression approaches for the protection of organ transplantsUBC Principal Investigators: Dr. Jayachandran Kizhakkedathu, department of pathology and laboratory medicine

Childhood Epigenetic Age Deviations and Developmental Differences (CEAD3)UBC Principal Investigator: Dr. Michael Kobor, department of medical genetics

Characterization and treatment of a novel conditional mouse model of pyridoxine-dependent epileptic encephalopathy caused by antiquitin mutations.UBC Principal Investigator: Dr. Blair Leavitt, department of medical genetics

Improving clinical practice recommendations for late preterm antenatal corticosteroids: incorporating a decision support tool to tackle the uncertain balance of risks and benefitsUBC Principal Investigator: Dr. Jessica Liauw, department of obstetrics & gynaecology

Enterovirus subversion of the autophagy pathwayUBC Principal Investigator: Dr. Honglin Luo, department of pathology and laboratory medicine

Reducing unsafe prescribing of prescription opioid medications to opioid nave patientsUBC Principal Investigators: Dr. Rita McCracken, department of family practice, Evan Wood, department of medicine

Maternal exposures during pregnancy as drivers of susceptibility to allergic asthma and Th2 inflammation.UBC Principal Investigator: Dr. Kelly McNagny, department of medical genetics

Self-Management for Amputee Rehabilitation using Technology (SMART) program: A peer supported mHealth approach for rehabilitation after lower limb amputationUBC Principal Investigators: Dr. William Miller, department of occupational science and occupational therapy, Maureen Ashe, department of family practice, William Mortenson, department of occupational science and occupational therapy, Michael Payne, medical microbiology

Evaluating tetrahydrocannabinol as an adjunct to opioid agonist therapy for individuals living with opioid use disorder: A Phase II, placebo-controlled, blinded, pilot study to assess safety and feasibilityUBC Principal Investigator: Dr. Michael-John Milloy, department of medicine

Engaging and retaining marginalized populations in primary health care in the downtown east side of VancouverUBC Principal Investigator: Dr. David Moore, department of medicine

Improved Assessment of Disease in Lymphoma Patients using Quantitative PET ImagingUBC Principal Investigator: Dr. Arman Rahmim, department of radiology

Delineating between pathophysiologic phenotypes of hypoxic ischemic brain injury after cardiac arrestUBC Principal Investigator: Dr. Mypinder Sekhon, department of medicine

Tissue resident and migratory group 2 innate lymphoid cells in health and diseaseUBC Principal Investigator: Dr. Fumio Takei, department of pathology & laboratory medicine

Neuro-cardiac predictors of treatment response to rTMS in depression: a mechanistic study using interleaved TMS-fMRIUBC Principal Investigator: Dr. Fidel Vila-Rodriguez, department of psychiatry

Low frequency repetitive transcranial magnetic stimulation (TMS) vs. intermittent Theta Burst Stimulation TMS effectiveness in depression and suicidal ideation: a randomized non-inferiority trialUBC Principal Investigator: Dr. Fidel Vila-Rodriguez, department of psychiatry

The role of PRDM16 in neuroendocrine prostate cancer development and aggressivenessUBC Principal Investigator: Dr. Yuzhuo Wang, department of urologic sciences

A prospective and longitudinal investigation of concussive and subconcussive mild traumatic brain injury mechanisms in ice hockeyUBC Principal Investigators: Dr. Alexander Rauscher, department of pediatrics, Lyndia (Chun) Wu, Faculty of Applied Science, Paul van Donkelaar, Faculty of Health and Social Development

Understanding Human Primary Atopic Disorders (Priority Announcement:Skin Conditions)UBC Principal Investigators: Dr. Stuart Turvey, department of pediatrics, Catherine Biggs, department of pediatrics

Read more:
Faculty of Medicine researchers receive $15M from CIHR's Project Grant program - UBC Faculty of Medicine

Recommendation and review posted by Bethany Smith

American economistMilton Friedmanrevealed that the secret to success in a capitalistic world lies in learning to play within the rules of the game. Business leaders have often clamored around this truth when playing the centuries-old game of economic strategy: a game, wherein the only rules involve engaging in open and free competition without deception or fraud.

This may be the case for those at the top of Americas societal hierarchy the wealthy, white men who reign over boardrooms and political podiums alike, dominating the most powerful positions for most of Americas history.

Yet for women, this is not, and has never been, completely true.

As the COVID-19 pandemic began to squeeze women from the US workforce, so too increased the news medias scrutiny on the unequal playing field faced by women in the workforce. However, long before the pandemic hit, women in the American workforce faced a much more difficult path to the top.

Women engage in a second kind of game; a game quietly played beneath the surface, like a secret handshake to an underground society wherein an invisible set of rules apply.

The idea is to be effective yet not too assertive. Be pleasant and agreeable without seeming too soft. Remember to be charming so people dont feel threatened by your ideas or your intelligence. Dont talk too loud. Dont talk too much. Dress in a way that is neither too feminine nor too masculine. Be empathetic but never emotional.

And for a woman of color, these rules are even more mysteriousand harder to discern. A woman of color constantly battles the widely preconceived notion that either by dint of genetics or environment her knowledge and abilities are lesser than others.

Yet her success also hinges on being pleasant, articulate, gregarious, and putting everyone at ease in her presence, lest she be deemed angry or dispensable. But above all else regardless of race or ethnicity a woman must always come to the boardroom or the podium wielding her best, most disarmingsmile.

We are so deeply entrenched in these beliefs that we unwittingly became our own gatekeepers.

Recently, one of us returned from a photo shoot for an award honoring trailblazing female leaders. The resulting photos showed a commanding businesswoman sitting at a boardroom table, flanked by two male colleagues. She was clearly and confidently assuming a leadership role. However, the photos engendered an overwhelming fear. The photos seemed to say, I dont look warm or likable enough.

The charming mask so often worn by women to appear less threatening had slipped, and the resulting photos revealed a powerful businesswoman. The fear of being rejected for looking overtly powerful is something a man would never consider.

Even the strongest, most accomplished women leaders cant escape these cultural expectations. While admired by many for her stoic strength, razor-sharp intellectualism, and unrelenting toughness,Kamala Harrisrecently came under fire just hours before winning the spot asJoe Bidens running mate. News coverage was riddled with sexist attacks on Harris lack of personal charm and warmth.

Unfortunately, Harris is just one of the many female political casualties. Bashed with sexist barbs due to perceived lack of likability and warmth, these women Hillary Clinton,Sarah Palin,Elizabeth Warren, to name a few disappeared in the public court of opinion.

For these women, the need for striking the perfect balance between being assertive without being bossy surpasses the need for intelligence, professional achievements, and even their policy.

Women at the top of their industry have found that to be successful in todays America means being smart and extremely effective but never so overtly as to bruise an ego.

Just ask the likes of fierce former CEO of Hewlett-Packard,Carly Fiorina, fashion mogulVictoria Beckham, and sports iconSerena Williamshow often they have been found lacking by the media for their inability to smile like women.

As we look to a near future in which the pandemic will most assuredly continue to hit women in the workforce the hardest there should be no doubt that now is the time to dissolve this game and strip ourselves of these subtle yet deeply ingrained rules that govern it.

To fully tap into the potential of womens strength, women must first endeavor to change the way we speak, worrying less about deliverance and more about the content of our words. This means being unfiltered, speaking unapologetically, refusing to let others speak for us. Perhaps even changing speech patterns rather than softening our voices, we must speak with a tone of authority.

This new approach boils down to a simple rule women need to remember: being likable is not our sole mission.

While it must be every womans goal to unapologetically toss aside the archaic rulebook that shapes our idea of the successful female leader, it is not just women who need to change. We must look into our culture, starting with how we raise our children.

For example, rather than solely emphasizing obedience, cooperation, and supportiveness, society must encourage girls to share their opinions, take risks, assume leadership roles, solve problems and praise them when they do so.

If we want more female leaders, we need to vote for them, support their business, and shine the light on female role models who are unapologetically using their voices to drive change.

The most important culture shift is also the simplest. We must all shift to hear what women have to say. We need to listen instead of scrutinizing. Allow women to express their ideas regardless of their looks or the way they speak. When we are able to support women based on their ability to lead, vision, and strategy rather than their people-pleasing demeanor we can all smile.

The opinions expressed herein are those of the authors and not of New York Medical College.

Here is the original post:
Want More Women in Leadership Roles? Focus on Their Strategy and Not Their Smile - The Globe Post

Recommendation and review posted by Bethany Smith

If youre a woman, youre probably intimately familiar with the abdominal pain and cramps that pop up once a month during your period. Generations of women have been taught that its normal to feel menstrual painbut a new wave of doctors say thats not always the case: Sometimes, pelvic pain can be a sign of a serious condition called endometriosis, and if you dont address it quickly, your future fertility could be at risk. These are some of the signs and symptoms that something more than just period pain is going on.

To understand endometriosis, first you need to know about the endometrium: Thats the lining inside the uterus that builds up once a month to allow for the implantation of a fertilized egg in the womb. If theres no fertilized egg, theres no need for a cushy lining, so the body sheds that layeralso know as having your period if youre a woman. Whats shed is a mixture of blood, vaginal secretions, and endometrial cells.

But sometimes, the blood flow gets mixed up, and instead of flowing out, it flows up, going back through the fallopian tubes and into the pelvis. Endometrial cells that mistakenly ended up in the pelvis can attach onto its walls, as well as the outside of the uterus, the fallopian tubes, or any of the organs within the pelvis. Those adventurous cells arent where theyre supposed to be, but they still try to perform the task they were designed for, and that is to collect blood to form a lining and release the blood if theres no baby on board.

Thats what endometriosis is: The growth of endometrial cells and development of thick tissue outside of the uterus that can lead to inflammation, lesions, and scarring. This tissue can grow on other organs, reducing blood flow and raising the risk of fertility issues. Endometriosis can cause intense painor none at all.

The biggest risk factor for this condition is being female (not much you can do there!). There also seems to be a genetic component involved, so if your mother, aunt, or sisters have endometriosis, you have a higher likelihood of getting it, too.

Experts estimate that 11% of reproductive-age women have endometriosis worldwide, yet here in the U.S., it can take up seven to 12 years for a proper diagnosis. That decade of pain can be attributed to a mix of factors, including limited access to care, a stigma around pelvic pain and menstruation-related complaints, and doctors who dont fully understand how to treat it.

Experts suspect endometriosis is caused by something know as retrograde menstruation. This is when menstrual fluid (blood, vaginal fluid, and endometrial cells) flows upwards rather than down and out of the body. In retrograde menstruation, the fluid is released into the pelvic cavity, overwhelming the bodys ability to remove it. This gives the endometrial cells the opportunity to find a new home. And thats the start of endometriosis.

Additionally, endometriosis can happen when endometrial cells are released into the abdomen during a surgery, such as a c-section. There are also theories that involve cells outside of the uterus mimicking endometrial cells when theyre activated by certain hormones, like estrogen.

For women who have severe cases of endometriosis, their main symptom is pain which can express itself in several different ways. Heres what to look for.

Chronic pelvic pain: There may be dull cramping throughout a womans cycle, not only when she is bleeding. Those who suffer from chronic pelvic pain (40% to 50% of those with endometriosis) often report that it gets worse when they have their period.

Constipation: If endometriosis occurs on the bowels or lower intestine, it can lead to constipation.

Heavy menstrual bleeding: Symptoms of so-called menorrhagia can include needing to use double sanitary protection (like a tampon and a pad), bleeding for more than seven days, passing blood clots larger than a quarter, and soaking through at least one pad or tampon every hour for several hours. Drop everything and go to the doctor ASAP if you have menstrual bleeding so bad that youre soaking through one pad or tampon every hour for more than two hours, bleeding between periods, or bleeding post-menopause. These can be symptoms of endometriosis, but also symptoms of other issues, including endometrial cancer.

Infertility: Between 30% and 50% of women who have endometriosis suffer from infertility issues. The causes are still being debated, but it could be that the endometriosis messes with the jobs of the ovaries and fallopian tubes. It could also be due to endocrine (hormone) or ovulatory disorders which interfere with the release and fertilization of healthy eggs. Or the normal shedding of the endometrial layer in the uterus is disrupted if endometriosis is present, and that causes infertility.

Painful sex: Between 40% and 50% of women with endometriosis report having deep dyspareunia, which is the fancy term for painful sex during deep penetration. So how do you know if pain during sex is related to endometriosis? If you have a burning sensation when your partner is first entering you, thats not probably endometriosis. If it is a knife-stabbing feeling when a partner is thrusting deeper, thats a red flag for the condition.

Sharp lower abdominal pain: This can be caused by an ovarian cyst that started as endometriosis. It can also be caused by endometriosis that attaches itself to two different organs, like an ovary and the large bowel, acting like connective tissue that binds these organs to each other. When thats jostled around, say during sex or a bowel movement, it can cause pain.

Painful urination: If endometriosis shows up outside the bladder, it can make urination painful, or blood can show up in the urine.

