An international team led by Eric A. Hendrickson of the University of Minnesota and Duncan Baird of Cardiff University has solved a key mystery in cancer research: What allows some malignant cells to circumvent the normal process of cell death that occurs when chromosomes get too old to maintain themselves properly?

Researchers have long known that chromosomal defects that occur as cells repeatedly divide over time are linked to the onset of cancer. Now, Hendrickson, Baird and colleagues have identified a specific gene that human cells require in order to survive these types of defects.

"We have identified a gene that, as cells age, seems to regulate whether the cells become cancerous or not," Hendrickson said. "This gene has never been identified before in this role, so this makes it a potentially very important therapeutic target."

As cells divide their telomeres -- the DNA "caps" that protect the ends of chromosomes from damage -- shorten, leaving the chromosomes vulnerable to sticking to each other. In normal cells, this chromosome stickiness is a death knell -- a signal to defective-cell cleanup crews to move in and finish them off. Malignant cells, however, are somehow able to elude the cleanup crews.

The current research, published in the August 7 issue of the journal Cell Reports, identifies an essential component that allows older cells to evade death. Using sophisticated gene-targeting techniques to disable particular genes in human cells and then studying the impact on telomere fusion, the researchers found that cells escaped death only when the gene Ligase 3 was active but not when its action, which appears to promote fusion within like chromosomes rather than between different chromosomes, was blocked.

"Telomere dysfunction has been identified in many human cancers, and as we have shown previously, short telomeres can predict the outcome of patients with [chronic lymphocytic leukemia] and probably many other tumor types," said Baird. "Thus, the discovery that Ligase 3 is required for this process is fundamentally important."

Interestingly, the research was made possible by a chance meeting between Hendrickson, who is an expert in using gene targeting to create cells missing key components (such as Ligase 3), and Baird, who is a leading expert in analyzing telomeres. When the two discovered at a scientific conference that they were both looking at the role of Ligase 3 in cancer, they decided to collaborate.

"The collaboration paid off as we were able to uncover something that neither one of us could have done on our own," Hendrickson says.

Importantly, additional studies are already underway. In particular, the reliance on Ligase 3 appears, in turn, to be dependent upon the activity of another key DNA repair gene, p53.

"Since p53 is the most commonly mutated gene in human cancer, it now behooves us to discover how these two genes are interacting and to see if we can't use that information to develop synergistic treatment modalities," says Hendrickson.

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Key piece to cancer cell survival puzzle found

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Jeffrey Smith #39;s #39;challenge #39; to Neil deGrasse Tyson EVISCERATED (part 1)
On August 5th, Jeffrey Smith, the creator of the #39;Institute for Responsible Technology #39; issued a challenge to Neil deGrasse Tyson. In it, he displays a TITANIC lack of knowledge on the topic...

By: Jeff Holiday

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Jeffrey Smith's 'challenge' to Neil deGrasse Tyson EVISCERATED (part 1) - Video

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Hari Pulakkat, ET Bureau Aug 8, 2014, 05.21AM IST

(Humanity will find it difficult)

Some British newspapers have been reporting the imminent harvest of a variety of nutrition-enriched genetically modified (GM) crop in the UK. It is a crop called camelina, also called false flax, a plant that usually grows in the Mediterranean. An institute called Rothamsted Research has tweaked the plant's genes and produced a variety that is full of omega-3 fatty acids, normally found only in oily fish.

Consumption of omega-3 fatty acids is supposed to be beneficial in a number of ways, and so this crop would provide the first real chance for vegetarians to get the vital nutrient through their normal diet. This would be great news for many people, but what is equally important is the fact that GM crops are set to finally break the resistance in Europe.

Despite considerable opposition from various pressure groups, GM crops are slowly advancing in Europe, with regulators relenting in several countries. Two months ago, almost all the environment ministers in Europe - only two countries resisted - decided to let individual countries follow their own course: whether to allow or not allow the cultivation of GM crops.

This will let the pro-GM countries go ahead with their plans, which will probably force the rest to consider GM crop trials and commercial launches. For some time now, Europe is cited as a model - often wrongly - to those around the world to resist commercial cultivation and even research in GM crops.

