Archive for the ‘Gene Therapy Research’ Category

Conference to Highlight Personal Genomics, Genomics in Medicine, Latest Advances in Sequencing and Diagnostic Technologies and Empowering Patients

Newswise The 4th Annual Consumer Genetics Conference, taking place October 3-5 at the Seaport Hotel in Boston, will include a keynote presentation by George Church that will provide a forthright and candid assessment of new sequencing technologies, including the emergence of nanopore DNA sequencing, current trends in personal genomics, and projections on the future path of medical genomics. A professor of genetics at the Harvard Medical School, Dr. Church will close the events first day in an address that touches on his new book which will be launched hours prior: Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves (co-authored with science writer Ed Regis).

One of the best known and most highly respected molecular geneticists in the country, George Church is a pioneer in two broad areas of molecular biology: DNA sequencing technology and synthetic biology. He is the founder of the Personal Genome Project and founder or advisor to numerous DNA sequencing and genome analysis companies, including 23andMe, Knome, NABsys and Genia major genomics, sequencing and direct-to-consumer genetics companies.

The opening day of the conference includes a number of marquee presentations, including Princeton professor Lee Silver (author of Remaking Eden), who will discuss whether the commercialization environment is currently optimized for personal genetic freedom. It will also include a featured presentation by Stan Lapidus, CEO/founder of SynapDx, who will describe successful business formation and value creation in diagnostics.

The second day of the conference will then offer varying perspectives on the business and translation of personalized genomics. Panel discussions will explore topics such as venture capital, investment banking and the financial cycle from funding to IPO, highlighting the metrics by which VCs and bankers make their decisions. Day two will also emphasize the physicians perspective on incorporating genomic technologies into the clinic and answer questions such as: how practical is it?

Day three will be all about empowering patients and applications of genomics into personal quests for disease propensities, prenatal and neonatal diagnostics, nutrition, vitamins, cosmetics, and weight management programs. 23andMe, the first company to seek FDA approval of its DNA test, and Knome, a provider of ground-breaking informatics technologies and human genome interpretation tools, will describe developments in exome and whole genome sequencing and how their products are helping to empower patients while improving clinical care.

For more information on the 4th Annual Consumer Genetics Conference, including a full program schedule, please visit http://www.consumergeneticsconference.com.

For media, to register for the Consumer Genetics Conference, please contact Lynn Blenkhorn at email: lynn.blenkhorn@fkhealth.com or by calling: 508-851-0930. If you cannot attend but would like to speak with one of the presenters by phone or Skype, we would be pleased to organize a phone interview on the day of their presentation.

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George Church, Founder of the Personal Genome Project, Just Announced as Keynote Speaker at Consumer Genetics Conference

12:00 AM

The Associated Press

NEW YORK - How does a tabby cat earn its stripes? With the right DNA.

click image to enlarge

Researchers say theyve found the gene that determines the coat of the common tabby, either the so-called mackerel pattern with narrow stripes, top row, or the blotchy classic pattern, bottom row.

The Associated Press

Scientists say they've found the gene that sets the common tabby pattern -- stripes or blotches.

It's one of several genes that collaborate to create the distinctive design of a cat's coat, and it's the first of the pattern genes to be identified.

Cats with narrow stripes, the so-called "mackerel" pattern, have a working copy of the gene. But if a mutation turns the gene off, the cat ends up with the blotchy "classic" pattern, researchers reported online Thursday in the journal Science.

It's called "classic" because "cat lovers really like the blotched pattern," said one of the authors, Greg Barsh. He works at both Stanford University and the HudsonAlpha Institute of Biotechnology in Huntsville, Ala.

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Scientists find gene behind the tabby coat

From where does a tabby cat get its stripes? The same place cheetahs get their spots.

A new study finds the same gene that is responsible for the cheetah's color patterns causes a tabby's stripes. Mutations in this newly identified gene transform a tabby's typical striped pattern into a less familiar "blotched" look. In cheetahs, similar mutations smear spots into thick stripes.

"What this is, is the first connection of a gene involved in pattern formation in cats to their molecular status," said study researcher Stephen O'Brien of the National Laboratory for Cancer Research.

Now "we know where the mutation is in this particular gene" to cause the pattern changes, O'Brien told LiveScience.

Stripes or spots? O'Brien and his colleagues contributed to the original sequencing of the domestic cat genome, which was completed in 2007. Besides being interesting from a basic science standpoint, O'Brien said, cat genetics may help researchers understand human disease and genetic development. [ The 10 Coolest Genomes Ever Sequenced ]

One mystery of cat development is how cats have come to have such varied coats, from solid colors to "mackerel" tabby patterns of thin vertical stripes. The researchers were particularly interested in what turns the mackerel pattern into a "blotched" tabby pattern, seen more often in European cats than American ones.

A map of kitty pedigrees allowed the researchers to narrow down the genetic culprit to one region of the chromosome containing three large genes.

They then sequenced the genomes of two batches of tabbies, one with blotched coats and the other striped ones, and narrowed the culprit further to a gene called Taqpep.

Three separate mutations of the Taqpep gene in the domestic cat and another mutation in the same gene in the king cheetah can cause the tabby pattern to go from striped to splotchy, and, in the cheetah, from spotty to striped, the researchers found.

This means the gene has mutated multiple times across kitties' evolutionary history.

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Found: Gene that gave tabby its stripes

Public release date: 20-Sep-2012 [ | E-mail | Share ]

Contact: B. Rose Huber rhuber@pitt.edu 412-624-4356 University of Pittsburgh

PITTSBURGHAlthough polyploids, which are plants with more than two sets of chromosomes, are common, how they contribute to the biodiversity has remained a mysteryuntil now. With the help of a $2 million grant from the National Science Foundation, researchers at the University of Pittsburgh and Oregon State University will use wild strawberry plants (Fragaria) to identify what role genetic diversity plays in polyploids, which make up 30-80% of all living plants. This will help scientists predict the ecological responses plants may have to environmental change.

"This deeply integrated comparative study of the wild relatives of the cultivated strawberrya species of world-wide economic importancewill provide foundational knowledge and contribute unparalleled resources that may be harnessed in efforts to ensure the sustainability of the strawberry and related crops such as the cherry, peach or apple, in the face of stress from non-living factors," said Tia-Lynn Ashman, principal investigator of the study and professor and associate chair of Pitt's Department of Biological Sciences.

The strawberry, a plant with 20 species (nearly half of which are polyploids), has centers of diversity in China and America and possesses numerous features that make it the perfect plant to examine. For example, Fragaria is susceptible to climate change, due to its early spring flowering and northern latitude or high-elevation distribution. Ashman says the wild strawberry will be the key to helping biologists resolve uncertainties about polyploidization's impact on the biodiversity.

"We will use common garden studies of natural and synthetic polyploids in the greenhouse and at climatically diverse sites to quickly identify the factors that underlie its functional traits and gene expression diversity," said Ashman.