Severe cramping: Known as dysmenorrhea, this affects 60% to 80% of women with endometriosis. To expel the endometrial lining, the uterus contracts. What triggers those uterine contractions are prostaglandins, which are hormone-like compounds that can cause pain and inflammation. More prostaglandins are linked to more painful menstrual cramps, and endometriosis is linked with a higher level of prostaglandins.

If youre saying to yourself: Wow, it wouldnt dawn on me to go see my gynecologist if Im having poop problemsId see a gastroenterologist! youve now identified one of the challenges with endometriosis. Because of the nature of the disease, its symptoms can cross over into other conditions, making it hard to get to the root of the issue. Without a specific screening test for endometriosis, it may take some trial and error before you receive a correct diagnosis.

Despite these symptoms, 20% to 25% of endometriosis patients are asymptomatic. For them, the discovery often comes when theyre tryingand failingto get pregnant. Still, it is definitely possible to get pregnant if you have endometriosis, and its something you and a reproductive endocrinologist and fertility specialist can discuss.

Asymptomatic patients may also learn about their endometriosis if the tissue mass gets very large and leads to excessive bloating. Other women find out when they have pelvic surgery for something elsesuch as a tubal ligation, or to have an appendix removedand the surgeon sees the endometriosis.

Before we get into the nitty gritty, its worth noting that the prevailing wisdom dictates that doctors begin treating endometriosis before theres a definite diagnosis. Thats because the only way to be sure that its present is to do a laparoscopy, a minimally invasive surgery in which a long thin camera and other tools are inserted into the pelvis through small incisions in the abdomen, and tissue samples are taken and studied by a pathologist. The procedure is expensive and time-consuming, so doctors may sometimes decide to begin treatment if all other indications are for endometriosis.

So what might some of those treatments be?

The first line of defense is NSAIDs, or nonsteroidal anti-inflammatory drugs, which block the bodys production of the hormonal compound prostaglandin, thus cutting down on pain, inflammation, and cramping. NSAIDs are most effective if you start to take them before your period starts. Talk to your doctor about dosage. Dont take more than is listed on the label unless directed by your doc, though he or she may want to bump you up to the prescription type.

Contraceptives that contain hormones, such as the pill, patch, ring, shots, or a hormonal IUD can treat endometriosis by managing a womans cycle or eliminating menses altogether.

A doctor may also opt to put you on a short stint of a nonsteroidal aromatase inhibitor, which is a class of drugs that prevents the cells in the body from making estrogen or by suppressing estrogen production. It essentially creates a menopause-like state. Doctors are wary of using it long-term because, down the road, estrogen suppression can lead to issues like osteoporosis, heart disease, and cognitive decline. But in some cases, turning off the estrogen gives the body time to clean out the endometriosis.

If medical remedies dont work, surgerys an option. Doctors typically do minimally invasive surgery and either cut out or laser off the endometriosis that they see. The good news: It can provide immediate relief of the symptoms. Bad news: For 40% to 80% of women, surgery doesnt provide a total cure, and pain returns within two years of the procedure. This happens because there can be areas of endometriosis so small that the surgeon missed them.

Beyond meds and surgery, researchers are investigating the role genetics play in endometriosis in hopes that it can them predict who will develop it, and aid in the creation of highly effective treatments, too. In the meantime, lifestyle changes may also help control the condition.

For example, we know that endometriosis is an inflammatory disease, and that inflammation can exacerbate painful symptoms. So reducing the amount of inflammatory foods (such as red meat and alcohol) in your diet can help, as can adding in anti-inflammatory foods like salmon, nuts, and olive oil.

Whats more, exercisesomething you may feel challenged to do when dealing with chronic painmay help to ease some symptoms, like cramping and bloating. You dont have to go all-in on marathon running or kickboxing to see a positive effect: Just 30 minutes of moderate exercise daily, like walking or jogging, can help ease your symptoms while improving your overall health and fitness.

Original post:
What are the Signs & Symptoms of Endometriosis? - HealthCentral.com

Recommendation and review posted by Bethany Smith

Esteemed cardiologist James T. Willerson, MD, of the Texas Heart Institute, who pioneered research in unstable atherosclerotic plaques and was the longest-serving editor of Circulation, died after a long illness on September 16, 2020, at age 81.

It's very easy to find his scientific contributions, which have been countless, said longtime friend and colleague Mohammad Madjid, MD (University of Texas Health Science Center, Houston). But if you knew him and saw how he worked, the thing that really stood out was how compassionate and genuine he was with his patients. He had an amazing rapport with them, and they knew he meant it when he said he was only one phone call away from them, 24-7, Madjid added. Over all the years that I knew him, I never saw him getting angry. He had a cool, gentle manner even under the most serious of circumstances.

Paul Ridker, MD (Harvard Medical School, Boston, MA), told TCTMD Willerson will be greatly missed.

Jim Willersons reach and influence were simply exceptional, he said. Early in my career, Jim reached out and was both supportive and inspirational. Over the years he became a friend and treasured research colleague.

Renu Virmani, MD (CVPath Institute, Gaithersburg, MD), said she got to know Willerson through his passion to advance the field of atherosclerosis and his desire to figure out how to predict future cardiac events so as to treat them before catastrophe occurred.

"While editor of Circulation, he encouraged everyone involved in research in this area, and I was one of the lucky ones whose career benefited from his passion, his curiosity, and his mentorship. I will always remember him as among the kindest and most humble leaders in our field," she said in an email. "His foresight did so much to advance knowledge in that field and I am deeply saddened by his passing."

In 2005, Willerson was the recipient of the TCT Career Achievement Award. Jim Willerson was a towering figure in medicine, Martin B. Leon, MD (NewYork-Presbyterian/Columbia University Irving Medical Center, New York, NY), TCTs founder and director, told TCTMD. He had a legendary work ethic, set new standards as editor-in-chief of Circulation, and always reverted to his patient-centered origins as a revered clinician. Jim was soft-spoken and extremely humble, which belied his raging intellect, thirst for knowledge, and commitment to excellence. He will be remembered as a true giant in cardiology, setting the stage for the modern era.

Gregg W. Stone, MD (Icahn School of Medicine at Mount Sinai, New York, NY), also a TCT director, called Willerson one of the true giants of medicine, as well as the consummate scientist, educator, editor, academician and caregiver.

He was also a warm person, inherently humble, but knew when to be outspoken and motivated generations of cardiologists. He will be greatly missed but always remembered, Stone remarked.

A Texas-Sized Life

Willerson was born on the edge of the Texas Hill Country in Lampasas to parents who were both physicians. He attended school in San Antonio and Austin before receiving his medical degree from Baylor College of Medicine in Houston. A championship swimmer in his college days, Willerson has a swimming scholarship named in his honor at his alma mater, the University of Texas at Austin.

In an interview published in 2018 in the European Heart Journal, he explained that a meeting arranged by his mother when he was just 14 years old, with the renowned cardiovascular surgeon Denton Cooley, MD, changed the arc of his life. Rather than a quick hello, Willerson recalled that the two spent 30 minutes speaking about Willersons interest in becoming a physician. The meeting was the start of an enduring friendship and collaboration with Cooley, who founded the Texas Heart Institute (THI) and performed the first successful artificial heart transplantation there in 1969. When Cooley stepped aside as president of THI at age 86, he chose Willerson to take the job. Willerson continued on, serving as president emeritus until his death.

He was the best role model that anyone could have, and the most lovable human you could ever want to be around. Mohammad Madjid

For many years, Madjid said, Willerson and Cooley worked in offices next-door to each other, remaining close until Cooleys death in 2016.

Throughout his long career, Willerson pioneered research on the detection and treatment of vulnerable atherosclerotic plaques, as well as genes and abnormal proteins. As a result of his research, he was awarded 15 patents, and his institution became the site of the first US Food and Drug Administration-approved trial of human stem cells to treat ischemic cardiomyopathies and congestive HF. Over his career, he published an estimated 1,000 scientific papers and wrote one of the first textbooks on nuclear cardiology.

Juan Granada, MD, CEO of the Cardiovascular Research Foundation (CRF), who spent time as a fellow atBaylor College of Medicine and worked closely with Willerson, said they shared an interest in vulnerable plaque research and translational medicine.

He was very entrepreneurial, very innovative, and one of the hardest working people that I ever met in my life, Granada noted. He recalled that during Willersons long tenure as editor of Circulation, he would often personally contact authors to sort through problems that cropped up during the review process.

This is essentially unheard of nowadays, but he would actually call you on the phone and say, Hey, I got this comment. Lets talk it through. He was amazing and unique in what he did, and he was a beautiful, caring person on top of it, Granada added.

To TCTMD, Madjid said of his mentor, He had my back through everything. When I was down, he was there. When I needed help or to talk, he was always there. He was the best role model that anyone could have, and the most lovable human you could ever want to be around.

Following the Texas Heart Institutes announcement of Willersons death, colleagues and friends took to Twitter to share their memories.

Photo Credit: Mohammad Madjid

Read more:
James T. Willerson, Revered Clinician, Editor, and Mentor, Dies at 81 - TCTMD

Recommendation and review posted by Bethany Smith

SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced that it presented the latest results from three Phase III studies from the Tecentriq (atezolizumab) clinical development program in triple-negative breast cancer (TNBC) at the European Society for Medical Oncology (ESMO) Virtual Congress 2020.

While we have made great progress in the treatment of many forms of breast cancer, TNBC remains an aggressive and difficult-to-treat disease, said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. We are proud of our work to address challenges and advance scientific understanding of cancer immunotherapy in the context of distinct chemotherapy regimens and in various TNBC treatment settings. Although the IMpassion131 study did not reach its endpoint, we are pleased to bring new treatment options for some TNBC patients, and remain committed to improving the lives of all women with early and advanced stages of this disease.

Results from the Phase III IMpassion031 study, evaluating Tecentriq in combination with chemotherapy (Abraxane [albumin-bound paclitaxel; nab-paclitaxel]; followed by doxorubicin and cyclophosphamide) in comparison to placebo plus chemotherapy (including nab-paclitaxel) demonstrated a statistically significant and clinically meaningful improvement in pathological complete response (pCR) for the treatment of people with early TNBC, regardless of PD-L1 expression. pCR was observed in 57.6% (95% CI: 49.7-65.2) of patients treated with Tecentriq in combination with chemotherapy, an increase of 16.5% from 41.1% (95% CI: 33.6-48.9) in patients treated with placebo plus chemotherapy (one-sided p=0.0044, significance boundary = 0.0184) in the intention-to-treat (ITT) population. The safety profile was consistent with the established profile of the individual medicines and no new safety concerns were identified.

The IMpassion031 study is the second positive Phase III study from Genentech demonstrating the benefit of Tecentriq in TNBC, and the first Tecentriq study to demonstrate benefit in early TNBC. Tecentriq in combination with nab-paclitaxel is currently approved in more than 70 countries worldwide, including the United States and across Europe, for the treatment of adults with unresectable locally advanced or metastatic TNBC in people whose tumors express PD-L1 (IC1%).

The final overall survival (OS) analysis of the Phase III IMpassion130 study, evaluating Tecentriq in combination with nab-paclitaxel compared with placebo plus nab-paclitaxel as a first-line treatment for patients with metastatic TNBC, was consistent with the first and second interim analyses. There was no significant difference in OS between the treatment groups in the ITT population. Clinically meaningful improvements in OS were seen with Tecentriq plus nab-paclitaxel in PD-L1-positive patients. The magnitude of OS improvements with Tecentriq in PD-L1-positive patients remained clinically meaningful, with an increase of 7.5 months in median OS with Tecentriq plus nab-paclitaxel compared with placebo plus nab-paclitaxel (hazard ratio [HR]=0.67 [95% CI: 0.530.86]). However, this result could not be formally tested due to the prespecified statistical testing hierarchy. The cumulative safety of the Tecentriq plus nab-paclitaxel combination remains consistent with the previously reported safety data for this study and the known risks of individual study medicines. No new safety concerns were identified with longer follow-up.

Finally, results from the Phase III IMpassion131 study, evaluating Tecentriq in combination with paclitaxel compared with placebo plus paclitaxel as a first-line treatment for patients with metastatic TNBC, did not show significant improvement for progression-free survival (PFS) in the PD-L1-positive population (HR=0.82 [95% CI: 0.60-1.12]). The OS data showed a negative trend; however, the study was not powered for the secondary endpoint of OS, and OS data were immature at the time of analysis (initial HR=1.55 [95% CI: 0.86-2.80] in the PD-L1-positive population, based on 21% of patients with an event; updated HR=1.12 [95% CI: 0.76-1.65], updated analysis based on 41% of patients with an event). The safety profile of Tecentriq plus paclitaxel was consistent with the established safety profile of the individual study medicines and no new safety concerns were identified.

Genentech has an extensive development program for Tecentriq, including multiple ongoing and planned Phase III studies across several types of lung, genitourinary, skin, breast, gastrointestinal, gynecological, and head and neck cancers. This includes studies evaluating Tecentriq both alone and in combination with other medicines.