If Europe cultivates GM crops on a large scale, resistance will slowly reduce in China and African countries, and later in India as well. All these countries have so far seen some resistance against GM crops. China, despite funding GM crop research, has been reluctant to commercialise these widely.

Africa has been uneven in its acceptance, with countries like South Africa being adopters and other countries like Tanzania and Kenya holding out. India commercialised Bt cotton more than a decade ago, but progress of GM crops in the country has been slow since then.

From a scientific viewpoint, genetic engineering is like atomic energy; it depends on how you use it. So while it is difficult to say that all GM crops are bad, there could be situations where they would do some damage, depending on the genes that one chooses to introduce.

Most of the genes being tried now are known to be safe. It is highly unlikely that they will cause damage to our agricultural system, but it is impossible to prove it the other way.

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Genetically modified crops: Ignoring genetic engineering at our own peril

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 7, 2014In vitro toxicity testing is rapidly being adopted in the pharmaceutical, chemical, and cosmetics industries, for example, as an alternative to animal studies to predict adverse health effects of drugs and personal care products and the health consequences of environmental exposures. An insightful Roundtable Discussion focused on how to apply these novel toxicology models to everyday hazard prediction, risk assessment, and decision making in industry is published in the preview issue of the new journal Applied In Vitro Toxicology, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Applied In Vitro Toxicology website.

In the Roundtable Discussion "Comments on How to Make the New Vision of Toxicity Testing in the 21st Century a Reality," Moderator Jim McKim, Editor-in-Chief of Applied In Vitro Toxicology and Founder and CEO, IONTOX, LLC, challenges the panelists to present a realistic view of how far the field has advanced in implementing the strategy put forth in a National Academy of Sciences report to improve toxicity testing.

Panelists Alan Goldberg, Consulting Editor of the Journal, Nicole Kleinstreuer, ILS/National Toxicology Program Interagency Center for Evaluation of Alternative Toxicological Methods (Research Triangle Park, NC), Francois Busquet, Center for Alternatives to Animal Testing (Konstanz, Germany), and Melvin Andersen, The Hamner Institutes for Health Sciences (RTP, NC) participate in an interactive discussion on the use of human cell models combined with high-throughput screening methods to test for toxicity, and the complexity of applying adverse outcome pathways (AOPs). The conversation covers topics ranging from policy issues, challenges related to data interpretation and understanding the information gained from in vitro models, the emergence of three-dimensional tissue culture models that integrate cells from multiple human organs, and the different approaches being used to assess risk from high-dose, short-term exposures compared to exposure to lower concentrations of a chemical over longer periods of time.

"Improved analytical technologies and improvements in human tissue models will allow us to change the animal safety testing paradigm," says Jim McKim.

###

About the Journal

Applied In Vitro Toxicology is a new peer-reviewed journal providing the latest research on the application of alternative in vitro testing methods for predicting adverse effects in the pharmaceutical, chemical, and personal care industries. Led by Editor-in-Chief James M. McKim, PhD, DABT, IONTOX, LLC, the Journal addresses important issues facing these diverse industries, including regulatory requirements; the reduction, refinement, and replacement of animal testing; new screening methods; evaluation of new cell and tissue models; and the most appropriate methods for assessing safety and satisfying regulatory demands. The Journal is published quarterly online with Open Access options and in print. A sample issue may be viewed on the Applied In Vitro Toxicology website (http://www.liebertpub.com/aivt).

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Expert insights on in vitro alternatives for drug and chemical toxicity testing

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The Sims 3 | Perfect Genetics Challenge Part 17: Engagement
In this part, Hunter proposes to Cassandra and Riley ages up into a teenager! Backstory: "Once upon a time, the Mighty Player sent a Sim to live in the world where all its creations were...

By: simplyapril

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The Sims 3 | Perfect Genetics Challenge Part 17: Engagement - Video

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QASA Protest outside UIA Durban 2014 Campus
"QASA is a co-ordinating, policy-making, governing and supporting organisation. The Association strives to prevent spinal cord injury, as well as protect and promote the interests of people...