This will allow her team to forge links between gene expression and functional variation, says Ashman, allowing them to determine where in the lineage the majority of genetic/functional diversity resides.

In addition to solving the unknown mysteries of multi-chromosome plants, the project also facilitates training by broad participation and international collaboration, including middle school science curriculum, involvement of high school teachers, next-generation sequencing workshops, cross-cutting training, and communication of research through academic journals.

Ashman's project falls under "Dimensions of Biodiversity" in NSF's investment in Science, Engineering, and Education for Sustainability program (SEES). The goal of the Dimensions of Biodiversity campaign is to transform, by 2020, how we describe and understand the scope and role of life on Earth. The SEES program addresses challenges in climate and energy research and education using a systems-based approach to understanding, predicting, and reacting to change in the natural, social, and built environments. Initial SEES efforts focused on coordination of a suite of research and education programs at the intersection of climate and environment, including specific attention to incorporating human dimensions.

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Pitt biologist receives $2 million to study genetic diversity of plants worldwide

The New Zealand Government needs to follow the lead of Austria and France who are taking action around their approval processes for genetic engineering (GE), the Green Party said today.

In response to a study finding that rats grew tumours and died after being fed GE Roundup ready corn, Austrias Minister for agriculture and the environment has asked the European Commission to review its approval processes. Frances Government have also ordered an investigation into the findings and are signalling that they may suspend imports of the corn.

"New Zealand needs to do the same but successive Governments seem too closely tied with the GE industry to be trusted to do so," Green Party genetic engineering spokesperson Steffan Browning said today.

"The National Government funded the recent biotech conference to the tune of $100,000 from the Ministry of Business, Innovation and Employment plus additional significant contributions from other departments; these are not the actions of a Government with their eyes open about GE.

"The New Zealand public want to know that the food approved for sale in this country is safe.

"Without changing the GE approval process and actually enforcing our labelling laws we cant be confident in that.

"We fought hard for proper labelling laws but they are not enforced, so New Zealanders cant actually show their opposition to GE through their purchasing.

"The fact is that this study shows we are right to be concerned and we need better approval processes that prove safety over the long term, instead of the short term feeding studies that decisions have been made on to date.

"This study has already started a strong discussion because people are really worried about the effects of these foods that have been approved to be in our stores now for a decade or longer.

"Of course this research is being described by some as controversial because there is big, big money involved in GE.

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NZ out of step on GE

After years of studying how cats get their color, researchers have pinpointed an elusive gene underlying spots on cheetahs, stripes in house cats and patterns across the feline world.

Called Taqpep, it and two other genes produce proteins central to a cascade of cell-level events that ultimately generate your kitty's distinctive coat.

"It's something we've been curious about for a long time," said geneticist Stephen O'Brien of the National Cancer Institute. "We've known just three genes were involved, but nobody knew what the genes were."

On the following pages, Wired talks to O'Brien about the findings, which were announced Sept. 20 in Science.

Feline coat patterns fall into two categories: stripes and spots. Though spots on a house cat may seem unusual to North American eyes, they're more common in Europe, where breeders have historically had different preferences, said O'Brien.

Earlier work by O'Brien and colleagues had pinpointed two other genes, called Agouti and Mc1r, as producing proteins that respectively control whether a coat is banded or solid, light or dark. Add Taqpep, and patterns start getting complicated.

Images: Helmi Flick

Citation: Specifying and Sustaining Pigmentation Patterns in Domestic and Wild Cats. By Christopher B. Kaelin, Xiao Xu, Lewis Z. Hong, Victor A. David, Kelly A. McGowan, Anne Schmidt-Kntzel, Melody E. Roelke, Javier Pino, Joan Pontius, Gregory M. Cooper, Hermogenes Manuel, William F. Swanson, Laurie Marker, Cindy K. Harper, Ann van Dyk,0 Bisong Yue, James C. Mullikin, Wesley C. Warren, Eduardo Eizirik, Lidia Kos, Stephen J. OBrien, Gregory S. Barsh, Marilyn Menotti-Raymond. Science, Vol. 337 No. 6101, Sept. 19, 2012

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From Cheetah Spots to Kitty's Stripes: The Genetics of Cat Coats

Public release date: 20-Sep-2012 [ | E-mail | Share ]

Contact: Emily Boynton emily_boynton@urmc.rochester.edu 585-273-1757 University of Rochester Medical Center

Just as women are advised to get plenty of folic acid around the time of conception and throughout early pregnancy, new research suggests another very similar nutrient may one day deserve a spot on the obstetrician's list of recommendations.

Consuming greater amounts of choline a nutrient found in eggs and meat during pregnancy may lower an infant's vulnerability to stress-related illnesses, such as mental health disturbances, and chronic conditions, like hypertension, later in life.

In an early study in The FASEB Journal, nutrition scientists and obstetricians at Cornell University and the University of Rochester Medical Center found that higher-than-normal amounts of choline in the diet during pregnancy changed epigenetic markers modifications on our DNA that tell our genes to switch on or off, to go gangbusters or keep a low profile in the fetus. While epigenetic markers don't change our genes, they make a permanent imprint by dictating their fate: If a gene is not expressed turned on it's as if it didn't exist.

The finding became particularly exciting when researchers discovered that the affected markers were those that regulated the hypothalamic-pituitary-adrenal or HPA axis, which controls virtually all hormone activity in the body, including the production of the hormone cortisol that reflects our response to stress and regulates our metabolism, among other things.

More choline in the mother's diet led to a more stable HPA axis and consequently less cortisol in the fetus. As with many aspects of our health, stability is a very good thing: Past research has shown that early exposure to high levels of cortisol, often a result of a mother's anxiety or depression, can increase a baby's lifelong risk of stress-related and metabolic disorders.

"The study is important because it shows that a relatively simple nutrient can have significant effects in prenatal life, and that these effects likely continue to have a long-lasting influence on adult life," said Eva K. Pressman, M.D., study author and director of the high-risk pregnancy program at the University of Rochester Medical Center. "While our results won't change practice at this point, the idea that maternal choline intake could essentially change fetal genetic expression into adulthood is quite novel."

Pressman, who advises pregnant women every day, says choline isn't something people think a lot about because it is already present in many things we eat and there is usually no concern of choline deficiency. Though much more research has focused on folate functionally very similar to choline and used to decrease the risk of neural tube defects like spina bifida a few very compelling studies sparked her interest, including animal studies on the role of choline in mitigating fetal alcohol syndrome and changing outcomes in Down syndrome.

A long-time collaborator with researchers at Cornell, Pressman joined a team led by Marie Caudill, Ph.D., R.D., professor in the Division of Nutritional Sciences at Cornell, in studying 26 pregnant women in their third trimester who were assigned to take 480 mg per day, an amount slightly above the standard recommendation of 450 mg per day, or about double that amount, 930 mg per day. The choline was derived from the diet and from supplements and was consumed up until delivery.