About the IMpassion031 study

The IMpassion031 study is a Phase III, multi-center, randomized, double-blind study evaluating the efficacy and safety of Tecentriq (atezolizumab) in combination with chemotherapy (Abraxane [albumin-bound paclitaxel; nab-paclitaxel]; followed by doxorubicin and cyclophosphamide) in comparison to placebo plus chemotherapy, in people with previously untreated, early TNBC. The primary endpoint is pCR using the American Joint Committee on Cancer (AJCC) staging system in the intention-to-treat (ITT) population and in the PD-L1-positive population. Secondary endpoints include overall survival (OS), event-free survival, disease-free survival and quality of life measures.

About the IMpassion130 study

The IMpassion130 study is a Phase III, multicenter, randomized, double-blind study evaluating the efficacy, safety and pharmacokinetics of Tecentriq plus nab-paclitaxel compared with placebo plus nab-paclitaxel in people with unresectable locally advanced or metastatic TNBC who have not received prior systemic therapy for metastatic breast cancer. The study enrolled 902 people who were randomized equally (1:1). The co-primary endpoints are PFS per investigator assessment (RECIST 1.1), and OS in the ITT population and PD-L1-positive population. Secondary endpoints include objective response rate and duration of response.

About the IMpassion131 study

The IMpassion131 study is a Phase III, multi-center, randomized, double-blind study evaluating the efficacy and safety of Tecentriq in combination with paclitaxel, in comparison to placebo plus paclitaxel, in people with previously untreated, inoperable, locally advanced or metastatic TNBC. The study enrolled 651 people who were randomized in a 2:1 ratio to receive Tecentriq or placebo plus paclitaxel. The primary endpoint is PFS per investigator assessment (RECIST 1.1) in the PD-L1-positive population, followed by intention-to-treat (ITT) population. Secondary endpoints include OS, objective response rate, and duration of response in the PD-L1-positive and ITT populations.

About triple-negative breast cancer

Breast cancer is the most common cancer among women worldwide. According to the American Cancer Society, close to 280,000 people in the United States will be diagnosed with invasive breast cancer, and more than 42,000 will die from the disease in 2020. Breast cancer is not one, but many diseases based on the biology of each tumor. In triple-negative breast cancer, tumor cells lack hormone receptors and do not have excess HER2 protein. Approximately 15 percent of breast cancers are triple-negative based on the results of diagnostic tests. It is an aggressive form of the disease with few treatment options.

About Tecentriq (atezolizumab)

Tecentriq is a monoclonal antibody designed to bind with a protein called PD-L1. Tecentriq is designed to bind to PD-L1 expressed on tumor cells and tumor-infiltrating immune cells, blocking its interactions with both PD-1 and B7.1 receptors. By inhibiting PD-L1, Tecentriq may enable the re-activation of T cells. Tecentriq may also affect normal cells.

Tecentriq U.S. Indications (pronounced t-SEN-trik)

Tecentriq is a prescription medicine used to treat adults with:

A type of bladder and urinary tract cancer called urothelial carcinoma.

Tecentriq may be used in patients with urothelial carcinoma if their bladder cancer has spread or cannot be removed by surgery, and if they have any one of the following conditions:

The approval of Tecentriq in these patients is based on a study that measured the amount of time until patients disease worsened. Continued approval for this use may depend on the results of an ongoing study to confirm benefit.

A type of lung cancer called non-small cell lung cancer (NSCLC).

Tecentriq may be used alone as the first treatment in patients with lung cancer if:

Tecentriq may be used with the medicines bevacizumab, paclitaxel, and carboplatin as the first treatment in patients with lung cancer if:

Tecentriq may be used with the medicines paclitaxel protein-bound and carboplatin as the first treatment in patients with lung cancer if:

Tecentriq may be used alone in patients with lung cancer if:

A type of breast cancer called triple-negative breast cancer (TNBC).

Tecentriq may be used with the medicine paclitaxel protein-bound in patients with TNBC when their breast cancer:

The approval of Tecentriq in these patients is based on a study that measured the amount of time until patients disease worsened. Continued approval for this use may depend on the results of an ongoing study to confirm benefit.

A type of lung cancer called small cell lung cancer (SCLC).

A type of liver cancer called hepatocellular carcinoma (HCC).

Tecentriq may be used with the medicine bevacizumab when a patients liver cancer:

A type of skin cancer called melanoma.

Tecentriq may be used with the medicines cobimetinib and vemurafenib when a patients melanoma:

It is not known if Tecentriq is safe and effective in children.

Important Safety Information

The most important information about Tecentriq is:

Tecentriq can cause the immune system to attack normal organs and tissues and can affect the way they work. These problems can sometimes become serious or life-threatening and can lead to death.

Patients should call or see their healthcare provider right away if they get any symptoms of the following problems or these symptoms get worse.

Tecentriq can cause serious side effects, including:

Getting medical treatment right away may help keep these problems from becoming more serious. A healthcare provider may treat patients with corticosteroid or hormone replacement medicines. A healthcare provider may delay or completely stop treatment with Tecentriq if patients have severe side effects.

Before receiving Tecentriq, patients should tell their healthcare provider about all of their medical conditions, including if they:

Patients should tell their healthcare provider about all the medicines they take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.

The most common side effects of Tecentriq when used alone include:

The most common side effects of Tecentriq when used in lung cancer with other anti-cancer medicines include:

The most common side effects of Tecentriq when used in TNBC with paclitaxel protein-bound include:

The most common side effects of Tecentriq when used in hepatocellular carcinoma with bevacizumab include:

The most common side effects of Tecentriq when used in melanoma with cobimetinib and vemurafenib include:

Tecentriq may cause fertility problems in females, which may affect their ability to have children. Patients should talk to their healthcare provider if they have concerns about fertility.

These are not all the possible side effects of Tecentriq. Patients should ask their healthcare provider or pharmacist for more information. Patients should call their doctor for medical advice about side effects of Tecentriq.

Report side effects to the FDA at (800) FDA-1088 or http://www.fda.gov/medwatch. Report side effects to Genentech at (888) 835-2555.

Please visit http://www.Tecentriq.com for the full Tecentriq Prescribing Information for additional Important Safety Information.

About Genentech in cancer immunotherapy

Genentech has been developing medicines to redefine treatment in oncology for more than 35 years, and today, realizing the full potential of cancer immunotherapy is a major area of focus. With more than 20 immunotherapy molecules in development, Genentech is investigating the potential benefits of immunotherapy alone, and in combination with various chemotherapies, targeted therapies and other immunotherapies with the goal of providing each person with a treatment tailored to harness their own unique immune system.

In addition to Genentechs approved PD-L1 checkpoint inhibitor, the companys broad cancer immunotherapy pipeline includes other checkpoint inhibitors, individualized neoantigen therapies and T cell bispecific antibodies. For more information visit http://www.gene.com/cancer-immunotherapy.

About Genentech

Founded more than 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious and life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit http://www.gene.com.

Read the original:
Genentech Presents New Data From Multiple Phase III Studies of Tecentriq in Triple-Negative Breast Cancer at ESMO Virtual Congress 2020 - Business...

Recommendation and review posted by Bethany Smith

Researchers say your biological sex affects gene expression in nearly every type of tissue influencing body fat, cancer and birth weight.

Gene expression is the amount of product created by a gene for cell function, the international team of researchers explained.

They said their findings could prove important for personalised medicine, creating new drugs and predicting patient outcomes.

"These discoveries suggest the importance of considering sex as a biological variable in human genetics and genomics studies," said project leader Barbara Stranger, an associate professor of pharmacology at Northwestern University Feinberg School of Medicine in Chicago.

Unreported links

The researchers analysed 44 types of healthy human tissue from 838 people to find out if there were differences between women and men in the average amount of gene expression.

They discovered that 37% of all human genes were expressed at different levels in women and men in at least one type of tissue.

They also identified 369 instances where a genetic variant present in males and females affected gene expression to a different degree in each sex. This led to the discovery of 58 previously unreported links between genes and blood pressure, cholesterol levels, breast cancer and body fat percentage.

Gender differences in gene expression were also found for genes involved in how the body responds to medications, how women control blood sugar levels in pregnancy, how the immune system functions and how cancer develops.

Critical component of personalised medicine

"If specific genes or genetic variants contribute differentially to a given trait in males and females, it could suggest sex-specific biomarkers, therapeutics and drug dosing," Stranger said in a Northwestern news release.

"In the future, such knowledge may form a critical component of personalised medicine or may reveal disease biology that remains obscured when considering males and females as a single group," she said.

The study was published in the journal Science.

Image credit: iStock

Excerpt from:
Your sex affects your genes for body fat, cancer and birth weight - Health24

Recommendation and review posted by Bethany Smith

KENILWORTH, N.J.--(BUSINESS WIRE)--AstraZeneca and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced final results from the Phase 3 PROfound trial which showed LYNPARZA demonstrated a statistically significant and clinically meaningful improvement in overall survival (OS) versus enzalutamide or abiraterone in men with metastatic castration-resistant prostate cancer (mCRPC) who have BRCA1/2 or ATM gene mutations. Patients had progressed on prior treatment with enzalutamide and/or abiraterone.

Prostate cancer is the second most common type of cancer in men, with an estimated 1.3 million new patients diagnosed worldwide in 2018. Approximately 20-30% of men with mCRPC have an homologous recombination repair (HRR) gene mutation, of which BRCA1/2 and ATM mutations are a subpopulation. Approximately 10-20% of early stage hormone-sensitive prostate cancer cases will develop into CRPC within approximately five years.

In the key secondary endpoint of OS in men with BRCA1/2 or ATM gene mutations, LYNPARZA reduced the risk of death by 31% vs. retreatment with enzalutamide or abiraterone (HR 0.69 [95% CI, 0.50, 0.97], p=0.0175). Median OS was 19.1 months for LYNPARZA vs. 14.7 months for enzalutamide or abiraterone, despite 66% of men on these treatments having crossed over to receive treatment with LYNPARZA following disease progression.

An exploratory analysis also showed a non-statistically significant improvement in OS in the overall trial population of men with HRR gene mutations (BRCA1/2, ATM, CDK12 and 11 other HRR-mutated [HRRm] genes), reducing the risk of death by 21% with LYNPARZA vs. enzalutamide or abiraterone (HR 0.79 [95% CI, 0.61, 1.03]. Median OS was 17.3 months vs. 14 months for enzalutamide or abiraterone.

The most common adverse reactions (ARs) 15% were anemia (50%), nausea (43%), fatigue/asthenia (42%), decreased appetite (31%), diarrhea (21%), vomiting (20%) and constipation (19%). Grade 3 or above ARs were anemia (23%), nausea (2%), fatigue or asthenia (3%), decreased appetite (2%) and diarrhea (1%). Twenty percent of patients on LYNPARZA discontinued treatment due to ARs and 23% had their dose reduced due to an AR.

Dr. Johann de Bono, one of the principal investigators of the PROfound trial and head of drug development at the Institute for Cancer Research and the Royal Marsden Hospital, said, LYNPARZA has demonstrated significant clinical benefit across key endpoints in PROfound and the final overall survival results for men with BRCA1/2 or ATM mutations reinforce its potential to change the standard of care for men with metastatic castration-resistant prostate cancer. The PROfound trial shows that LYNPARZA can play an important role in this new era of precision medicine in prostate cancer, bringing targeted therapy at a molecular level to patients with a historically poor prognosis and few treatment options.

Dr. Jos Baselga, executive vice president, Oncology R&D, AstraZeneca said, These results help to transform the treatment landscape in certain men with metastatic castration-resistant prostate cancer, where overall survival has been very difficult to achieve. LYNPARZA is the only PARP inhibitor to demonstrate overall survival versus enzalutamide or abiraterone for men with BRCA or ATM mutations. We look forward to continuing to bring LYNPARZA to these patients around the world.

Dr. Roy Baynes, senior vice president and head of global clinical development, chief medical officer, Merck Research Laboratories, said, The PROfound trial is the first positive Phase 3 trial using molecular biomarker testing to help identify treatment options for certain men with metastatic castration resistant prostate cancer. These results further underpin the importance of genomic testing for HRR gene mutations to help identify this at-risk patient population and help physicians make treatment decisions. These results demonstrate the potential of LYNPARZA for mCRPC patients with certain HRR mutations.

Final OS results from the PROfound trial were presented on Sunday, Sept. 20, 2020, during the Presidential Symposium at the European Society for Medical Oncology (ESMO) Virtual Congress 2020 and published simultaneously in The New England Journal of Medicine.

Summary of OS results

OS data cut-off date was March 20, 2020.

Men with BRCA1/2 and ATM mutations (Cohort A)Secondary Endpoint

Overall populationof men with HRR mutations(Cohorts A+B)Exploratory Endpoint

LYNPARZA n=162

Control

n=83

LYNPARZA n=256

Control

n=131

Median, months

19.1

14.7

17.3

14.0

Hazard ratio (95% CI)

0.69 (0.50, 0.97)

0.79 (0.61, 1.03)

P-value

0.0175

N/A

The Phase 3 PROfound trial had met its primary endpoint in August 2019, showing significantly improved radiographic progression-free survival (rPFS) in men with mutations in BRCA1/2 or ATM genes, and had met a key secondary endpoint of rPFS in the overall HRRm population, which formed the basis of the U.S. Food and Drug Administration approval in May 2020. Regulatory reviews are ongoing in the EU and other regions.