By: Pedro Buccellato

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QASA Protest outside UIA Durban 2014 Campus - Video

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WOW....regenerative medicine with stem cells natural activation !
NEW 100% NATURAL STEM CELLS ACTIVATOR !

By: Juan Perez

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WOW....regenerative medicine with stem cells natural activation ! - Video

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UC San Francisco researchers have identified cells' unique features within the developing human brain, using the latest technologies for analyzing gene activity in individual cells, and have demonstrated that large-scale cell surveys can be done much more efficiently and cheaply than was previously thought possible.

"We have identified novel molecular features in diverse cell types using a new strategy of analyzing hundreds of cells individually," said Arnold Kriegstein, MD, PhD, director of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. "We expect to use this approach to help us better understand how the complexity of the human cortex arises from cells that are spun off through cell division from stem cells in the germinal region of the brain."

The research team used technology focused on a "microfluidic" device in which individual cells are captured and flow into nano-scale chambers, where they efficiently and accurately undergo the chemical reactions needed for DNA sequencing. The research showed that the number of reading steps needed to identify and spell out unique sequences and to successfully identify cell types is 100 times fewer than had previously been assumed. The technology, developed by Fluidigm Corporation, can be used to individually process 96 cells simultaneously.

"The routine capture of single cells and accurate sampling of their molecular features now is possible," said Alex Pollen, PhD, who along with fellow Kriegstein-lab postdoctoral fellow Tomasz Nowakowski, PhD, conducted the key experiments, in which they analyzed the activation of genes in 301 cells from across the developing human brain. Their results were published online August 3 in Nature Biotechnology.

Kriegstein said the identification of hundreds of novel biomarkers for diverse cell types will improve scientists' understanding of the emergence of specialized neuronal subtypes. Ultimately, the combination of this new method of focusing on gene activity in single cells with other single-cell techniques involving microscopic imaging is likely to reveal the origins of developmental disorders of the brain, he added.

The process could shed light on several brain disorders, including lissencephaly, in which the folds in the brain's cortex fail to develop, as well as maladies diagnosed later in development, such as autism and schizophrenia, Kriegstein said.

According to the Nature Biotechnology study co-authors, this strategy of analyzing molecules in single cells is likely to find favor not only among researchers who explore how specialized cells arise at specific times and locations within the developing organism, but also among those who monitor cell characteristics in stem cells engineered for tissue replacement, and those who probe the diversity of cells within tumors to identify those responsible for survival and spread of cancerous cells.

No matter how pure, in any unprocessed biological sample there are a variety of cells representing various tissue types. Researchers have been sequencing the combined genetic material within these samples. To study which genes are active and which are dormant, they use the brute repetition of sequencing steps to capture an adequate number of messenger RNA sequences, which are transcribed from switched-on genes. However, it is difficult to conclude from mixed tissue samples which genes are expressed by particular cell types.

Pollen and Nowakowski showed that fewer steps -- and less time and money -- are needed to distinguish different cell types through single-cell analysis than had previously been thought.

"We are studying an ecosystem of different, but related, cell types in the brain," Pollen said. "We are breaking that community down into the different populations of cells with the goal of understanding their functional parts and components so we can accurately predict how they will develop."

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Single-cell analysis holds promise for stem cell and cancer research

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A method of growing human cells from tissue removed from a patient's gastrointestinal (GI) tract eventually may help scientists develop tailor-made therapies for inflammatory bowel disease and other GI conditions.

Reporting online recently in the journal Gut, researchers at Washington University School of Medicine in St. Louis said they have made cell lines from individual patients in as little as two weeks. They have created more than 65 such cell lines using tissue from 47 patients who had routine endoscopic screening procedures, such as colonoscopies. A cell line is a population of cells in culture with the same genetic makeup.

The scientists said the cell lines can help them understand the underlying problems in the GI tracts of individual patients and be used to test new treatments.

"While it has been technically possible to isolate intestinal epithelial stem cells from patients, it has been challenging to use the material in ways that would benefit them on an individual basis," said co-senior investigator Thaddeus S. Stappenbeck, MD, PhD, a professor of pathology and immunology. "This study advances the field in that we have developed new methods that allow for the rapid expansion of intestinal epithelial stem cells in culture. That breaks a bottleneck and allows us to develop new ways to test drug and environmental interactions in specific patients."