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Nutrient in eggs and meat may influence gene expression from infancy to adulthood

Assistant professor of physics Meni Wanunu uses nanopores to read a gene sequence one strand of DNA at a time.

(Phys.org)In the last five years, next-generation gene sequencing has brought down the cost of unlocking a single genome from $10 million to $10,000. While the savings is unprecedented, more can still be done to reduce the cost even further, an effort that would enable a host of applications in medical research and healthcare.

Meni Wanunu, an assistant professor of physics at Northeastern University, says his work in nanopore sequencing represents one such effort. Traditionally, Wanunu has used nanopores as a DNA readout device, wherein a single strand of DNA passes through the pore causing minute changes to the surrounding electrical signal that reports on its structure.

But now he's doing the opposite: "We'll use the nanopore to hold a molecule fixed in space," Wanunu explains.

Backed by a recent $825,000 grant from the National Institutes of Health, Wanunu will apply nanopores to another sequencing technology that reads exactly one strand of DNA at atime.

Pacific Biosciences, Wanunu's grant partner, has designed a sequencing device called a SMRT Cell for single-molecule, real-time analysis. SMRT cells have the potential to bring gene-sequencing costs down to $100 per genome, but they must first overcome some significanthurdles.

Each aluminum SMRT cell contains 150,000 holes. Each hole is 100 nanometers wide and should contain one "polymerase," a molecule whose native responsibility in a living cell is to replicate a DNA sequence, one nucleotide base at a time. Polymerases are nature's best DNA sequencers and SMRT cells take advantage of a molecule with millions of years of evolution behindit.

But according to Wanunu, only about 37 percent of the holes in a SMRT cell can theoretically contain exactly one polymerase, because there's no technology to put exactly one polymerase in each hole. While 100 nanometers may seem small, one of Wanunu's nanopores is 100 timessmaller.

The goal of the research backed by the new grant is to match each SMRT cell hole with a single nanopore. Sitting above the nanopore, each polymerase will be attached to an anchor below it, thus preventing the former from floating away.

By ensuring that there is a single polymerase in each hole, the nanopore approach will increase the number of gene sequences that can be read at once, improving the overall yield of the SMRT cell. Additionally, since nanopores are so small, it's possible to create a voltage gradient across them, driving charged DNA strands toward the holes, and thus increasing the sensitivity of the sequencer to DNA molecules.

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Nanopores promise cost savings in gene sequencing

COLORADO SPRINGS, Colo.--(BUSINESS WIRE)--

Cannabis Science (CBIS), a pioneering U.S. Biotech Company developing pharmaceutical products for global public health challenges, reports on a recent press release by the San Francisco NBC news, with new studies by Scientists at California Pacific Medical Center, which have shown that cannabidiol, (CBD), has the ability to "turn off" a gene that causes breast and other types of cancers to metastasize, according to the San Francisco Chronicle newspaper.

NBC News reports, The drug "has been shown to reduce pain and nausea" in cancer patients. AIDS patients also use cannabis to eat, sleep and otherwise be more functional. Turns out that cannabidiol has none of the psychotropic effects of marijuana as a whole. The researchers hope to move to clinical trials on humans soon to test the cannabidiol inhibition of metastasis, reported in the San Francisco Chronicle. What they found is that the cannabinoid turns off the overexpression of ID-1, which makes the cells lose their ability to travel to distant tissues. In other words, it keeps the cells more local and blocks their ability to metastasize. (spread to a new location) The researchers stressed cannabidiol works only on cancer cells that have these high levels of ID-1 and these do not include all cancerous tumors but, rather, aggressive, metastatic cells. But they've found such high levels in leukemia, colorectal, pancreatic, lung, ovarian, brain and othercancers.

Cannabis Science appreciates this additional scientific support that this report provides for our two target drug development programs as the Company moves forward with CS-TATI-1, and based on the success of previous skin cancer patients who self-administered cannabis-based treatments, the Company is focusing on the use of CS-S/BCC-1 topical cannabis-based preparations for the treatment of basal and squamous cell carcinomas.

Dr. Robert Melamede states, Cannabis Science is excited for the increasing scientific support for our projects. In the near future, we will share new developments, as well a the progress we have made with our earlier defined initiatives. Our professional expansion and development, as detailed in our latest news releases,was driven by the science of how cannabinoids can benefit both HIV/AIDS and Cancer Patients.

NBC News: http://www.msnbc.msn.com/id/49094732#.UFsvfY7nuZY

San Francisco Chronicle: http://www.sfgate.com/health/article/Pot-compound-seen-as-tool-against-cancer-3875562.php#page-1

About CS-S/BCC-1

Cannabis Science is currently working with CBR International to develop a Pre-IND Application to the FDA that focuses on the use of CS-S/BCC-1 topical cannabis-based preparations for the treatment of basal and squamous cell carcinomas. Cannabis Science has already seen success with 4 self-medicated skin cancer patients. These patients have been self-administering using cannabis-based extracts applied topically to their carcinomas and tumors. These patients have experienced shrinking and apparent eradication of their skin cancer, backed by positive reports from their doctors, which is why the Company is confident about the eminent success of this new drug to be developed.

About CS-TATI-1

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NBC News Reports that Cannabidiol (CBD) "Turns Off" the Cancer Gene Involved in Metastasis Findings by Scientists at ...

April Flowers for redOrbit.com Your Universe Online

A research team from the Allen Institute for Brain Science reports that human brains share a consistent genetic blueprint and possess enormous biochemical complexity. The findings, published in Nature, stem from the first in-depth and large-scale analysis of the vast data set publicly available in the Allen Human Brain Atlas.

The Allen Human Brain Atlas fully integrates different kinds of data across different scales of brain exploration in an open, public online resource. It details genes at work throughout the human brain with data incorporated from magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) as well as histology and gene expression data derived from both microarray and in situ hybridization approaches.

The results of this new study are based on extensive analysis of the Allen Human Brain Atlas, specifically the detailed all-genes, all-structures survey of genes at work throughout the human brain. This enormous dataset profiles 400 to 500 distinct brain areas per hemisphere using microarray technology. It comprises more than 100 million gene expression measurements covering three individual human brains to date, including two clinically unremarkable brains donated by a 24-year-old and 39-year-old man, and half a brain from a third man.

Among other findings, these data show that 84% of all genes are expressed somewhere in the human brain and in patterns that are largely similar from one brain to the next.

This study demonstrates the value of a global analysis of gene expression throughout the entire brain and has implications for understanding brain function, development, evolution and disease, said Ed Lein, Ph.D., Associate Investigator at the Allen Institute for Brain Science and co-lead author on the paper.

These results only scratch the surface of what can be learned from this immense data set. We look forward to seeing what others will discover.