AstraZeneca and Merck are exploring additional trials in metastatic prostate cancer including the ongoing Phase 3 PROpel trial, with first data expected in 2021, evaluating LYNPARZA as a first-line medicine for patients with mCRPC in combination with abiraterone acetate versus abiraterone acetate alone.

About PROfound

PROfound is a prospective, multi-center, randomized, open-label, Phase 3 trial evaluating the efficacy and safety of LYNPARZA versus enzalutamide or abiraterone in patients with mCRPC who have progressed on prior treatment with abiraterone or enzalutamide and have a qualifying HRR tumor mutation (BRCA1/2, ATM, CDK12, BARD1, BRIP2, CHEK1, CHEK2, PALB2, PPP2R2A, RAD51B, RAD51D, RAD54L).

The trial was designed to analyze patients with HRRm genes in two cohorts: the primary endpoint was rPFS in those with mutations in BRCA1/2 or ATM genes and then, if LYNPARZA showed clinical benefit, a formal analysis was performed of the overall trial population of patients with HRRm genes (BRCA1/2, ATM, CDK12 and 11 other HRR mutated genes; a key secondary endpoint).

In the U.S., patients are selected for treatment with LYNPARZA based on the following FDA-approved companion diagnostics:

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

There are no contraindications for LYNPARZA.

WARNINGS AND PRECAUTIONS

Myelodysplastic Syndrome/Acute Myeloid Leukemia (MDS/AML): Occurred in <1.5% of patients exposed to LYNPARZA monotherapy, and the majority of events had a fatal outcome. The duration of therapy in patients who developed secondary MDS/AML varied from <6 months to >2 years. All of these patients had previous chemotherapy with platinum agents and/or other DNA-damaging agents, including radiotherapy, and some also had a history of more than one primary malignancy or of bone marrow dysplasia.

Do not start LYNPARZA until patients have recovered from hematological toxicity caused by previous chemotherapy (Grade 1). Monitor complete blood count for cytopenia at baseline and monthly thereafter for clinically significant changes during treatment. For prolonged hematological toxicities, interrupt LYNPARZA and monitor blood count weekly until recovery.

If the levels have not recovered to Grade 1 or less after 4 weeks, refer the patient to a hematologist for further investigations, including bone marrow analysis and blood sample for cytogenetics. Discontinue LYNPARZA if MDS/AML is confirmed.

Pneumonitis: Occurred in <1% of patients exposed to LYNPARZA, and some cases were fatal. If patients present with new or worsening respiratory symptoms such as dyspnea, cough, and fever, or a radiological abnormality occurs, interrupt LYNPARZA treatment and initiate prompt investigation. Discontinue LYNPARZA if pneumonitis is confirmed and treat patient appropriately.

Embryo-Fetal Toxicity: Based on its mechanism of action and findings in animals, LYNPARZA can cause fetal harm. A pregnancy test is recommended for females of reproductive potential prior to initiating treatment.

Females

Advise females of reproductive potential of the potential risk to a fetus and to use effective contraception during treatment and for 6 months following the last dose.

Males

Advise male patients with female partners of reproductive potential or who are pregnant to use effective contraception during treatment and for 3 months following the last dose of LYNPARZA and to not donate sperm during this time.

Venous Thromboembolic Events: Including pulmonary embolism, occurred in 7% of patients with metastatic castration-resistant prostate cancer who received LYNPARZA plus androgen deprivation therapy (ADT) compared to 3.1% of patients receiving enzalutamide or abiraterone plus ADT in the PROfound study. Patients receiving LYNPARZA and ADT had a 6% incidence of pulmonary embolism compared to 0.8% of patients treated with ADT plus either enzalutamide or abiraterone. Monitor patients for signs and symptoms of venous thrombosis and pulmonary embolism, and treat as medically appropriate, which may include long-term anticoagulation as clinically indicated.

ADVERSE REACTIONSFirst-Line Maintenance BRCAm Advanced Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: nausea (77%), fatigue (67%), abdominal pain (45%), vomiting (40%), anemia (38%), diarrhea (37%), constipation (28%), upper respiratory tract infection/influenza/ nasopharyngitis/bronchitis (28%), dysgeusia (26%), decreased appetite (20%), dizziness (20%), neutropenia (17%), dyspepsia (17%), dyspnea (15%), leukopenia (13%), UTI (13%), thrombocytopenia (11%), and stomatitis (11%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: decrease in hemoglobin (87%), increase in mean corpuscular volume (87%), decrease in leukocytes (70%), decrease in lymphocytes (67%), decrease in absolute neutrophil count (51%), decrease in platelets (35%), and increase in serum creatinine (34%).

ADVERSE REACTIONSFirst-Line Maintenance Advanced Ovarian Cancer in Combination with Bevacizumab

Most common adverse reactions (Grades 1-4) in 10% of patients treated with LYNPARZA/bevacizumab compared to a 5% frequency for placebo/bevacizumab in the first-line maintenance setting for PAOLA-1 were: nausea (53%), fatigue (including asthenia) (53%), anemia (41%), lymphopenia (24%), vomiting (22%) and leukopenia (18%). In addition, the most common adverse reactions (10%) for patients receiving LYNPARZA/bevacizumab irrespective of the frequency compared with the placebo/bevacizumab arm were: diarrhea (18%), neutropenia (18%), urinary tract infection (15%), and headache (14%).

In addition, venous thromboembolic events occurred more commonly in patients receiving LYNPARZA/bevacizumab (5%) than in those receiving placebo/bevacizumab (1.9%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients for LYNPARZA in combination with bevacizumab in the first-line maintenance setting for PAOLA-1 were: decrease in hemoglobin (79%), decrease in lymphocytes (63%), increase in serum creatinine (61%), decrease in leukocytes (59%), decrease in absolute neutrophil count (35%), and decrease in platelets (35%).

ADVERSE REACTIONSMaintenance Recurrent Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA in the maintenance setting for SOLO-2 were: nausea (76%), fatigue (including asthenia) (66%), anemia (44%), vomiting (37%), nasopharyngitis/upper respiratory tract infection (URI)/influenza (36%), diarrhea (33%), arthralgia/myalgia (30%), dysgeusia (27%), headache (26%), decreased appetite (22%), and stomatitis (20%).

Study 19: nausea (71%), fatigue (including asthenia) (63%), vomiting (35%), diarrhea (28%), anemia (23%), respiratory tract infection (22%), constipation (22%), headache (21%), decreased appetite (21%), and dyspepsia (20%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the maintenance setting (SOLO-2/Study 19) were: increase in mean corpuscular volume (89%/82%), decrease in hemoglobin (83%/82%), decrease in leukocytes (69%/58%), decrease in lymphocytes (67%/52%), decrease in absolute neutrophil count (51%/47%), increase in serum creatinine (44%/45%), and decrease in platelets (42%/36%).

ADVERSE REACTIONSAdvanced gBRCAm Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer after 3 or more lines of chemotherapy (pooled from 6 studies) were: fatigue/asthenia (66%), nausea (64%), vomiting (43%), anemia (34%), diarrhea (31%), nasopharyngitis/upper respiratory tract infection (URI) (26%), dyspepsia (25%), myalgia (22%), decreased appetite (22%), and arthralgia/musculoskeletal pain (21%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer (pooled from 6 studies) were: decrease in hemoglobin (90%), mean corpuscular volume elevation (57%), decrease in lymphocytes (56%), increase in serum creatinine (30%), decrease in platelets (30%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSgBRCAm, HER2-negative Metastatic Breast Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in OlympiAD were: nausea (58%), anemia (40%), fatigue (including asthenia) (37%), vomiting (30%), neutropenia (27%), respiratory tract infection (27%), leukopenia (25%), diarrhea (21%), and headache (20%).

Most common laboratory abnormalities (Grades 1-4) in >25% of patients in OlympiAD were: decrease in hemoglobin (82%), decrease in lymphocytes (73%), decrease in leukocytes (71%), increase in mean corpuscular volume (71%), decrease in absolute neutrophil count (46%), and decrease in platelets (33%).

ADVERSE REACTIONSFirst-Line Maintenance gBRCAm Metastatic Pancreatic Adenocarcinoma

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: fatigue (60%), nausea (45%), abdominal pain (34%), diarrhea (29%), anemia (27%), decreased appetite (25%), constipation (23%), vomiting (20%), back pain (19%), arthralgia (15%), rash (15%), thrombocytopenia (14%), dyspnea (13%), neutropenia (12%), nasopharyngitis (12%), dysgeusia (11%), and stomatitis (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: increase in serum creatinine (99%), decrease in hemoglobin (86%), increase in mean corpuscular volume (71%), decrease in lymphocytes (61%), decrease in platelets (56%), decrease in leukocytes (50%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSHRR Gene-mutated Metastatic Castration Resistant Prostate Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA for PROfound were: anemia (46%), fatigue (including asthenia) (41%), nausea (41%), decreased appetite (30%), diarrhea (21%), vomiting (18%), thrombocytopenia (12%), cough (11%), and dyspnea (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for PROfound were: decrease in hemoglobin (98%), decrease in lymphocytes (62%), decrease in leukocytes (53%), and decrease in absolute neutrophil count (34%).

DRUG INTERACTIONS

Anticancer Agents: Clinical studies of LYNPARZA with other myelosuppressive anticancer agents, including DNA-damaging agents, indicate a potentiation and prolongation of myelosuppressive toxicity.

CYP3A Inhibitors: Avoid coadministration of strong or moderate CYP3A inhibitors when using LYNPARZA. If a strong or moderate CYP3A inhibitor must be coadministered, reduce the dose of LYNPARZA. Advise patients to avoid grapefruit, grapefruit juice, Seville oranges, and Seville orange juice during LYNPARZA treatment.

CYP3A Inducers: Avoid coadministration of strong or moderate CYP3A inducers when using LYNPARZA.

USE IN SPECIFIC POPULATIONS

Lactation: No data are available regarding the presence of olaparib in human milk, its effects on the breastfed infant or on milk production. Because of the potential for serious adverse reactions in the breastfed infant, advise a lactating woman not to breastfeed during treatment with LYNPARZA and for 1 month after receiving the final dose.

Pediatric Use: The safety and efficacy of LYNPARZA have not been established in pediatric patients.

Hepatic Impairment: No adjustment to the starting dose is required in patients with mild or moderate hepatic impairment (Child-Pugh classification A and B). There are no data in patients with severe hepatic impairment (Child-Pugh classification C).

Renal Impairment: No dosage modification is recommended in patients with mild renal impairment (CLcr 51-80 mL/min estimated by Cockcroft-Gault). In patients with moderate renal impairment (CLcr 31-50 mL/min), reduce the dose of LYNPARZA to 200 mg twice daily. There are no data in patients with severe renal impairment or end-stage renal disease (CLcr 30 mL/min).

INDICATIONS

LYNPARZA is a poly (ADP-ribose) polymerase (PARP) inhibitor indicated:

First-Line Maintenance BRCAm Advanced Ovarian Cancer

For the maintenance treatment of adult patients with deleterious or suspected deleterious germline or somatic BRCA-mutated (gBRCAm or sBRCAm) advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

First-Line Maintenance HRD Positive Advanced Ovarian Cancer in Combination with Bevacizumab

In combination with bevacizumab for the maintenance treatment of adult patients with advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy and whose cancer is associated with homologous recombination deficiency (HRD) positive status defined by either:

Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

Maintenance Recurrent Ovarian Cancer

For the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube or primary peritoneal cancer, who are in complete or partial response to platinum-based chemotherapy.

Advanced gBRCAm Ovarian Cancer

For the treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated (gBRCAm) advanced ovarian cancer who have been treated with 3 or more prior lines of chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

gBRCAm HER2-negative Metastatic Breast Cancer

Original post:
LYNPARZA Reduced Risk of Death by 31% vs. Enzalutamide or Abiraterone for Men with BRCA1/2 or ATM-Mutated Metastatic Castration Resistant Prostate...

Recommendation and review posted by Bethany Smith

Male Breast Cancer Treatment Market forecast to 2026

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Male Breast Cancer Treatment Market size, development, key opportunity, application and forecast to 2026 | Pfizer, Roche, GlaxoSmithKline, Sanofi,...

Recommendation and review posted by Bethany Smith

Its been quite a tough year for our wildlife population.

At least 30,000 koalas across the country lost their lives in last summers devastating bushfires - and in New South Wales alone, up to 71 per cent of the population was wiped out.

Watch the full story above

Now, legislation aimed to protect the species has received backlash from some landowners.

But amongst the bad news, the country has banded together for our furry friends.

State and Federal governments have pledged millions of dollars to the cause, and people all over the country have knitted mittens to aid those affected by the fires.

But theres still a long way to go to save our koalas.