To grow the human cells, the researchers adapted a system used to grow intestinal epithelial stem cells in mice. In the GI tract, epithelial cells line the inner surface of the esophagus, stomach and intestines.

"An additional important feature of this system is that we can isolate stem cell lines from intestinal biopsies," said first author Kelli L. VanDussen, PhD, a postdoctoral fellow in Stappenbeck's laboratory. "These biopsies are very small tissue fragments that are routinely collected by a gastroenterologist during endoscopy procedures. We have refined this technique, so we have nearly 100 percent success in creating cell lines from individual patient biopsies."

The researchers developed an experimental system that created high levels of critical factors to isolate and expand intestinal epithelial stem cells, including a signaling protein called Wnt and a related protein called R-spondin, which enhances the Wnt signal. They also exposed the cells to a protein called Noggin, which prevented the cells from differentiating into other cell types that live in the GI tract.

After growing the intestinal cell lines, the investigators collaborated with Phillip I. Tarr, MD, the Melvin E. Carnahan Professor of Pediatrics and director of the Division of Pediatric Gastroenterology and Nutrition, to conduct experiments and see how the cells interacted with bacterial pathogens like E. coli.

This showed that pathogenic strains of E. coli attached to intestinal epithelial cells. That attachment is thought to be the critical step in stimulating disease. The investigators said the experimental system they created should lead to new methods to uncover therapies for treating bacterial infections of the intestine.

"In the past, the only really robust method for studying GI epithelial cells was to use cancer cell lines," said co-senior investigator Matthew A. Ciorba, MD, a gastroenterologist and assistant professor of medicine. "However, cancer cells behave differently than the noncancerous GI epithelium, which is affected in patients with conditions such as inflammatory bowel disease. This technique now allows us to study cells identical to the ones that live in a patient's GI tract. Plus, we can grow the cell lines quickly enough that it should be possible to develop a personalized approach to understanding a patient's disease and to tailor treatment based on a patient's underlying problem."

Continued here:
Growing human GI cells may lead to personalized treatments

Recommendation and review posted by simmons

PUBLIC RELEASE DATE:

6-Aug-2014

Contact: Robert Miranda cogcomm@aol.com Cell Transplantation Center of Excellence for Aging and Brain Repair

Putnam Valley, NY. (Aug. 6, 2014) Recent studies have shown that transplanting induced pluripotent stem cell-derived neural stem cells (iPS-NSCs) can promote functional recovery after spinal cord injury in rodents and non-human primates. However, a serious drawback to the transplantation of iPS-NSCs is the potential for tumor growth, or tumorogenesis, post-transplantation.

In an effort to better understand this risk and find ways to prevent it, a team of Japanese researchers has completed a study in which they transplanted a human glioblastoma cell line into the intact spinal columns of laboratory mice that were either immunodeficient or immunocompetent and treated with or without immunosuppresant drugs. Bioluminescent imaging was used to track the transplanted cells as they were manipulated by immunorejection.

The researchers found that the withdrawal of immunosuppressant drugs eliminated tumor growth and, in effect, created a 'safety lock' against tumor formation as an adverse outcome of cell transplantation. They also confirmed that withdrawal of immunosuppression led to rejection of tumors formed by transplantation of induced pluripotent stem cell derived neural stem/progenitor cells (iPS-NP/SCs).

Although the central nervous system has shown difficulty in regenerating after damage, transplanting neural stem/progenitor cells (NS/PCs) has shown promise. Yet the problem of tumorogenesis, and increases in teratomas and gliomas after transplantation has been a serious problem. However, this study provides a provisional link to immune therapy that accompanies cell transplantation and the possibility that inducing immunorejection may work to reduce the likelihood of tumorogenesis occurring.

"Our findings suggest that it is possible to induce immunorejection of any type of foreign-grafted tumor cells by immunomodulation," said study co-author Dr. Masaya Nakamura of the Keio University School of Medicine. "However, the tumorogenic mechanisms of induced pluripotent neural stem/progenitor cells (iPS-NS/PCs) are still to be elucidated, and there may be differences between iPS-NS/PCs derived tumors and glioblastoma arising from genetic mutations, abnormal epigenetic modifications and altered cell metabolisms."