The team expects their work to serve as a baseline against which others can compare the genetic activity of diseased brains, and so shed light on factors that underlie neurological and psychiatric conditions.

The human brain is the most complex structure known to mankind and one of the greatest challenges in modern biology is to understand how it is built and organized, said Seth Grant, a professor of molecular neuroscience at Edinburgh University who worked on the brain map.

This allows us for the first time to overlay the human genome on to the human brain. It gives us essentially the Rosetta stone for understanding the link between the genome and the brain, and gives us a path forward to decoding how genetic disorders impact and produce brain disease, he said.

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Researchers Track Gene Expression To Create Atlas of Human Brain

SAN FRANCISCO & BOSTON--(BUSINESS WIRE)--

Third Rock Ventures, LLC today announced the formation of MyoKardia, Inc. with a $38 million Series A financing of the company. MyoKardia is developing a pipeline of novel small molecule therapeutics that address key clinical needs for patients with genetic heart disease. The companys first programs include hypertrophic and dilated cardiomyopathy, which together afflict approximately 1 million people in the United States, and for which no novel therapeutics have been brought to market in over a decade. MyoKardias proprietary drug discovery platform brings together advances from the fields of cardiovascular genomics and heart muscle biology to enable its scientists to target certain heart disease at its source. This genetically targeted approach has the potential to revolutionize the treatment of cardiomyopathies, and ultimately a broader spectrum of cardiovascular disease, including heart failure. The company is founded by world leaders in the fields of muscle biology and cardiovascular genetics: James Spudich, Ph.D., Professor of Biochemistry, Stanford University, Leslie Leinwand, Ph.D., Professor of Molecular, Cellular and Developmental Biology, University of Colorado, Christine Seidman, M.D., Professor of Medicine and Genetics, Harvard Medical School and Director of the Cardiovascular Genetics Center at Brigham and Womens Hospital, and Jonathan Seidman, Ph.D., Professor of Genetics, Harvard Medical School.

The last decade has been challenging for those pursuing novel therapeutics in the cardiovascular space, in part because most treatments target symptoms far downstream of the root cause, said Dr.Leinwand. MyoKardias approach addresses this challenge head on by employing genetics to more precisely define the disease and who we want to treat, and by employing cutting-edge muscle biochemistry and a novel platform to determine how we want to treat. Our initial targets are genetic cardiomyopathies, but this could very well be a novel and tractable therapeutic discovery approach to even larger diseases like heart failure.

Abnormalities in the basic unit of heart muscle, called the sarcomere, have been identified as the driving cause for a variety of heart disease, and the most common cause of hypertrophic and dilated cardiomyopathy. Mutations in the proteins of the sarcomere cause disease by rendering the muscle either hyper or hypo contractile. MyoKardias platform brings together recent assay and protein expression advances pioneered by its founders with genetic insights to enable a personalized medicine approach. This allows for the rapid development of mutation-specific sarcomeric allosteric modulators that rebalance contractility, therefore stopping and potentially reversing the course of disease. MyoKardias approach will leverage resident expertise in sarcomere genetics, in-vivo and in-vitro disease models, next-generation biochemical and biophysical assay development, and medicinal chemistry. Together, these capabilities will provide for the efficient progression of multiple programs in DCM, HCM, and other genetic cardiomyopathies and heart disease related to sarcomere dysfunction.

With MyoKardias platform, we have the ability to exquisitely characterize the biochemistry and biophysics of the human mutated sarcomere, said Dr. Spudich. This not only allows us to better understand what drives pathophysiology, it also points us toward potential mutant specific solutions.

Our goal is to provide treatments for patients with genetic diseases for whom the options to date have been profoundly limited, said Charles Homcy, M.D., interim chief executive officer of MyoKardia and venture partner at Third Rock Ventures. With this Series A financing, we can meet our goals. We now have the resources and capabilities to effectively translate the insights of our founders and employees into multiple clinical products that positively impact patient lives.

Hypertrophic and dilated cardiomyopathies, MyoKardias first two focus disease areas, are the most common forms of heart muscle disease and the most common diagnosis leading to cardiac transplantation. More than 60 million people worldwide have cardiomyopathy or carry a cardiomyopathy gene mutation, including approximately 1 million patients in the United States. Despite this large patient population and the persisting unmet clinical need, there is a lack of novel therapeutics being developed that directly target these diseases.

About Genetic Cardiomyopathy

Genetic cardiomyopathies are conditions that arise from mutation in a critical heart muscle protein. Hypertrophic cardiomyopathy (HCM) produces thickening of the heart walls and is best known as a leading cause of sudden cardiac death in young athletes. Dilated cardiomyopathy (DCM) produces weakening of the heart walls and enlargement of the heart chambers. Cardiomyopathy can occur at any age, and more than 30,000 children, from newborns to 18-year-olds, suffer from some form of cardiomyopathy in the United States a patient population comparable to the number of people living with cystic fibrosis.

About MyoKardia, Inc.

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Third Rock Ventures Launches MyoKardia with $38 Million to Address Genetic Heart Disease

Public release date: 20-Sep-2012 [ | E-mail | Share ]

Contact: Emmanouil Dermitzakis emmanouil.dermitzakis@unige.ch 41-223-795-483 Universit de Genve

We are not all the same when it comes to illness. In fact, the risk of developing a disease such as diabetes or heart disease varies from one individual to another. A study led by Emmanouil Dermitzakis, Louis-Jeantet Professor at the Faculty of Medicine of the University of Geneva (UNIGE) reveals that the genetic predisposition to develop certain diseases may differ from one individual to another depending on their sex. Together with his collaborators, the professor has shown that genetic variants have a different impact on the level of gene expression between men and women. The results of this research have been published in the scientific journal Genome Research.

For decades geneticists have been interested in genetic variants that affect the level of gene expression. These variants spark the interest of researchers because they play a role in the predisposition to certain diseases. Professor Dermitzakis' team from UNIGE, in collaboration with Oxford University, focused on the fundamental differences in the genetics of gene expression between men and women. After analyzing the impact of genetic variants on the level of gene expression in women, and then in men, the scientists have found that the effect of certain variants affecting gene expression and the genetic risk of developing a disease resulting from these genetic variants is different depending on the sex of the individual.

Everyone will agree that men and women are different but, beyond the obvious, genetics brings to light more subtle differences. The researchers found that even with the same DNA mutation in men and in women, the impact on the level of gene expression will be different. Of all the genetic variants that have an impact on the level of gene expression, about 15% work differently depending on whether they are acting upon a man or a woman.

We already knew that certain environmental factors like diet had a variable impact depending on the sex of an individual. Today, we are able to confirm that genetic variants have a different impact on the level of gene expression in men and women; that is to say that although two individuals of opposite sex both have a same variant predisposing them to a disease, they will not have the same propensity to develop it, states Professor Dermitzakis.