Its not good, to put it very bluntly, said Chad Staples, a zookeeper from Mogo and Featherdale Wildlife Parks.

The fires were devastating for so many species but a tree-dwelling species is going to be affected far worse.

They were already under intense pressure prior to the fires, so its not good.

A tree-dwelling species is going to be affected far worse.

Australian forests need fire to regenerate, and its very natural - but that was a big-scale, high-intensity fire, and that wiped out a lot.

If koala populations were already in big numbers, you would have that flow come back in as the forest comes back.

But because wed already isolated so many of those pockets, for them to breed back to those numbers will take decades.

As part of the rehabilitation process, its important that we keep as much of their habitat as possible.

They will come back if we can allow them to, Staples said.

With the help of zoos, we can always breed koalas to go back - but if theres nowhere for them to go back to, its pretty dire.

Koala corridors are also important so one group of koalas will not get cut off from others.

Koalas need to be able to breed with different groups within their species - and without corridors, they also cant get to new food sources or escape fires.

If you have a pocket of good habitat, that is great for that area, but you need genetic drift, Staples said.

If you have any sort of island population, theres nothing coming in or going out, so youre essentially bottlenecking - and its a very short-term solution.

The corridor allows for males to move between changing genetics and strengthening the whole genome of the population.

In some more uplifting news, Archer, a koala at Featherdale Wildlife Park, has become a dad for the first time.

And the names of Archers two baby joeys have been chosen with a little help from royalty.

The female joey is being named after Princess Eugenie, and the male is being named Jack, after her husband, Staples said.

Theyve been massive supporters and theyre dying to come back out when everyone can travel again.

Go here to read the rest:
Australia's 2020 bushfires wiped out 71 per cent of NSW's koala population - and restoring the numbers will take 'decades' - 7NEWS.com.au

Recommendation and review posted by Bethany Smith

BOTHELL, Wash. & KENILWORTH, N.J.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq: SGEN) and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced two new strategic oncology collaborations.

The companies will globally develop and commercialize Seattle Genetics ladiratuzumab vedotin, an investigational antibody-drug conjugate (ADC) targeting LIV-1, which is currently in phase 2 clinical trials for breast cancer and other solid tumors. The collaboration will pursue a broad joint development program evaluating ladiratuzumab vedotin as monotherapy and in combination with Mercks anti-PD-1 therapy KEYTRUDA (pembrolizumab) in triple-negative breast cancer, hormone receptor-positive breast cancer and other LIV-1-expressing solid tumors. Under the terms of the agreement, Seattle Genetics will receive a $600 million upfront payment and Merck will make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics is eligible for progress-dependent milestone payments of up to $2.6 billion.

Separately, Seattle Genetics has granted Merck an exclusive license to commercialize TUKYSA (tucatinib), a small molecule tyrosine kinase inhibitor, for the treatment of HER2-positive cancers, in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics will receive $125 million from Merck as an upfront payment and is eligible for progress-dependent milestones of up to $65 million.

Collaborating with Merck on ladiratuzumab vedotin will allow us to accelerate and broaden its development program in breast cancer and other solid tumors, including in combination with Mercks KEYTRUDA, while also positioning us to leverage our U.S. and European commercial operations, said Clay Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. The strategic collaboration for TUKYSA will help us reach more patients globally and benefit from the established commercial strength of one of the worlds premier pharmaceutical companies.

These two strategic collaborations will enable us to further diversify Mercks broad oncology portfolio and pipeline, and to continue our efforts to extend and improve the lives of as many patients with cancer as possible, said Dr. Roger M. Perlmutter, President, Merck Research Laboratories. We look forward to working with the team at Seattle Genetics to advance the clinical program for ladiratuzumab vedotin, which has shown compelling signals of efficacy in early studies, and to bring TUKYSA to even more patients with cancer around the world.

Ladiratuzumab Vedotin Collaboration Details

Under the terms of the agreement, Seattle Genetics and Merck will collaborate and equally share costs on the global development of ladiratuzumab vedotin and other LIV-1-targeting ADCs. The companies have agreed to jointly develop and share future costs and profits for ladiratuzumab vedotin on a 50:50 basis worldwide. Merck will pay Seattle Genetics $600 million upfront and make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics will be eligible to receive up to $2.6 billion in milestone payments, including $850 million in development milestones and $1.75 billion in sales milestones.

The companies will jointly develop and commercialize ladiratuzumab vedotin and equally share profits worldwide. The companies will co-commercialize in the U.S. and Europe. Seattle Genetics will be responsible for marketing applications for approval in the U.S. and Canada, and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in Europe and in countries outside the U.S. and Canada, and will record sales in countries outside the U.S., Europe and Canada. Including the upfront payment, equity investment proceeds and potential milestone payments, Seattle Genetics is eligible to receive up to $4.2 billion.

The closing of the equity investment is contingent on completion of review under the Hart-Scott-Rodino Antitrust Improvements Act of 1976 (HSR Act).

TUKYSA Collaboration Details

Under the terms of the agreement, Merck has been granted exclusive rights to commercialize TUKYSA in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics retains commercial rights and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in its territory, supported by the positive results from the HER2CLIMB clinical trial.

Merck will also co-fund a portion of the TUKYSA global development plan, which encompasses several ongoing and planned trials across HER2-positive cancers, including breast, colorectal, gastric and other cancers set forth in a global product development plan. Seattle Genetics will continue to lead ongoing TUKYSA global development planning and operational execution. Merck will solely fund and conduct country-specific clinical trials necessary to support anticipated regulatory applications in its territory.

Seattle Genetics will receive from Merck $125 million as an upfront payment and is eligible to receive progress-dependent milestones of up to $65 million. Seattle Genetics will also receive $85 million in prepaid research and development payments to be applied to Mercks global development funding obligations. In addition, Seattle Genetics would receive tiered royalties on sales of TUKYSA in Mercks territory.

The financial impact of these collaborations is not included in Seattle Genetics 2020 guidance.

Seattle Genetics Conference Call Details

Seattle Genetics management will host a conference call to discuss these collaborations today at 6:00 a.m. Pacific Time (PT); 9:00 a.m. Eastern Time (ET). The event will be simultaneously webcast and available for replay from the Seattle Genetics website at http://www.seattlegenetics.com, under the Investors section. Investors may also participate in the conference call by calling 844-763-8274 (domestic) or +1 412-717-9224 (international). The conference ID is 10147850.

About Ladiratuzumab Vedotin

Ladiratuzumab vedotin is a novel investigational ADC targeted to LIV-1. Most metastatic breast cancers express LIV-1, which also has been detected in several other cancers, including lung, head and neck, esophageal and gastric. Ladiratuzumab vedotin utilizes Seattle Genetics proprietary ADC technology and consists of a LIV-1-targeted monoclonal antibody linked to a potent microtubule-disrupting agent, monomethyl auristatin E (MMAE) by a protease-cleavable linker. This novel ADC is designed to bind to LIV-1 on cancer cells and release the cell-killing agent into target cells upon internalization. Ladiratuzumab vedotin may also cause antitumor activity through other mechanisms, including activation of an immune response by induction of immunogenic cell death.

About TUKYSA (tucatinib)

TUKYSA is an oral, small molecule tyrosine kinase inhibitor (TKI) of HER2, a protein that contributes to cancer cell growth. TUKYSA in combination with trastuzumab and capecitabine was approved by the U.S. Food and Drug Administration (FDA) in April 2020 for adult patients with advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received one or more prior anti-HER2-based regimens in the metastatic setting. In addition, TUKYSA received approval in Canada, Singapore, Australia and Switzerland under the Project Orbis initiative of the FDA Oncology Center of Excellence that provides a framework for concurrent submission and review of oncology products among international partners. A marketing application is under review in the European Union.

TUKYSA is being evaluated in several ongoing clinical trials and additional studies are planned. Current trials include the following:

For additional information, visit http://www.clinicaltrials.gov.

TUKYSA Important Safety Information

Warnings and Precautions

If diarrhea occurs, administer antidiarrheal treatment as clinically indicated. Perform diagnostic tests as clinically indicated to exclude other causes of diarrhea. Based on the severity of the diarrhea, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Monitor ALT, AST, and bilirubin prior to starting TUKYSA, every 3 weeks during treatment, and as clinically indicated. Based on the severity of hepatoxicity, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Adverse Reactions

Serious adverse reactions occurred in 26% of patients who received TUKYSA. Serious adverse reactions in 2% of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea (2%), abdominal pain (2%), and seizure (2%). Fatal adverse reactions occurred in 2% of patients who received TUKYSA including sudden death, sepsis, dehydration, and cardiogenic shock.

Adverse reactions led to treatment discontinuation in 6% of patients who received TUKYSA; those occurring in 1% of patients were hepatotoxicity (1.5%) and diarrhea (1%). Adverse reactions led to dose reduction in 21% of patients who received TUKYSA; those occurring in 2% of patients were hepatotoxicity (8%) and diarrhea (6%).

The most common adverse reactions in patients who received TUKYSA (20%) were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash.

Lab Abnormalities

In HER2CLIMB, Grade 3 laboratory abnormalities reported in 5% of patients who received TUKYSA were: decreased phosphate, increased ALT, decreased potassium, and increased AST. The mean increase in serum creatinine was 32% within the first 21 days of treatment with TUKYSA. The serum creatinine increases persisted throughout treatment and were reversible upon treatment completion. Consider alternative markers of renal function if persistent elevations in serum creatinine are observed.

Drug Interactions

Use in Specific Populations

For more information, please see the full Prescribing Information for TUKYSA here.

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High or Mismatch Repair Deficient Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Microsatellite Instability-High or Mismatch Repair Deficient Colorectal Cancer

KEYTRUDA is indicated for the first-line treatment of patients with unresectable or metastatic MSI-H or dMMR colorectal cancer (CRC).

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Tumor Mutational Burden-High

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic tumor mutational burden-high (TMB-H) [10 mutations/megabase (mut/Mb)] solid tumors, as determined by an FDA-approved test, that have progressed following prior treatment and who have no satisfactory alternative treatment options. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with TMB-H central nervous system cancers have not been established.

Cutaneous Squamous Cell Carcinoma

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cutaneous squamous cell carcinoma (cSCC) that is not curable by surgery or radiation.

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

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Seattle Genetics and Merck Announce Two Strategic Oncology Collaborations - Business Wire

Recommendation and review posted by Bethany Smith

Fact.MR has recently added a new research report on the global CRISPR and Cas Genes market size to its repository. This report aims to help readers in understanding key technologies as well as product developments in this market during the forecast period of 2020 to 2026. Analysts at Fact.MR highlight that the global CRISPR and Cas Genes market will show growth at a prominent CAGR of 21.2% during the period of analysis.

This report intends to offer an in-depth analysis of various important aspects such as opportunities, drivers, challenges, and restraints of the global CRISPR and Cas Genes market. In addition to this, it provides detailed data on various key players working in this market together with important data on their diverse business strategies to maintain their prominent market position.

The overall share, volume, and other additional important information of important players is also precisely presented in the latest report on the global CRISPR and Cas Genes market. Apart from this, readers get a clear idea about emerging players and the competitive landscape of the market for CRISPR and Cas Genes during the forecast period of 2020 to 2026. This aside, the report covers important data on strengths, weaknesses, and threats of all important vendors in the global CRISPR and Cas Genes market.

The report on the global CRISPR and Cas Genes market offers detailed analysis on various activities that impact on the growth of this market. Thus, the report includes reliable data on partnerships, new product launches, mergers, and acquisitions occurring in the global CRISPR and Cas Genes market during the period of analysis.

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Fact.MRs latest report delivers a complete study of the impact of COVID-19 on the CRISPR and Cas Genes market in the present situation. At the same time, it gives readers an idea about the potential effects of the COVID-19 pandemic during the forecast period of 2020 to 2026. The report gives region-wise as well as country-wise data related to the impact of COVID-19 on the growth of the global CRISPR and Cas Genes market. Apart from this, the report talks about diverse strategies executed by industry leaders to deal with this critical situation. This information is intended to assist all key entities while handling critical situations and continuing the work successfully during this pandemic.

The global CRISPR and Cas Genes market study delivers data on the present market situation on regional as well as global levels. In addition to this, it offers forecasts on market development during the assessment period. To offer this top-notch study, the analysts at Fact.MR has utilized diverse industrial as well as digitalization tools. These tools have helped them to present futuristic insights to readers on the global CRISPR and Cas Genes market. In addition to this, the report covers a basic overview of the CRISPR and Cas Genes market and its taxonomy. This data helps in improving the overall reader experience.

Depending on product type, the CRISPR and Cas Genes market report is divided into the following segments:

Based on end-use, the CRISPR and Cas Genes market report is bifurcated into:

Major players profiled in the report on the global CRISPR and Cas Genes market include:

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Key regions covered in the global CRISPR and Cas Genes market report are:

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CRISPR and Cas Genes Market to Witness Positive Growth owing to Outbreak of COVID-19, Projects Fact.MR - The Cloud Tribune

Recommendation and review posted by Bethany Smith

Researchers say they have potentially developed a new, more convenient tests for the coronavirus that uses the genetic technology known as CRISPR and could produce results in less than an hour.