The researchers concluded that their model might be a reliable tool to target human spinal cord tumors in preclinical studies and also useful for studying the therapeutic effect of anticancer drugs against malignant tumors.

"This study provides evidence that the use of, and subsequent removal of, immunosuppression can be used to modulate cell survival and potentially remove tumor formation by transplanted glioma cells and provides preliminary data that the same is true for iPS-NS/PCs." said Dr. Paul Sanberg, distinguished professor at the Center of Excellence for Aging and Brain Repair, University of South Florida. "Further study is required to determine if this technique could be used under all circumstances where transplantation of cells can result in tumor formation and its reliability in other organisms and paradigms."

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Researchers seek 'safety lock' against tumor growth after stem cell transplantation

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By Partnership for Public Service August 5

Dr. Griffin Rodgers spends most of his waking hours leading the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), but he also manages to carve out time to work on a life-long passion discovering a cure for sickle cell disease.

Long before becoming the director of NIDDK, Rodgers was credited with discovering the first effective therapy for sickle cell disease, an inherited blood disorder that affects more than 90,000 Americans, most of them African-Americans. The disease, which affects millions of people throughout the world, can damage bones, joints and internal organs, cause acute and chronic pain, and often result in premature death.

Prior to his discovery of a drug treatment in the 1990s, the only options for sickle cell patients were blood transfusions for pain and supportive care.

This initial breakthrough has been followed by the recent announcement that Rodgers and a team of National Institutes of Health (NIH) researchers have developed a modified blood stem-cell transplant regimen that is highly effective in reversing sickle cell disease in adults. The findings, based on a clinical trial of 30 patients, represent a potentially transformative treatment.

Dr. Neal Young, chief of NIHs Hematology Branch of the National Heart, Lung and Blood Institute, said Rodgers has been the driving force behind the advanced medical treatments for people with sickle cell disease. His work, said Young, is a very big deal because it will save the lives and alleviate the suffering of thousands of people.

Dr. Thomas Starzl, a physician and researcher who performed the worlds first liver transplant, wholeheartedly concurred.

Griffin Rodgers work on sickle cell disease has been revolutionary, said Starzl. I can only give him rave reviewsfive stars.

Rodgers grew up in New Orleans where he had three high school friends who became debilitated with sickle cell disease. Two of those friends died in their teenage years and the third passed away a few years after high school.

These deaths left a tremendous impression on Rodgers, who pursued a medical career that led him to NIH in 1984 where he began his work on sickle cell disease. Over the years as he made his mark in the laboratory and the clinical setting, Rodgers also progressed through the managerial ranks, heading NIDDKs Molecular and Clinical Hematology Branch starting in 1998, becoming deputy director of NIDDK in 2001 and director of the institute in 2007.

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NIH scientist transforming treatment of sickle cell disease

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PHYTOSCIENCE PHILIPPINES DOUBLE SKIN CELL THERAPY REVIEW
PHYTOSCIENCE PHILIPPINES DOUBLE SKIN CELL THERAPY REVIEW A RARE OPPORTUNITY TO ALL FILIPINOS BE A PART OF THE PHYTOSCIENCE PIONEERING TEAM 2013 Best Selling ...

By: phytoscience double stem cell philippines

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PHYTOSCIENCE PHILIPPINES DOUBLE SKIN CELL THERAPY REVIEW - Video

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(PRWEB UK) 7 August 2014

BioEden the specialist tooth stem cell bank stands by its pledge to make personalised stem cell therapy an affordable reality by launching Access Membership at just 5 per month.

With stem cell therapy holding the promise of longer and better lives in the future, the cost and the ease of finding a stem cell match has been an issue, given that the cost of private stem cell banking requires an initial cash outlay of up to 4000.

Not any more.

BioEden the leading specialist tooth stem cell bank, has added Access Membership to parents finding themselves financially unable to bank their child's cells for future use. "It doesnt sit well with us that a parent could be unable to access what could be a life saving service for their child, for financial reasons," said Group CEO Mr Tony Veverka.