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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Men and women are different in terms of genetic predispositions

AMES, Iowa, Sept. 20, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics (NLNK) announced today that Dr. Charles Link, Chairman and CEO, will participate in a panel discussion entitled "Innovation in Immunotherapy and Vaccines" at the University of Connecticut Stamford Campus on Monday September 24, 2012. The panel will be lead by Dr. Phil Greenberg of the Fred Hutchinson Cancer Center. The panel discussion will be recorded and a webcast will be available in the investor relations section of the NewLink website, http://www.NewLinkGenetics.com, on or about Thursday September 27, 2012.

About NewLink Genetics Corporation

NewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small-molecule immunotherapy product candidates intended to treat a wide range of oncology indications. NewLink's product candidates are designed with an objective to harness multiple components of the innate immune system to combat cancer, either as a monotherapy or in combination with current treatment regimens, without incremental toxicity. NewLink's lead product candidate, HyperAcute(R) Pancreas cancer immunotherapy (algenpantucel-L) is being studied in a Phase 3 clinical trial in surgically-resected pancreatic cancer patients (patient information is available at http://www.pancreaticcancer-clinicaltrials.com). This clinical trial is being performed under a Special Protocol Assessment with the U.S. Food and Drug Administration. NewLink and its collaborators have completed patient enrollment for a Phase 1/2 clinical trial evaluating its HyperAcute(R) Lung cancer immunotherapy (tergenpumatucel-L) product candidate for non-small cell lung cancer and a Phase 2 clinical trial for its HyperAcute(R) Melanoma cancer immunotherapy product candidate. NewLink also is developing indoximod (d-1-methyltryptophan, or D-1MT), a small-molecule, orally bioavailable product candidate from NewLink's proprietary indoleamine-(2,3)-dioxygenase, or IDO, pathway inhibitor technology. Through NewLink's collaboration with the National Cancer Institute, NewLink is studying indoximod in various chemotherapy and immunotherapy combinations in two Phase 1B/2 safety and efficacy clinical trials. For more information please visit http://www.linkp.com.

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NewLink CEO to Participate in Panel Entitled "Innovation in Immunotherapy and Vaccines"

When Dr. M. Alan Permutt, a physician-scientist at Washington University, died in June, he left behind an important finding: the WSF1 gene.

Permutt discovered it in 1998 and found that mutations in the gene were the marker for a rare disorder known as Wolfram syndrome.

Parents usually realize their children have the condition when they're diagnosed with type I diabetes. Eventually it causes hearing and vision loss, as well as nerve cell damage and motor difficulties. Life expectancy for those who have it is about 30.

Dr. Fumihiko Urano, associate professor of endocrinology, metabolism and lipid research at Washington U., continued Permutt's work and was part of a team that recently identified the mechanism behind that mutation.

The findings will not only help scientists understand Wolfram syndrome but could also lead to new treatments for type 2 diabetes and common neurological diseases, such as Alzheimer's disease and Parkinson's disease.

Urano didn't initially intend to study Wolfram syndrome. He was looking at a type of cell stress called endoplasmic reticulum dysfunction and its role in diabetes and aging. Every cell has endoplasmic reticulum. It's a network of membranes that synthesizes lipids and proteins, regulates calcium in the cell, transports cellular materials and signals death of the cell.

"We hypothesized that the Wolfram gene is a prototype of endoplasmic reticulum," he said.

With that in mind, he and Permutt established an international registry of patients with Wolfram syndrome in 2010. And rather than just study what goes wrong during the genetic mutation, they also tried to understand the basic functions of the WFS1 gene by studying patient samples and creating animal models.

They found that the WFS1 gene helps produce cyclic adenosine monophosphate or cyclic AMP that is crucial for producing insulin. The mutation in the gene disrupts the production of cyclic AMP. A lack of cyclic AMP can also lead to nerve cell dysfunction and even death.

"We were kind of surprised to know that WSF1 is so important for the production of cyclic AMP," Urano said. "It's such a fundamental function of our cells, and that's why patients with Wolfram have many manifestations including diabetes, optic atrophy, hearing loss and nerve damage."

View original post here:
Work at Washington U. holds hope for those with Wolfram syndrome

20 September 2012

Immediate withdrawal of unsafe GE corn vital

Research released yesterday shows the Governments lax policy on genetic engineering is putting the health of New Zealanders at risk, the Green Party said today.

The peer-reviewed research, published in the Journal of Food and Toxicology, shows disturbing results about the health effects of eating a genetically engineered corn that has been approved for human consumption in New Zealand for the last 10 years.

The rats in this study, fed with Roundup ready corn with levels of Roundup that are within approved limits, developed mutations and tumours at a hugely alarming rate.

There are now huge concerns over the safety of this corn. Eating this corn has now been proven to cause the growth of tumours, so why was it approved a decade ago without the necessary evidence that it was safe to eat? Green Party genetic engineering spokesperson Steffan Browning asked today.

New Zealand has more than 70 GE foods approved for sale in New Zealand to date, and these approvals were mostly based on health studies that were 90 days long or less. This new research recorded effects for two years and the tumours and deaths showed up after that previous 90 day cut off point.

We now know that eating this corn, called NK603, causes tumours and we cant be sure that any products containing these GE foods currently out there being eaten by New Zealanders are safe either.

FSANZ must immediately recall any products that have this strain of GE corn as an ingredient and reassess all previous approvals for long term eating safety.

New Zealanders dont want to be part of a science experiment. They rely on the Government to make sure these products are safe before they are released for human consumption.

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Immediate withdrawal of unsafe GE corn vital

Research released yesterday shows the Governments lax policy on genetic engineering is putting the health of New Zealanders at risk, the Green Party said today.

The peer-reviewed research, published in the Journal of Food and Toxicology, shows disturbing results about the health effects of eating a genetically engineered corn that has been approved for human consumption in New Zealand for the last 10 years.

The rats in this study, fed with Roundup ready corn with levels of Roundup that are within approved limits, developed mutations and tumours at a hugely alarming rate.

"There are now huge concerns over the safety of this corn. Eating this corn has now been proven to cause the growth of tumours, so why was it approved a decade ago without the necessary evidence that it was safe to eat?" Green Party genetic engineering spokesperson Steffan Browning asked today.

"New Zealand has more than 70 GE foods approved for sale in New Zealand to date, and these approvals were mostly based on health studies that were 90 days long or less. This new research recorded effects for two years and the tumours and deaths showed up after that previous 90 day cut off point.

"We now know that eating this corn, called NK603, causes tumours and we cant be sure that any products containing these GE foods currently out there being eaten by New Zealanders are safe either.

"FSANZ must immediately recall any products that have this strain of GE corn as an ingredient and reassess all previous approvals for long term eating safety.

"New Zealanders dont want to be part of a science experiment. They rely on the Government to make sure these products are safe before they are released for human consumption.