The researchers at Massachusetts Institute of Technology and the Broad Institute say the new test, known as STOPCovid, was found to be as accurate as the current molecular test known as aPCR test. They tested 400 patient samples and the new test was found to detect 93% of positive cases.Their findings were published in theNew England Journal of Medicine this week.

"We found that we could essentially match the gold standard," said Jonathan Gootenberg, a McGovern Institute fellow at MIT. "This could be done very rapidly and without expensive instrumentation."

Omar Abudayyeh, another MIT McGovern fellow working on the research, said the test is sensitive and can detect even a low amount of the virus. He said the testing would be most useful as a regular diagnostic tool that would be repeatedly test patients.

"If you're cheap enough and easy enough to run every day, you're going to capture someone when their viral load is high enough that you'll be able to take them out into quarantine before they can spread," Abudayyeh said.

The researchers useda CRISPR-based process to concentrate viral genetic material in a test sample. They said that would eliminate the need for the testing materials that are currently in short supply because of the pandemic, and a commercial lab would not have to process the results.

"Using these technologies will really allow for much more rapid testing down from days to sometimes less than an hour," said MIT McGovern fellow Jonathan Gootenberg. "That would enable a drastic change in how the tracing and handling of the pandemic is done."

They hope to further simplify the test so it can be used by patients at home. Gootenberg said they are working with clinical test developers to have this type of test on the market in a few months.

The researchers worked with other scientists at the University of Washington, Fred Hutchinson Cancer Research Center, Brigham and Women's Hospital, and the Ragon Institute.

See the article here:
MIT, Harvard Researchers Say They're Close To A New Rapid COVID Test - WBUR

Recommendation and review posted by Bethany Smith

An opioid-blocking vaccine could spare many people a lifetime of drug addiction, if and when its developed. COVID-19 exposed Africas inability to mitigate a pandemic; the silver lining is that it focused a spotlight on neglected tropical diseases that plague countries on the continent. Researchers in Israel are using CRISPR gene editing to improve cannabis production, helping ensure a stable supply of medical marijuana for patients all over the world.

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Join geneticist Kevin Folta and GLP editor Cameron English on this episode of Science Facts and Fallacies as they break down these latest news stories:

A vaccine for opioid addiction could spare many people a lifetime of drug decadency, and all the tragic side effects that come with it. Three candidate vaccines are currently undergoing clinical trials, but a new study suggests that such a drug may not be effective when its most needed, because the bodys immune system may counteract the vaccines effect.

Drug policy reform advocates have also challenged the ethics of developing an opioid vaccine. Why, they ask, should the federal government invest money in a speculative vaccine when it could fund proven harm-reduction strategies that ultimately reduce drug use? Moreover, could people convicted of drug offenses be required to get an opioid immunization, and who would pay for it?

Plagued by conflict, corrupt governments, poverty and lacking health care infrastructure, Africa was woefully unprepared to combat the coronavirus that rapidly made its way across the globe early in 2020. COVID-19 didnt strike Africa as hard as it did other parts of the world, fortunately enough, but it has highlighted a critical and often overlooked problem in Africa: neglected tropical diseases (NTDs).

As the name implies, these conditions get little attention from the international medical community, because they primarily afflict people in poor countries. A small contingency of infectious disease experts and philanthropies is committed to helping governments tackle the problem, however Africa ultimately has to reform its political institutions and invest in the health care infrastructure that can prevent and treat NTDs.

Researchers are improving all sorts of crops with CRISPR gene editing: everything from wheat, tomatoes and applesto cannabis. A biotech startup in Israel is utilizing the powerful new breeding technique to develop disease-resistant marijuana that can be easily grown from seed (instead of cloned) under greenhouse conditions, the goal being to produce a more stable supply of medical-grade cannabis for patients all over the world.

Subscribe to the Science Facts and Fallacies Podcast on iTunes and Spotify.

Kevin M. Folta is a professor in the Horticultural Sciences Department at the University of Florida. Follow Professor Folta on Twitter @kevinfolta

Cameron J. English is the GLPs managing editor. BIO. Follow him on Twitter @camjenglish

Continued here:
Podcast: CRISPR-edited weed; opioid addiction vaccine; Africa's neglected diseases - Genetic Literacy Project

Recommendation and review posted by Bethany Smith

CRISPR Therapeutics (NASDAQ:CRSP) has had a great run on the share market with its stock up by a significant 19% over the last three months. However, we decided to pay attention to the companys fundamentals which dont appear to give a clear sign about the companys financial health. Specifically, we decided to study CRISPR Therapeutics ROE in this article.

Return on equity or ROE is an important factor to be considered by a shareholder because it tells them how effectively their capital is being reinvested. Simply put, it is used to assess the profitability of a company in relation to its equity capital.

View our latest analysis for CRISPR Therapeutics

The formula for return on equity is:

Return on Equity = Net Profit (from continuing operations) Shareholders Equity

So, based on the above formula, the ROE for CRISPR Therapeutics is:

2.1% = US$20m US$911m (Based on the trailing twelve months to June 2020).

The return is the income the business earned over the last year. So, this means that for every $1 of its shareholders investments, the company generates a profit of $0.02.

Thus far, we have learned that ROE measures how efficiently a company is generating its profits. Based on how much of its profits the company chooses to reinvest or retain, we are then able to evaluate a companys future ability to generate profits. Assuming everything else remains unchanged, the higher the ROE and profit retention, the higher the growth rate of a company compared to companies that dont necessarily bear these characteristics.

It is quite clear that CRISPR Therapeutics ROE is rather low. Even compared to the average industry ROE of 14%, the companys ROE is quite dismal. Hence, the flat earnings seen by CRISPR Therapeutics over the past five years could probably be the result of it having a lower ROE.

Next, on comparing with the industry net income growth, we found that CRISPR Therapeutics reported growth was lower than the industry growth of 27% in the same period, which is not something we like to see.

The basis for attaching value to a company is, to a great extent, tied to its earnings growth. What investors need to determine next is if the expected earnings growth, or the lack of it, is already built into the share price. Doing so will help them establish if the stocks future looks promising or ominous. Is CRISPR Therapeutics fairly valued compared to other companies? These 3 valuation measures might help you decide.

CRISPR Therapeutics doesnt pay any dividend, meaning that potentially all of its profits are being reinvested in the business. However, this doesnt explain why the company hasnt seen any growth. So there could be some other explanations in that regard. For instance, the companys business may be deteriorating.

Overall, we have mixed feelings about CRISPR Therapeutics. Even though it appears to be retaining most of its profits, given the low ROE, investors may not be benefitting from all that reinvestment after all. The low earnings growth suggests our theory correct. That being so, the latest analyst forecasts show that the company will continue to see an expansion in its earnings. To know more about the companys future earnings growth forecasts take a look at this free report on analyst forecasts for the company to find out more.

PromotedIf youre looking to trade CRISPR Therapeutics, open an account with the lowest-cost* platform trusted by professionals, Interactive Brokers. Their clients from over 200 countries and territories trade stocks, options, futures, forex, bonds and funds worldwide from a single integrated account.

This article by Simply Wall St is general in nature. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. We aim to bring you long-term focused analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Simply Wall St has no position in any stocks mentioned. *Interactive Brokers Rated Lowest Cost Broker by StockBrokers.com Annual Online Review 2020

Have feedback on this article? Concerned about the content? Get in touch with us directly. Alternatively, email editorial-team@simplywallst.com.

Original post:
CRISPR Therapeutics AGs (NASDAQ:CRSP) Stock Is Rallying But Financials Look Ambiguous: Will The Momentum Continue? - Simply Wall St

Recommendation and review posted by Bethany Smith

MONDAY 14th September

August transfers from Alibaba show Ant Financial inheriting up to one quarter of the e-commerce giants US portfolio, making it a patent power in its own right. Read more here

The Supreme People's Court hasgranted Chinas first anti-suit injunction in a patent case, ordering Conversant not to enforce aGerman sales ban it won against Huawei in August. Read more here

In extraordinary step, DOJ antitrust head Makan Delrahim calls onthe IEEE to consider changes tolicensing rules which have been bitterly opposed by many top SEP owners. Read more here

TUESDAY 15th September

The Broad Institute has been handed a significant win by the PTAB in its ongoing CRISPR patent battle with UCAL Berkeley. Read more here

Confronting critical challenges, Taiwan's tech companies must find a way to create patent value - IAMspeaks with IP leaders from Foxconn, AU Optronics and others. Read more here

Ireland-based Solas OLED flexes its financial muscle and accuses group of tech giants of infringing patents that originated with Casio. Read more here

WEDNESDAY 16th September

The High Court of Australia could overturn a 112-year-old doctrine of patent exhaustion precedent in a much-awaited ruling that will havebroad commercial implications. Read more here

Speaking at IPBC Connect, the EPO and USPTO leaders say covid-induced changes are here to stay and warn of decreased user engagement caused by the pandemic. Read more here

Efficient infringement is an anathema to Apple, says company CEO Cook in letter to Congressman that also praises the eBay decision and calls for further study of the plague of PAEs. Read more here

THURSDAY 17th September

Ninestar, part of a formidable stable of Chinese companies focused on printing technology, is back in Canons crosshairs after a successful defence against the Japanese giant at the ITC. Read more here

There is growing pressure on US federal agencies and government departments to enforce the patents they own, especially in the life sciences arena. Read more here

The covered business method programme at the PTAB has ended, but efforts to extend it are now being made as influential banking group eyes broader conversation about patents. Read more here

FRIDAY 18th September

Settlements worth hundreds of millions of dollars with the likes of Apple and Samsung have put Korean university KAIST in the licensing big leagues. Read more here

The technological and geographic scope of InterDigitals patent portfolio means new chief licensing officer Eeva Hakoranta has a lot to play with. Read more here

Companies implementing 5G standards must consider the licensing implications of a large chunk of patents that currently lie under the radar. Read more here

SATURDAY 19th September

In this weeks Saturday Opinion, Scott Cleland argues that Googles most effective revenue growth engines have all depended, to an extent at least, on infringing IP owned by leading competitors. Read more here

Book your place at IPBC Connect today

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China's first anti-suit injunction; Apple CEO rejects efficient infringement; CRISPR patent battle latest; EPO and USPTO heads' covid warning; CBM...

Recommendation and review posted by Bethany Smith

This article was originally published here

Nat Commun. 2020 Sep 18;11(1):4711. doi: 10.1038/s41467-020-18575-6.

ABSTRACT

The recent outbreak of novel coronavirus (SARS-CoV-2) causing COVID-19 disease spreads rapidly in the world. Rapid and early detection of SARS-CoV-2 facilitates early intervention and prevents the disease spread. Here, we present an All-In-One Dual CRISPR-Cas12a (AIOD-CRISPR) assay for one-pot, ultrasensitive, and visual SARS-CoV-2 detection. By targeting SARS-CoV-2s nucleoprotein gene, two CRISPR RNAs without protospacer adjacent motif (PAM) site limitation are introduced to develop the AIOD-CRISPR assay and detect the nucleic acids with a sensitivity of few copies. We validate the assay by using COVID-19 clinical swab samples and obtain consistent results with RT-PCR assay. Furthermore, a low-cost hand warmer (~$0.3) is used as an incubator of the AIOD-CRISPR assay to detect clinical samples within 20 min, enabling an instrument-free, visual SARS-CoV-2 detection at the point of care. Thus, our method has the significant potential to provide a rapid, sensitive, one-pot point-of-care assay for SARS-CoV-2.

PMID:32948757 | DOI:10.1038/s41467-020-18575-6

Originally posted here:
Ultrasensitive and visual detection of SARS-CoV-2 using all-in-one dual CRISPR-Cas12a assay - DocWire News

Recommendation and review posted by Bethany Smith

ReportsnReports added Latest Emerging Gene Therapies Market Research Report offers crucial data on numerous market situations, for example, ability improvement elements, elements controlling the advancement, market possibilities, and risks to the global market. Also, the report widely facilities round competitive evaluation of Emerging Gene Therapies Market. The competitive evaluation section includes key producers, recent players, providers, market strategies, ability chances, operation panorama, and evaluation of the traits of the Emerging Gene Therapies Market.

Request for FREE Sample Report @ https://www.reportsnreports.com/contacts/requestsample.aspx?name=1854862

Top Company Profile Analysis in this Report-

AmgenGilead SciencesNovartisSanofiGlaxoSmithKlinePfizer

Emerging Gene Therapies Market Report provides a comprehensive overview of the emerging gene therapy market. The report discusses gene therapy and the technology behind gene editing, outlining the advantages, limitations and current evidence for the platforms under development. The report discusses relevant clinical studies targeting specific therapeutic indications and highlights examples of current challenges within the field, with a focus on therapies that target the eye, liver, and blood.

Additionally, the report provides a background to the CRISPR patent litigation, a key factor within the gene editing company landscape. It provides profiles of six companies developing gene editing platforms, considers the gene therapy interests of the main pharmaceutical companies, and discusses current regulatory trends in the development of gene therapies.