Parents can access the stem cell banking service for just 5 per month, and can become a member of the plan as soon as the baby is born. To date the option for stem cell banking at birth has been umbilical cord blood banking, an invasive process which provides haemopoetic stem cell banking at a cost.

Now parents have the option to choose tooth stem cell banking or to add this to cord blood banking at a very low monthly cost.

Tooth stem cells have considerable advantages over cord blood cells;

And now, thanks to BioEden, cost doesnt have to be a barrier.

So how can 5 a month give access to such a specialist service?

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BioEden fights the financial cost of stem cell banking by bringing their specialist service to the people for just 5 ...

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NEW DELHI: Union health minister Harsh Vardhan on Wednesday called upon citizens to voluntarily register themselves as bone marrow donors to help enhance the chances of patients with blood cancer and other blood-related diseases get genetically compatible donors.

"Unlike blood donation, in the case of unrelated donor, the chances are one in a million that a donor's Human Leukocyte Antigen (HLA) will match with the needy patient's. Therefore, there is a requirement of having millions of registered donors," Vardhan said while speaking at the launch of a "Public Initiative of Bone Marrow Donation" at All India Institute of Medical Science (AIIMS) here.

A willing donor can register himself at the Asian Indian Donor Marrow Registry (AIDMR) at AIIMS. He will have to undergo an initial test done for which 10 ml of blood is taken. The test is called HLA typing.

In case they turn out to be HLA match for the needy patient, they will be requested to donate their bone marrow or peripheral blood stem cells to patients of blood-cancer and other disorders, he said.

Vardhan said the health ministry will soon start a facility for the bone marrow donation in Safdurjung Hospital, which will intensify the initiative for bone marrow donation in the country.

"There is a need for the NGOs and several other health organisations to spread awareness in the society to curb all kinds of myths and superstitions that deter the individuals from being donors, which is a noble cause," he said.

On the occasion, Vardhan registered himself as a bone marrow donor and gave his blood sample for the HLA testing.

"One should at least understand that for the patients suffering from blood-related diseases like blood cancer, leukaemia, thalassemia, anaemia and many other diseases, a simple commitment to donate bone marrow can save a patient's life at the cost of nothing," Vardhan told IANS.

The AIDMR at AIIMS has set a target of registering 100,000 bone marrow donors in the first year and expand the register up to half a million donors in the next five years.

Vardhan also called for donation of body organs and cadavers, which can save life of the needy patients, and also serve the purposes of medical research.

Link:
India needs more bone marrow donors: Health minister Harsh Vardhan

Recommendation and review posted by Bethany Smith

Union Health Minister Harsh Vardhan Wednesday called upon citizens to voluntarily register themselves as bone marrow donors to help enhance the chances of patients with blood cancer and other blood-related diseases get genetically compatible donors.

"Unlike blood donation, in the case of unrelated donor, the chances are one in a million that a donor's Human Leukocyte Antigen (HLA) will match with the needy patient's. Therefore, there is a requirement of having millions of registered donors," Vardhan said while speaking at the launch of a "Public Initiative of Bone Marrow Donation" at All India Institute of Medical Science (AIIMS) here.

A willing donor can register himself at the Asian Indian Donor Marrow Registry (AIDMR) at AIIMS. He will have to undergo an initial test done for which 10 ml of blood is taken. The test is called HLA typing.

In case they turn out to be HLA match for the needy patient, they will be requested to donate their bone marrow or peripheral blood stem cells to patients of blood-cancer and other disorders, he said.

Vardhan said the health ministry will soon start a facility for the bone marrow donation in Safdurjung Hospital, which will intensify the initiative for bone marrow donation in the country.

"There is a need for the NGOs and several other health organisations to spread awareness in the society to curb all kinds of myths and superstitions that deter the individuals from being donors, which is a noble cause," he said.

On the occasion, Vardhan registered himself as a bone marrow donor and gave his blood sample for the HLA testing.

"One should at least understand that for the patients suffering from blood-related diseases like blood cancer, leukaemia, thalassemia, anaemia and many other diseases, a simple commitment to donate bone marrow can save a patient's life at the cost of nothing," Vardhan told IANS.