"Despite legal requirements, most GE foods are unlabelled so New Zealanders cant even choose to avoid them.

"I am hopeful that this study is on the top of the Minister for Food Safetys reading list this morning and that she will take immediate action to protect the health of New Zealanders.

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Immediate withdrawal of unsafe GE corn vital - Greens

It was a summer trip Hobe Sounds Grant Casto wont likely soon forget.

Casto, 17, traveled to Nuremberg, Germany, in late June to present a research paper in the study of genetics. He participated in the European Human Genetics Conference, attending with his grandfather, Richard J. Crout, an associate dean of research and a professor of dentistry and medicine at West Virginia University schools of dentistry and medicine

Going to a different country and seeing all these people from different countries come together to share their work that they found on genetics, I learned a lot about different diseases and all these new genetic disorders theyre finding, said Casto. He meet students and instructors from several nations at the event.

During the conference, Casto presented a research paper on the effects of genetics on dental health, such as cavities. Casto, whose parents work in dental care, said growing up in a family of medical professionals helped to spark his interest in science and medicine.

Ive liked science ever since I was young, he said. My long-term goal is to be an endodontist like my dad.

This fall, Casto has shifted his concentration back to his studies as a junior at the Clark Advanced Learning Center, a public charter high school on Southeast Salerno Road in Stuart where he is a junior. He currently maintains 3.8 grade-point while taking an academic curriculum that concentrates on science and college-level courses at Indian River State College. Casto said he hopes to attend West Virginia University and enroll in dental school while also pursuing a Ph.D in genetics.

Besides his studies, he has performed in years past with a local youth symphony, playing various instruments. He also volunteers at the Boys and Girls Club of Martin County. Casto said that the volunteer work is part of program through his school in which students help to organize events for children at the club, including holiday activities.

(I enjoy) seeing the kids happy, he said of his volunteer experiences.

What are your hobbies?

Music. I like pets. I like to take care of them. I have a parakeet, a blue-tounged skink, a leopard geck.

Continued here:
Love of science lifts Hobe Sound teen to genetics conference in Germany

Public release date: 19-Sep-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, September 19, 2012-- Researchers have successfully developed a stable population of neural crest cells derived from mice that can be grown in large quantities in the laboratory and that demonstrates the potential to develop into many different cell types needed throughout the body. This powerful new research tool for understanding stem cell biology and human development and disease is described in an article published in Stem Cells and Development, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Stem Cells and Development website.

Mamoru Ishii and colleagues from University of Southern California, Los Angeles, and California Institute of Technology, Pasadena, CA, present their work leading to the development of two neural crest cell lines with stem cell characteristics in the article "A Stable Cranial Neural Crest Cell Line from Mouse." The 09-1 cell line is capable of differentiating into four main cell types: bone, muscle, brain, and cartilage/connective tissue.

"This exciting report is the first to characterize cranial neural crest cell lines isolated from the mouse embryo, which definitively demonstrate multipotency and long-term propagation," says Editor-in-Chief Graham C. Parker, PhD, research professor, Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine.

###

About the Journal

Stem Cells and Development is an authoritative peer-reviewed journal that will increase its frequency to 24 times per year beginning in 2013, both print and online. The Journal is dedicated to communication and objective analysis of developments in the biology, characteristics, and therapeutic utility of stem cells, especially those of the hematopoietic system. Complete tables of content and a free sample issue may be viewed online at the Stem Cells and Development website.

About the Publisher

Mary Ann Liebert, Inc. is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Cellular Reprogramming, Tissue Engineering, and Human Gene Therapy. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc. website.

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New cranial neural crest cell line developed

Public release date: 19-Sep-2012 [ | E-mail | Share ]

Contact: Bill Schappert bschappert@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, September 19, 2012More than 900 million people worldwide are active users of the social networking site Facebook, and it is estimated that as many as one-third report using Facebook to check on the activities of former romantic partners. The effects of remaining Facebook friends with an ex-lover or even just following their activities online can disrupt a person's ability to heal emotionally and move on with his or her life, according to an article in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal published by Mary Ann Liebert Inc., publishers (http://www.liebertpub.com). The article is available free online on the Cyberpsychology, Behavior, and Social Networking website.

The study entitled "Facebook Surveillance of Former Romantic Partners: Associations with PostBreakup Recovery and Personal Growth" assessed the effects of continued Facebook contact with an ex-partner and of Facebook surveillance, in which there is no actual online contact, but one individual monitors the Facebook page and postings of another.

The study collected data from 464 participants to evaluate their Facebook usage and their emotional recovery and personal adjustment following the breakup of a romantic relationship. It evaluated parameters such as negative feelings, sexual desire and emotional longing for the ex-partner, and feelings of reduced personal growth as measures of distress and the ability to move forward with their lives.

"This study sees again virtual life mirroring real life. Just as real life contact with ex-partners may inhibit growth, healing, and well-being, so may virtual contact," says Brenda K. Wiederhold, PhD, MBA, BCIA, Editor-in-Chief of Cyberpsychology, Behavior, and Social Networking, from the Interactive Media Institute, San Diego, CA.

###

About the Journal

Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly in print and online that explores the psychological and social issues surrounding the Internet and interactive technologies. Complete tables of content and a sample issue (http://online.liebertpub.com/toc/cpb/14/6) may be viewed online on the Cyberpsychology, Behavior, and Social Networking website.

About the Publisher

More here:
Can post-breakup Facebook surveillance delay emotional recovery?

Newswise WINSTON-SALEM, N.C. Sept. 19, 2012 A genetic mutation that occurred thousands of years ago might be the answer to how early humans were able to move from central Africa and across the continent in what has been called the great expansion, according to new research from Wake Forest Baptist Medical Center.

By analyzing genetic sequence variation patterns in different populations around the world, three teams of scientists from Wake Forest Baptist, Johns Hopkins University School of Medicine and the University of Washington School of Medicine, Seattle, demonstrated that a critical genetic variant arose in a key gene cluster on chromosome 11, known as the fatty acid desaturase cluster or FADS, more than 85,000 years ago. This variation would have allowed early humans to convert plant-based polyunsaturated fatty acids (PUFAs) to brain PUFAs necessary for increased brain size, complexity and function. The FADS cluster plays a critical role in determining how effectively medium-chain PUFAs found in plants are converted to the long-chain PUFAs found in the brain.

This research is published online today in PLOS One.

Archeological and genetic studies suggest that homo sapiens appeared approximately 180,000 years ago, but stayed in one location around bodies of water in central Africa for almost 100,000 years. Senior author Floyd H. Ski Chilton, Ph.D., professor of physiology and pharmacology and director of the Center for Botanical Lipids and Inflammatory Disease Prevention at Wake Forest Baptist, and others have hypothesized that this location was critical, in part, because early humans needed large amounts of the long-chain PUFA docosahexaenoic acid (DHA), which is found in shellfish and fish, to support complex brain function.