Emerging Gene Therapies Market Report explores how emerging gene editing products will compete with established products, their relative competitive strengths, and upcoming value inflection points within the field.

Scope of this Report- What are the key emerging products within the gene therapy landscape? Which companies have the strongest pipeline of innovative products? How will gene editing disrupt existing gene therapy products? What are the regulatory trends for emerging gene therapies? What are the interests of pharmaceutical companies within the field?

Reasons to buy this Report- Achieve an up-to-date understanding of the area, with a comprehensive reference of key products within the gene therapy landscape, compared across technology-specific relevant characteristics such as editing mechanism and delivery vector. Conduct competitive analysis using indication-specific, side-by-side comparisons of the latest data for key gene therapy products in the strategically relevant areas of eye, blood, and liver. Conduct strategic analysis using an overview of gene therapy specific considerations for evaluating and developing gene therapy products the CRISPR patent space, emerging regulatory trends, innovation leaders and the interests of pharma in gene therapy.

Single User License: US $ 2995

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Table of Contents1.1 List of Tables 71.2 List of Figures 82 Introduction 102.1 Gene Therapy Definitions 102.2 Report Coverage the Emerging Gene Therapy Pipeline 112.3 History of Gene Therapy 122.4 Limitations of Gene Transfer 132.5 The Development of Targeted Gene Editing 132.6 Overview of Gene Editing Platforms 132.6.1 Zinc Fingers (1996) 132.6.2 Transcription Activator-Like Effectors (2011) 142.6.3 The CRISPR/Cas System (2013) 152.6.4 Effectors for Targeting Domains 192.6.5 Comparison of Gene Editing Systems 192.6.6 Summary of Gene Editing Systems 192.7 Overview of In Vivo Gene Therapy 212.7.1 Editing is Dependent on Cell Type, Stage, and Repair Pathway 212.7.2 Delivery 212.7.3 Emerging Safety Concerns with Editing Platforms 242.7.4 Editing Products are Reliant on the Target Cells Cycle Stage and DNA Repair Machinery 272.7.5 Advantages of Gene Editing over Gene Transfer 282.7.6 Integration into Safe Harbor Sites 282.7.7 The Increasing Complexity of Gene Therapy 302.7.8 Summary of In Vivo Gene Therapy 313 Gene Therapy Near Term Product Pipeline 333.1 Leber Congenital Amaurosis 333.1.1 Unmet Need 333.1.2 Molecular Genetics 333.1.3 Luxturna (Voretigene neparvovec) 333.1.4 Editas Medicine: EDIT-101 353.1.5 Trial Design 363.1.6 EDIT-101 and Off-Target Effects 373.1.7 The Potential Advantage of EDIT-101 is the Longevity of its Therapeutic Effect 373.1.8 Summary LCA 383.2 Choroideremia 383.3 Hurler Syndrome (MPS I) 393.3.1 Key Clinical Studies 403.3.2 Regenex: RGX-111 403.3.3 Sangamo Therapeutics: SB-318 403.4 Hunter Syndrome (MPS II) 413.4.1 Unmet Need 413.4.2 Sangamo Therapeutics: SB-913 413.4.3 Immusoft Corporation: Cell Therapy 433.5 Sanfilippo Syndrome (MPS III) 433.5.1 Lysogene: LYS-SAF302 433.6 Summary MPS Disorders 443.7 Hemophilia 443.7.1 Hemophilia A 463.7.2 Summary Hemophilia A 503.7.3 Hemophilia B 513.7.4 Summary Hemophilia B 533.8 Hemoglobinopathies 543.8.1 Beta Thalassemia: Unmet Need 543.8.2 Beta Thalassemia: Molecular Genetics 553.8.3 Sickle Cell Disease: Unmet Need 563.8.4 Sickle Cell Disease: Molecular Genetics 563.9 Cellular Therapies for Hemoglobinopathies 573.9.1 Blue Bird Bio: BB-305 (LentiGlobin) 573.9.2 Sangamo: ST-400 603.9.3 CRISPR Therapeutics: CTX-001 613.9.4 Summary: Cellular Therapies for Hemoglobinopathies 623.10 Duchenne Muscular Dystrophy 633.10.1 Unmet Need 633.10.2 Molecular Genetics 633.10.3 ExonDys 51 Sarepta Therapeutics 643.10.4 Solid BioSciences: SGT-001 663.10.5 Exonics Therapeutics: CRISPR Approach 673.10.6 Summary Duchenne Muscular Dystrophy 684 Competitive Landscape 694.1 Regulatory Considerations for Developing Gene Therapy Products 694.1.1 Product Characteristics 694.1.2 Clinical Study Design for Gene Therapy Products 694.1.3 Disease specific guidance 704.1.4 Reimbursement and Payment 714.1.5 Summary Regulatory Considerations 724.2 Intellectual Property CRISPR/Cas 724.2.1 Licensing, Exploitation, and MPEG Pool 744.3 Company Analysis: Gene Editing Companies 754.3.1 Sangamo Therapeutics 754.3.2 CRISPR Therapeutics 794.3.3 Casebia Therapeutics 814.3.4 Editas Medicine 824.3.5 Intellia Therapeutics 844.3.6 Homology Medicines 864.4 Company Analysis: Pharma 874.4.1 Amgen 874.4.2 Gilead Sciences 874.4.3 Novartis 874.4.4 Sanofi 884.4.5 GlaxoSmithKline 884.4.6 Pfizer 885 Appendix 895.1 References 895.2 Report Methodology 98

and more

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Emerging Gene Therapies Market Report- Technological, Clinical, Regulatory and Competitive Landscape | Amgen, Gilead Sciences - The Daily Chronicle

Recommendation and review posted by Bethany Smith

RALEIGH, N.C., Sept.15, 2020 /PRNewswire/ --The AKC Canine Health Foundation, a non-profit organization dedicated to advancing the health of all dogs and their owners, has published a review of the current state of genetic testing in dogs. This valuable resource is intended to help dog breeders, owners, and veterinarians make sound decisions with regard to interpreting and understanding the implications of genetic test results.

Creation of this resource was initiated by 2019 AKC Board Chairman, Bill Feeney, and funded by the AKC Canine Health Foundation (CHF) and the Orthopedic Foundation for Animals (OFA). It was completed by Dr. Liza Gershony, a 2019 CHF Clinician Scientist Fellow, and Dr. Anita Oberbauer, CHF-funded researcher and recipient of the 2019 Asa Mays, DVM, Excellence in Canine Health Research Award - both from the University of California, Davis. The whitepaper was introduced by Dr. Oberbauer at the September 2020 American Kennel Club Delegates' meeting and is available on the CHF website at akcchf.org/geneticswhitepaper2020.

"While scientific advances in the area of canine DNA testing are exciting, they have also led to a desperate need for continued education," says Eddie Dziuk, Chief Operating Officer of the Orthopedic Foundation for Animals and member of the AKC Delegates Canine Health Committee."Dog breeders, owners, and even veterinary professionals often struggle with questions such as test purpose, accuracy, breed specificity/appropriateness, and interpretation of results. The genetics whitepaper is a long awaited and needed resource to address today's most pressing questions and make better use of these powerful tools to breed healthier dogs."

"The AKC Canine Health Foundation and its donors hope that dog breeders and caregivers use this resource to make informed and thoughtful decisions regarding their breeding plans and disease prevention and treatment strategies for individual dogs," states Dr. Calvin Carpenter, CHF Executive Director. "Genetic testing is most impactful when properly used as one of many tools available to dog owners."

The genetics whitepaper provides a foundation in canine genetics valuable to anyone involved in the care of and decision making for individual dogs or breeding stock. Practical applications and limitations of existing genetic tests are reviewed for the lay audience. This resource is offered as a tool to help improve the health of current and future generations of dogs.

About CHFSince 1995, the AKC Canine Health Foundation has leveraged the power of science to address the health needs of all dogs. With more than $58 million in funding to date, the Foundation provides grants for the highest quality canine health research and shares information on the discoveries that help prevent, treat and cure canine diseases. The Foundation meets and exceeds industry standards for fiscal responsibility, as demonstrated by their highest four-star Charity Navigator rating and GuideStar Platinum Seal of Transparency. Learn more at http://www.akcchf.org.

SOURCE AKC Canine Health Foundation

http://www.akcchf.org

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AKC Canine Health Foundation Publishes Whitepaper on the State of Genetic Testing in Dogs - PRNewswire

Recommendation and review posted by Bethany Smith

Dr. Emily Bromley, Guest columnist

Health Matters: Newborn Screening and Baby Safety

Did you know more babies arrive in September than in any other month? Whether due to cold winter nights or the magic of the holidays, we doctors and nurses who work in hospital birthing centers are always busy this time of year.

We love partnering and celebrating with moms, parents and families as we welcome newborns into the world. Nothing brings joy like a baby.

And we all want to help keep these new bundles of joy safe and healthy.

In September we recognize Newborn Screening Awareness and Baby Safety Month.

While still in the hospital, all babies are given a "heel stick" blood test to detect if the baby has any rare diseases or conditions so appropriate treatment can begin.

The newborn screening test will detect cystic fibrosis, phenylketonuria (PKU) and more than 50 other possible treatable conditions.

After delivery, we'll also put erythromycin ointment in the newborn's eyes, and give a vitamin K shot to help with blood clotting along with giving a hepatitis B vaccine.

This routine screening and treatment helps ensure babies reach their best health potential right from the start.

There's also an opportunity for prenatal and genetic testing before and during pregnancy, for moms and parents who are interested in preparing for their future family.

Horizon screening tests will determine if a parent is a recessive gene carrier of a disease, increasing the likelihood of passing it down to an infant.

And while screening provides information to best care and plan for a baby, there's a handful of items to keep in mind to keep a baby safe.

It starts in the hospital where nurses help show new parents how to clean, feed and generally care for a newborn. Our caring nurses are committed to making new moms feel comfortable and confident before taking the newborn home.

Other safety basics include "baby proofing" your home so as the baby starts to crawl, they won't get into anything hazardous or dangerous.

Sleep safety is also very important. A proper, safe crib is essential with nothing in it for the baby to suffocate in or become tangled with.

Car seat safety is also vital. If you need help checking a car seat, you may schedule an appointment with a certified technician by contacting Life Resources of Northern Michigan at 231-796-4919. There will also be a car seat safety check from 3 p.m. to 6 p.m. Oct. 16 at the Reed City Fire Department, 523 Morse St., Reed City.

Babies. We all know they're precious. Let's keep them safe and healthy!

I'm happy to "deliver" this baby screening and baby safety news to you.

-- Emily Bromley, MD, is an obstetrician at Spectrum Health Big Rapids Hospital Obstetrics, Gynecology and Urology.

Read more:
Health Matters: Newborn Screening and Baby Safety - The Pioneer

Recommendation and review posted by Bethany Smith

Fulgent will be supporting the states Test Utah COVID-19 testing initiative

TEMPLE CITY, Calif., Sept. 15, 2020 (GLOBE NEWSWIRE) -- Fulgent Genetics, Inc. (NASDAQ: FLGT) (Fulgent Genetics or the company), a technology company providing comprehensive testing solutions through its scalable technology platform, today announced a new partnership with the State of Utah for COVID-19 testing.

Through a competitive bidding process, the Utah Department of Health selected Fulgent Genetics to utilize the companys FDA EUA-approved RT-PCR test for its Test Utah COVID-19 testing initiative. This initiative was developed to increase availability of COVID-19 testing solutions for residents across the state of Utah to help stem the spread of COVID-19. Fulgents RT-PCR test is being administered at a number of fixed sites and mobile units in select counties across the state, with the potential to expand as the program grows. Samples are collected on-site and processed at Fulgents lab in Temple City, California and results are delivered to patients within an average of 24 hours of sample receipt.

We are pleased to be selected as a partner by the Utah Department of Health for their Test Utah initiative, which is making COVID-19 testing more readily available for residents of Utah, commented Brandon Perthuis, Chief Commercial Officer of Fulgent Genetics. The State of Utah joins the growing list of municipalities, healthcare providers and organizations that have selected Fulgents RT-PCR test for their COVID-19 testing needs. Our rapid turnaround time, reliable testing solutions combined with our user-friendly platforms and applications continue to be reasons why Fulgent is selected as a testing partner in these competitive situations.

As we look to stop the spread of COVID-19 and save lives across the state of Utah, we are pleased to be working with Fulgent Genetics as part of our Test Utah initiative to offer our residents a convenient and reliable testing solution for COVID-19, said Utah Governor Gary Herbert. The goal of our Test Utah initiative is to dramatically increase the rate of COVID-19 testing in the state so residents can have better access to testing and help stem the spread of COVID-19, so we can get back to normal as quickly as possible. We are thankful to have Fulgent as a partner to offer reliable and timely COVID-19 testing solutions.

For more information on the State of Utahs Test Utah program, please visit http://www.testutah.com.