The AIDMR at AIIMS has set a target of registering 100,000 bone marrow donors in the first year and expand the register up to half a million donors in the next five years.

Vardhan also called for donation of body organs and cadavers, which can save life of the needy patients, and also serve the purposes of medical research.

More here:
India needs more bone marrow donors: Harsh Vardhan

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PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Charli Scouller c.scouller@qmul.ac.uk 020-788-27943 Queen Mary, University of London

For the first time, scientists have uncovered new information on how stem cells in the human bowel behave, revealing vital clues about the earliest stages in bowel cancer development and how we may begin to prevent it.

The study, led by Queen May University of London (QMUL) and published today in the journal Cell Reports, discovered how many stem cells exist within the human bowel and how they behave and evolve over time. It was revealed that within a healthy bowel, stem cells are in constant competition with each other for survival and only a certain number of stem cells can exist within one area at a time (referred to as the 'stem cell niche'). However, when investigating stem cells in early tumours, the researchers saw increased numbers of stem cells within each area as well as intensified competition for survival, suggesting a link between stem cell activity and bowel cancer development.

The study involved studying stem cells directly within the human body using a specially developed 'toolkit'. The toolkit worked by measuring random mutations that naturally accrue in ageing stem cells. The random mutations recorded how the stem cells had behaved, similarly to how the rings on a tree trunk record how a tree grew over time. The techniques used were unique in that scientists were able to study the human stem cells within their natural environment, giving a much more accurate picture of their behaviour.

Until this research, the stem cell biology of the human bowel has remained largely a mystery. This is because most stem cell research is carried out in mice, and it was uncertain how research findings in mice could be applied to humans. However, the scientists in fact found the stem cell biology of human bowels to have significant similarities to mice bowels. This means researchers can continue investigating stem cell activity within mice with the knowledge it is representative of humans - hopefully speeding up bowel cancer research.

Importantly, these new research methods can also now be applied to investigate stem cells in other parts of the human body such as skin, prostate, lung and breast, with the aim of accelerating cancer research in these areas too.

Dr Trevor Graham, Lecturer in Tumour Biology and Study Author at Queen Mary University of London, comments: "Unearthing how stem cells behave within the human bowel is a big step forward for stem cell research. Until now, stem cell research was mostly conducted in mice or involved taking the stem cells out of their natural environment, thus distorting their usual behaviour. We now want to use the methods developed in this study to understand how stem cells behave inside bowel cancer, so we can increase our understanding of how bowel cancer grows. This will hopefully shed more light on how we can prevent bowel cancer the fourth most common cancer in the UK. We are positive this research lays important foundations for future bowel cancer prevention work, as well as prevention work in other cancers."

Dr Marnix Jansen, Histopathologist and Study Author at Queen Mary University of London, comments: "This study was made possible through the involvement of patients either diagnosed with bowel cancer or born with a tendency to develop bowel cancer. Only by investigating tissues taken directly from patients could we study how bowel cancers develop. Our work underlines the importance of patient involvement in scientific research if we are to tackle bowel cancer and help the greatest number of people."

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Scientists uncover stem cell behavior of human bowel for the first time

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Mary Beth O'Leary moleary@cell.com 617-397-2802 Cell Press

While neurons normally fail to regenerate after spinal cord injuries, neurons formed from human induced pluripotent stem cells (iPSCs) that were grafted into rats with such injuries displayed remarkable growth throughout the length of the animals' central nervous system. What's more, the iPSCs were derived from skin cells taken from an 86-year-old man. The results, described in the Cell Press journal Neuron, could open up new possibilities in stimulating neuron growth in humans with spinal cord injuries

"These findings indicate that intrinsic neuronal mechanisms readily overcome the barriers created by a spinal cord injury to extend many axons over very long distances and that these capabilities persist even in neurons reprogrammed from very aged human cells," said senior author Mark Tuszynski, MD, PhD, professor of neurosciences and director of the UC San Diego Center for Neural Repair.

After Dr. Tuszynski and his colleagues converted the skin cells into iPSCs, which can be coaxed to develop into nearly any other cell type, the team reprogrammed the cells to become neurons, embedded them in a matrix containing growth factors, and then grafted them into 2-week-old spinal cord injuries in rats.