This may have kept early humans tethered to the water in central Africa where there was a constant food source of DHA, Chilton said. There has been considerable debate on how early humans were able to obtain sufficient DHA necessary to maintain brain size and complexity. Its amazing to think we may have uncovered the region of genetic variation that arose about the time that early humans moved out of this central region in what has been called the great expansion.

Once this trait arose, the study shows that it was under intense selective pressure and thus rapidly spread throughout the population of the entire African continent. "The power of genetics continually impresses me, and I find it remarkable that we can make inferences about things that happened tens of thousands of years ago by studying patterns of genetic variation that exist in contemporary populations," said Joshua M. Akey, Ph.D., lead scientist at the University of Washington.

This conversion meant that early humans didnt have to rely on just one food source, fish, for brain growth and development. This may have been particularly important because the genetic variant arose before organized hunting and fishing could have provided more reliable sources of long-chain PUFAs, Akey said.

To investigate the evolutionary forces shaping patterns of variation in the FADS gene cluster in geographically diverse populations, the researchers analyzed 1,092 individuals representing 15 different human populations that were sequenced as part of the 1000 Genome Project and 1,043 individuals from 52 populations from the Human Genome Diversity Panel database. They focused on the FADS cluster because they knew those genes code for the enzymatic steps in long-chain PUFA synthesis that are the least efficient.

Chilton said the findings were possible because of the collaboration of internationally recognized scientists from three distinct and diverse disciplines fatty acid biochemistry (Wake Forest Baptist), statistical genetics (Johns Hopkins) and population genetics (University of Washington). This new information builds on Chiltons 2011 research findings published in BMC Genetics that showed how people of African descent have a much higher frequency of the gene variants that convert plant-based medium-chain omega-6 PUFAs found in cooking oils and processed foods to long-chain PUFAs that cause inflammation. Compared to Caucasians, African Americans in the United States have much higher rates of hypertension, type 2 diabetes, stroke, coronary heart disease and certain types of cancer. The current observation provides another important clue as to why diverse racial and ethnic populations likely respond differently to the modern western diet, Chilton said.

This research was supported by National Institutes of Health grants, P50 AT002782 and a Clinical and Translational Science Award grant to The Johns Hopkins Medical Institutions. Additional support was received from the Wake Forest Health Sciences Center for Public Health Genomics. Additional support came from the Mary Beryl Patch Turnbull Scholar Program and the MOSAIC initiative of Johns Hopkins University.

See the original post:
Genetic Mutation May Have Allowed Early Humans to Migrate Throughout Africa

Public release date: 19-Sep-2012 [ | E-mail | Share ]

Contact: Bonnie Davis bdavis@wakehealth.edu 336-399-8274 Wake Forest Baptist Medical Center

WINSTON-SALEM, N.C. Sept. 19, 2012 A genetic mutation that occurred thousands of years ago might be the answer to how early humans were able to move from central Africa and across the continent in what has been called "the great expansion," according to new research from Wake Forest Baptist Medical Center.

By analyzing genetic sequence variation patterns in different populations around the world, three teams of scientists from Wake Forest Baptist, Johns Hopkins University School of Medicine and the University of Washington School of Medicine, Seattle, demonstrated that a critical genetic variant arose in a key gene cluster on chromosome 11, known as the fatty acid desaturase cluster or FADS, more than 85,000 years ago. This variation would have allowed early humans to convert plant-based polyunsaturated fatty acids (PUFAs) to brain PUFAs necessary for increased brain size, complexity and function. The FADS cluster plays a critical role in determining how effectively medium-chain PUFAs found in plants are converted to the long-chain PUFAs found in the brain.

This research is published online today in PLOS One.

Archeological and genetic studies suggest that homo sapiens appeared approximately 180,000 years ago, but stayed in one location around bodies of water in central Africa for almost 100,000 years. Senior author Floyd H. "Ski" Chilton, Ph.D., professor of physiology and pharmacology and director of the Center for Botanical Lipids and Inflammatory Disease Prevention at Wake Forest Baptist, and others have hypothesized that this location was critical, in part, because early humans needed large amounts of the long-chain PUFA docosahexaenoic acid (DHA), which is found in shellfish and fish, to support complex brain function.

"This may have kept early humans tethered to the water in central Africa where there was a constant food source of DHA," Chilton said. "There has been considerable debate on how early humans were able to obtain sufficient DHA necessary to maintain brain size and complexity. It's amazing to think we may have uncovered the region of genetic variation that arose about the time that early humans moved out of this central region in what has been called the 'great expansion.'"

Once this trait arose, the study shows that it was under intense selective pressure and thus rapidly spread throughout the population of the entire African continent. "The power of genetics continually impresses me, and I find it remarkable that we can make inferences about things that happened tens of thousands of years ago by studying patterns of genetic variation that exist in contemporary populations," said Joshua M. Akey, Ph.D., lead scientist at the University of Washington.

This conversion meant that early humans didn't have to rely on just one food source, fish, for brain growth and development. This may have been particularly important because the genetic variant arose before organized hunting and fishing could have provided more reliable sources of long-chain PUFAs, Akey said.

To investigate the evolutionary forces shaping patterns of variation in the FADS gene cluster in geographically diverse populations, the researchers analyzed 1,092 individuals representing 15 different human populations that were sequenced as part of the 1000 Genome Project and 1,043 individuals from 52 populations from the Human Genome Diversity Panel database. They focused on the FADS cluster because they knew those genes code for the enzymatic steps in long-chain PUFA synthesis that are the least efficient.

More:
Genetic mutation may have allowed early humans to migrate throughout Africa, research says

If you are tired of Googling the possible consequences of genetic inheritance and the severity of hereditary cases related to cancer, then Slidell Memorial Hospitals Regional Cancer Center might just be the ticket to that information.

On Sept. 6, hospital officials announced that their business has unleashed a new frontier in the fight against cancer; something they say comes in the form of a Genetics Clinic, now open to the community.

For patients diagnosed with cancer, if their type of cancer has an inherited aspect, their family members must confront the possibility they may be at increased risk of also developing cancer, said SMH in a news release.

Such scenario is the direct reason the hospital has recently opened a genetics clinic.

Our program will provide genetic counseling and testing to people who are at increased risk for hereditary cancer, said Mathew McElveen, M.D., medical oncologist and SMHRCC medical director. This is about helping them make informed medical decisions based on their own personal risk assessment.

Genetics risk assessments can have a huge impact on a persons life by allowing them to better manage their health and reduce their risk of ever developing cancer, said Clinical Geneticist Duane W. Superneau, M.D., medical director of Our Lake of the Lake Genetics Services.

Superneau will see clients twice a month at the SMHRCC Genetics Clinic in Slidell.