About Fulgent Genetics

Fulgent Genetics proprietary technology platform has created a broad, flexible test menu and the ability to continually expand and improve its proprietary genetic reference library while maintaining accessible pricing, high accuracy and competitive turnaround times. Combining next generation sequencing (NGS) with its technology platform, the company performs full-gene sequencing with deletion/duplication analysis in an array of panels that can be tailored to meet specific customer needs. In 2019, the company launched its first patient-initiated product, Picture Genetics, a new line of at-home screening tests that combines the companys advanced NGS solutions with actionable results and genetic counseling options for individuals. Since March 2020, the company has commercially launched several tests for the detection of SARS-CoV-2, the virus that causes the novel coronavirus (COVID-19), including NGS and reverse transcription polymerase chain reaction (RT-PCR) - based tests. The company has received Emergency Use Authorization (EUA) from the U.S. Food and Drug Administration (FDA) for the RT-PCR-based tests for the detection of SARS-CoV-2 using upper respiratory specimens (nasal, nasopharyngeal, and oropharyngeal swabs) and for the at-home testing service through Picture Genetics. A cornerstone of the companys business is its ability to provide expansive options and flexibility for all clients unique testing needs through a comprehensive technology offering including cloud computing, pipeline services, record management, web portal services, clinical workflow, sequencing as a service and automated lab services.

About Picture Genetics

Through its Picture Genetics platform launched in 2019, Fulgent Genetics offers consumers direct access to its advanced genetic testing and analytics capabilities from the ease and comfort of home, at an affordable price point. The Picture Genetics platform provides a holistic approach to at-home genetic screening by including oversight from independent physicians as well as genetic counseling options to complement Fulgent Genetics comprehensive genetic testing analysis. The Picture Genetics platform currently offers multiple tests, providing medically actionable, clinical-level results with professional medical follow-up in one easy process. Visit http://www.picturegenetics.com for more information.

Story continues

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Examples of forward-looking statements in this press release include statements about, among other things: managements beliefs, judgments and estimates regarding Fulgents testing solutions, including its technology platforms and RT-PCR testing solution; the companys identification and evaluation of opportunities and its ability to capitalize on opportunities to grow its business; and its expected lab capacity and results turnaround times.

Forward-looking statements are statements other than historical facts and relate to future events or circumstances or the companys future performance, and they are based on managements current assumptions, expectations and beliefs concerning future developments and their potential effect on the companys business. These forward-looking statements are subject to a number of risks and uncertainties, which may cause the forward-looking events and circumstances described in this press release to not occur, and actual results to differ materially and adversely from those described in or implied by the forward-looking statements. These risks and uncertainties include, among others: the ongoing impacts of the COVID-19 pandemic, including the preventive public health measures that may continue to impact demand for its tests and the pandemics effects on the global supply chain; the market potential for, and the rate and degree of market adoption of, the companys tests, including its newly-developed tests for COVID-19 and genetic testing generally; the companys ability to capture a sizable share of the developing market for genetic and COVID-19 testing and to compete successfully in these markets, including its ability to continue to develop new tests that are attractive to its various customer markets, its ability to maintain turnaround times and otherwise keep pace with rapidly changing technology; the companys ability to maintain the low internal costs of its business model, particularly as the company makes investments across its business; the companys ability to maintain an acceptable margin on sales of its tests, particularly in light of increasing competitive pressures and other factors that may continue to reduce the companys sale prices for and margins on its tests; risks related to volatility in the companys results, which can fluctuate significantly from period to period; risks associated with the composition of the companys customer base, which can fluctuate from period to period and can be comprised of a small number of customers that account for a significant portion of the companys revenue; the companys ability to grow and diversify its customer base and increase demand from existing and new customers; the companys investments in its infrastructure, including its sales organization and operational capabilities, and the extent to which these investments impact the companys business and performance and enable it to manage any growth it may experience in future periods; the companys level of success in obtaining coverage and adequate reimbursement and collectability levels from third-party payors for its tests; the companys level of success in establishing and obtaining the intended benefits from partnerships, joint ventures or other relationships; the companys compliance with the various evolving and complex laws and regulations applicable to its business and its industry; risks associated with the companys international operations; the companys ability to protect its proprietary technology platform; and general industry, economic, political and market conditions. As a result of these risks and uncertainties, forward-looking statements should not be relied on or viewed as predictions of future events.

The forward-looking statements made in this press release speak only as of the date of this press release, and the company assumes no obligation to update publicly any such forward-looking statements to reflect actual results or to changes in expectations, except as otherwise required by law.

The companys reports filed with the U.S. Securities and Exchange Commission (SEC), including its annual report on Form 10-K for the year ended December 31, 2019 filed with the SEC on March 13, 2020 and the other reports it files from time to time, including subsequently filed quarterly and current reports, are made available on the companys website upon their filing with the SEC. These reports contain more information about the company, its business and the risks affecting its business.

Investor Relations Contact:The Blueshirt GroupNicole Borsje, 415-217-2633; nborsje@blueshirtgroup.com

Media Contact:The Blueshirt GroupJeff Fox, 415-828-8298, jeff@blueshirtgroup.com

Continued here:
Fulgent Genetics to Provide COVID-19 Testing Solutions for the State of Utah - Yahoo Finance

Recommendation and review posted by Bethany Smith

Supreme Court justice Ruth Bader Ginsburg has died at age 87. Ginsburg is most noted for her lifelong fight for equality for women. USA TODAY

Supreme Court Associate Justice Ruth Bader Ginsburg, who died Friday evening,had overcome four bouts with pancreatic, lung and colon cancer dating back two decades.

Ginsburg, 87,could not beat the most recent spread to her liver and died from complications of metastatic pancreatic cancer.

In January, she announcedshe was cancer-free, sayinga periodic scan and biopsy revealed lesions on her liver but that chemotherapy treatment that began in May was "yielding positive results." But by July,Ginsburg said she wasbattling cancer againand was undergoing chemotherapy after a lesion was found on her liver.

"It's fairly uncommon to have so many cancers successfully treated and then to be able to live through them, certainly as long as she did and to tolerate the treatment of these in her 80s, it's a testament to her," said Dr.Kiran Turaga, director of theSurgical Gastrointestinal Cancer Program at the University of Chicago Medicine.

Ginsburg had her first bout of cancer in 1999 when doctors discovered colon cancer at an early stage by accident due to an unrelated abdominal infection. A decade later, when Ginsburg was undergoing regular screenings, doctors discovered pancreatic cancer and removed parts of herpancreas, along with her spleen. In 2018, shehad two cancerous growths removed from her lungs again discovered by chance after she fell and broke several ribs. And last year, Ginsburgwas treatedfor a malignant tumor on her pancreas.

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Ginsburg had yet to graduate high school when her mother,Celia Bader, died from cervical cancer. Years later, her husband, Martin Ginsburg, was diagnosed with testicular cancer and underwent two surgeries. He died in 2010 of complications from metastatic cancer. The two had been married for 56 years.

"Like too many Americans, Justice Ginsburg had an extensive history with cancer having lost her mother and husband to the disease," Gary M. Reedy, CEO of the American Cancer Society, said in a statement Friday. "Her personal health history and active survivorship made her an inspiration for many patients and survivors and helped inform her deep commitment to public health policy."

Compared to colon cancer, pancreatic cancer is less common but more deadly. About 57,000 people will be diagnosed with pancreatic cancer this year, and about 47,000 people will die from it, according to the American Cancer Society. While pancreatic cancer accounts for about 3% of all cancers in the U.S., it accounts for about 7% of all cancer deaths.

"It has remained one of the most, if not the most difficult cancer for us to treat," said Dr. Brian Wolpin, director of the Gastrointestinal Cancer Center and Hale Family Center for Pancreatic Cancer Research at Dana-Farber Cancer Institute. "It does tend to present late, and there are not many specific symptoms for pancreatic cancer. They tend to be things like abdominal discomfort or weight loss."

The cancer also tends to be more aggressive,Wolpin said. It grows faster than other types of cancer and is less responsive to treatment.Less than 10% of patientssurvive five years or more after diagnosis, Wolpin said.

"She lived 10 years with this disease. She beat the odds, and it was a remarkable fight," saidDr. Timothy Donahue, chief of surgical oncology at UCLAs Jonsson Comprehensive Cancer Center. "But its not uncommon for this disease to have a long latency period and then come back or recur even more than 10 years later, so we continue to surveil these patients years after their diagnosis."

Pancreatic cancer can be painful because the pancreas is located near many nerve endings, Donahue said. It often causes back pain, he said.

"Not only is it painful, its very difficult to live with because of the weight loss and the extremely poor energy levels," Donahuesaid. "Theres something particular about this tumor that causes many issues for these patients much more so than other comparable cancers."

There are two compartments of the pancreas, andtwo larger categories of pancreatic cancer, Donahue said. Steve Jobs, for example, died from complications of a rare form of pancreatic cancer that is less aggressive.

There's no colonoscopy or mammogram equivalent for pancreatic cancer, and it's often discovered incidentally, experts say.

"We don't have a good detection. You can have a tiny little cancer, and you can operate on it, but it still has a high risk of coming back,"said Dr. Mary Mulcahy, oncologist at Lurie Cancer Center at Northwestern Memorial Hospital.

But researchers are looking into how blood-based tests may be used to screen for pancreatic cancer.

"These are still reasonably early days. Theres no standard blood test that we use yet," Wolpin said. "How we would then apply that in a large population would be hard to figure out."

Others are investigating the role of a specific cancer-causing genetic mutation, known as KRAS, which is implicated in nearly all pancreatic cancer cases, according to Donahue. There's a campaign underway to encourage all patients newly diagnosed with pancreatic cancer to get their genes sequenced so researchers can learn more about the genetics of the disease, Donahue said.

"Universal genetic testing is important not only because it might influence some of the treatments they receive for their own cancer, but also whether their immediate family members need to speak with a genetic counselor about receiving a genetic test themselves," saidAnirban Maitra, a pancreatic cancer researcher at MD Anderson Cancer Center.

'RGB': How 'Notorious' Ruth Bader Ginsburg became a pop-culture icon

Ruth Bader Ginsburg's last wish: 'I will not be replaced until a new president is installed'

While pancreatic cancer typically affects people who are older, colon canceris increasingly affecting young Americans.Deaths from colon and rectal cancers have been declining for several decades due to improved screening and treatment measures, but deaths among young people have been increasing slightly in recent years, according to researchers.

Late last month, actor Chadwick Bosemandied from colon cancerat just 43.

But science is making huge strides. In the U.S., the five-year survival rate for all cancers combined has increased substantially since the early 1960s, from 39% to 70% among white people and from 27% to 64% among Black people, according to the American Cancer Society.

"Even today, people think cancer is a death diagnosis," Turaga said. "But in the last three years, there are so many new years of treating cancers. We're making so much progress."

Contributing: Richard Wolf, Ken Alltucker, Kristine Phillips

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The Greenwood Genetic Centers (GGCs) annual Race the Helix 5K and 1-mile run/walk is celebrating its 10th year of raising awareness for families impacted by genetic disorders and providing funds to support the programs and research of the Greenwood Genetic Center.

Because of the COVID-19 pandemic, this years event will be virtual.

Runners and walkers can register at http://www.runsignup.com and complete their 5K run or 1-mile walk anywhere they choose between Sept. 26 and Oct. 3.

Participants are invited to post their participation on social media and share their race times and photos with event coordinators.

Race the Helix has become something that we look forward to hosting on our campus each fall, and it is disappointing not be able to celebrate this milestone year in person with all of our friends and supporters, said Bill Tiller, Executive Director of the GGC Foundation. But on the bright side, a virtual race means that we can share GGCs message of hope with participants far beyond our usual reach for an in-person event.

Race the Helix started in 2011 when Stephen and Jodi Shenal of Greenwood reached out to the Center with the idea as a way to show their appreciation for the care their family received after the birth of their daughter, Ryleigh, who has a rare chromosome deletion.

When Ryleigh was first diagnosed, her geneticist, Dr. Steve Skinner told us Remember, Ryleigh is still the same beautiful baby she was before this diagnosis, said Jodi. Those word comforted me then, and over these past ten years, GGCs compassionate care has provided our family with hope and encouragement beyond measure.

Along with Ryleigh, who will celebrate her 10th birthday in November, Race the Helix has grown each year both in the number of participants, as well as in funds raised for the GGC Foundation.

Last year the Greenwood event brought in over $30,000 to support GGC initiatives that benefit families worldwide.

GGCs caring employees have truly become an extension of our family, said Stephen. Were thrilled that this little idea that Jodi and I had 10 years ago has taken off in such a big way. We cant wait to see the reach of the virtual event across the country and even around the world.

All proceeds benefit the GGC Foundation which supports GGCs research and educational programs and helps defray the cost of genetic testing for uninsured or underinsured patients.

Registration for Race the Helix can be found at http://www.GGC.org or http://www.RunSignUp.com. There is a $25 fee for the 5K race. The 1-mile run/walk is free thanks to event sponsors.

Submitted by Lori Bassett

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Race the Helix 5K celebrates 10th anniversary with virtual event - Index-Journal

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