All support work, such as scheduling appointments and lab work, will be done on-site at SMHRCC, McElveen said. This means patients in the city of Slidell and the surrounding community will not have to travel very far for such testing and counseling.

The National Cancer Institute states that a cancer genetics clinic, such as the one just setup at SMHRCC, is a core component of a comprehensive cancer program because these services allow affected families access to cancer prevention and early-detection methods. Several issues that indicate a person could benefit from an assessment include: family history of early-onset cancers, family member on same side with same or related cancer, family member has more than one type of cancer, or family is of Jewish ancestry with a family history of breast, ovarian or pancreatic cancers, or family history of a rare type of cancer or tumor.

Most cases Superneau will deal with will pertain to cancer, but any patient with a non-cancer genetic disorder, can also be seen in the clinic.

More here:
Slidell Memorial Hospital brings new age to local genetics

Sharks are color blind, new research suggests, with the toothy predators likely forever seeing the world in black and white.

The study, published in the latest Royal Society Biology Letters, is the first to investigate the genetic basis and spectral tuning of the shark visual system.

The ramifications could be huge, helping to save both sharks and people.

"The work will have a major influence on human interactions with sharks," co-author Nathan Hart, a research associate professor at the University of Western Australia's School of Animal Biology and The Oceans Institute, told Discovery News.

NEWS: Sharks Get Worry-Free Tans

"Firstly, this knowledge may enable us to design fishing gear that is more specific for target fish species and thus reduces unnecessary bycatch of sharks," Hart continued. "Secondly, it may help us to design equipment that is less attractive to sharks (wetsuits and surfboards, for example) that may help to reduce attacks on humans."

Building on a study from last year, Hart and his colleagues isolated and sequenced genes encoding shark photopigments involved in vision. Photopigments are light-sensitive molecules. Through a biochemical process, they signal this detection of light to the rest of the visual system.

Photopigments are found in two places: rods and cones. The former type is more sensitive and is generally used under very dim light. The latter type is smaller and less sensitive, but is faster responding, applying more to brighter-light conditions.

The researchers determined that the studied sharks, in this case two wobbegong species, are cone monochromats. This means that the sharks only had one type of cone and one type of rod gene, supporting that they are color-blind. The findings strengthen earlier speculation about not only wobbegongs, but other shark species.

NEWS: Shark Paradise Found

Continued here:
Genetics confirms sharks are color blind

NEW YORK, Sept. 19, 2012 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) ("NeoStem" or the "Company"), a rapidly emerging market leader in the fast growing cell therapy market, today announced that Company management has been invited to participate at BIOX, the Noble Financial Capital Markets' Life Sciences Exposition on Monday, September 24. Company management will make a webcasted company presentation and participate in a cell therapy panel.

Noble Financial Capital Markets Investor Conference - BIOX Life Sciences Exposition

For more information about the conference, please visit http://www.nobleresearch.com/BIOX.htm.

About NeoStem, Inc.

NeoStem, Inc. continues to develop and build on its core capabilities in cell therapy, capitalizing on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a significant role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. We are emerging as a technology and market leading company in this fast developing cell therapy market. Our multi-faceted business strategy combines a state-of-the-art contract development and manufacturing subsidiary, Progenitor Cell Therapy, LLC ("PCT"), with a medically important cell therapy product development program, enabling near and long-term revenue growth opportunities. We believe this expertise and existing research capabilities and collaborations will enable us to achieve our mission of becoming a premier cell therapy company.

Our contract development and manufacturing service business supports the development of proprietary cell therapy products. NeoStem's most clinically advanced therapeutic, AMR-001, is being developed at Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011. Amorcyte is developing a cell therapy for the treatment of cardiovascular disease and is enrolling patients in a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is collaborating with Becton-Dickinson in the early clinical exploration of a T-cell therapy for autoimmune conditions. In addition, pre-clinical assets include our VSELTM Technology platform as well as our mesenchymal stem cell product candidate for regenerative medicine. Our service business and pipeline of proprietary cell therapy products work in concert, giving us a competitive advantage that we believe is unique to the biotechnology and pharmaceutical industries. Supported by an experienced scientific and business management team and a substantial intellectual property estate, we believe we are well positioned to succeed.

For more information on NeoStem, please visit http://www.neostem.com.

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's or its partners' successful development of AMR-001 and other cell therapeutics, the size of the market for such products, its competitive position in such markets, the Company's ability to successfully penetrate such markets and the market for its CDMO business, and the efficacy of protection from its patent portfolio, as well as the future of the cell therapeutics industry in general, including the rate at which such industry may grow. Forward looking statements also include statements with respect to satisfying all conditions to closing the disposition of Erye, including receipt of all necessary regulatory approvals in the PRC. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors, including but not limited to (i) the Company's ability to manage its business despite operating losses and cash outflows, (ii) its ability to obtain sufficient capital or strategic business arrangement to fund its operations, including the clinical trials for AMR-001, (iii) successful results of the Company's clinical trials of AMR-001 and other cellular therapeutic products that may be pursued, (iv) demand for and market acceptance of AMR-001 or other cell therapies if clinical trials are successful and the Company is permitted to market such products, (v) establishment of a large global market for cellular-based products, (vi) the impact of competitive products and pricing, (vii) the impact of future scientific and medical developments, (viii) the Company's ability to obtain appropriate governmental licenses and approvals and, in general, future actions of regulatory bodies, including the FDA and foreign counterparts, (ix) reimbursement and rebate policies of government agencies and private payers, (x) the Company's ability to protect its intellectual property, (xi) the company's ability to successfully divest its interest in Erye, and (xii) matters described under the "Risk Factors" in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 20, 2012 and in the Company's other periodic filings with the Securities and Exchange Commission, all of which are available on its website. The Company does not undertake to update its forward-looking statements. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem to Present at Noble Capital Markets' Life Sciences Exposition on September 24

19 September 2012 Last updated at 01:39 ET

Dundee University researchers believe they have found a way to predict the effectiveness of chemotherapy drugs in fighting ovarian cancer.

Scientists have discovered a gene called FGF1 was highly active in aggressive, advanced ovarian cancers.

They observed it was present at higher levels in cancer cells that were resistant to a common treatment for the disease.

The team hope the findings help to develop new cancer treatments.

Researchers measured amounts of a variety of genes in 187 ovarian cancer patients and found each cancer had a unique range of active genes.

However, FGF1 appeared to playing the greatest role in determining how cancers behave.

The team, based at the University's School of Medicine, found the gene called FGF1 was found at higher levels in cancer cells that are resistant to platinum chemotherapy treatments, such as carboplatin and cisplatin.

As a result, women with high levels of FGF1 are less likely to respond to these drugs and have a poorer prognosis.

The scientist believe measuring how active the gene is could predict which women with ovarian cancer will benefit from the drugs.

Originally posted here:
Gene key to chemotherapy efficacy