Three months later, the team found mature neurons and extensive nerve fiber growth across long distances in the rats' spinal cords, including through the wound tissue and even extending into the brain. Despite numerous connections between the implanted neurons and existing rat neurons, functional recovery of the animals' limbs was not restored. The investigators noted that several iPSC grafts contained scars that may have blocked beneficial effects.

Dr. Tuszynski, along with lead author Paul Lu, PhD, of the UC San Diego Department of Neurosciences, and their collaborators are now working to identify the best way to translate neural stem cell therapies for patients with spinal cord injuries, using grafts derived from the patients' own cells.

###

Neuron, Lu et al.: "Long-Distance Axonal Growth from Human Induced Pluripotent Stem Cells After Spinal Cord Injury."

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Human skin cells reprogrammed as neurons regrow in rats with spinal cord injuries

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Newswise Building upon previous research, scientists at the University of California, San Diego School of Medicine and Veterans Affairs San Diego Healthcare System report that neurons derived from human induced pluripotent stem cells (iPSC) and grafted into rats after a spinal cord injury produced cells with tens of thousands of axons extending virtually the entire length of the animals central nervous system.

Writing in the August 7 early online edition of Neuron, lead scientist Paul Lu, PhD, of the UC San Diego Department of Neurosciences and colleagues said the human iPSC-derived axons extended through the white matter of the injury sites, frequently penetrating adjacent gray matter to form synapses with rat neurons. Similarly, rat motor axons pierced the human iPSC grafts to form their own synapses.

The iPSCs used were developed from a healthy 86-year-old human male.

These findings indicate that intrinsic neuronal mechanisms readily overcome the barriers created by a spinal cord injury to extend many axons over very long distances, and that these capabilities persist even in neurons reprogrammed from very aged human cells, said senior author Mark Tuszynski, MD, PhD, professor of Neurosciences and director of the UC San Diego Center for Neural Repair.

For several years, Tuszynski and colleagues have been steadily chipping away at the notion that a spinal cord injury necessarily results in permanent dysfunction and paralysis. Earlier work has shown that grafted stem cells reprogrammed to become neurons can, in fact, form new, functional circuits across an injury site, with the treated animals experiencing some restored ability to move affected limbs. The new findings underscore the potential of iPSC-based therapy and suggest a host of new studies and questions to be asked, such as whether axons can be guided and how will they develop, function and mature over longer periods of time.

While neural stem cell therapies are already advancing to clinical trials, this research raises cautionary notes about moving to human therapy too quickly, said Tuszynski.

The enormous outgrowth of axons to many regions of the spinal cord and even deeply into the brain raises questions of possible harmful side effects if axons are mistargeted. We also need to learn if the new connections formed by axons are stable over time, and if implanted human neural stem cells are maturing on a human time frame months to years or more rapidly. If maturity is reached on a human time frame, it could take months to years to observe functional benefits or problems in human clinical trials.

In the latest work, Lu, Tuszynski and colleagues converted skin cells from a healthy 86-year-old man into iPSCs, which possess the ability to become almost any kind of cell. The iPSCs were then reprogrammed to become neurons in collaboration with the laboratory of Larry Goldstein, PhD, director of the UC San Diego Sanford Stem Cell Clinical Center. The new human neurons were subsequently embedded in a matrix containing growth factors and grafted into two-week-old spinal cord injuries in rats.

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Dramatic Growth of Grafted Stem Cells in Rat Spinal Cord Injuries

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The Dr Hadwen Trust awarded 135,078 to Dr Catherine Wright, a lecturer at the Department of Life Sciences at Glasgow Caledonian University and a member of the Institute for Applied Health Research's Diabetes and Biomedical Sciences research group.

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The grant will fund a three-year research programme which will allow the university's skin tissue bank to continue providing human skin tissue and cells that can be used for studies related to diabetes research.

This includes issues such as wound healing, as well as the development of human stem cells - which would help to replace the need for animal experimentation.

Dr Wright said: "The funding will allow us to employ a full-time member of staff to assist the academics to run the tissue bank and develop new types of human cell models that can replace animal experiments."

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Diabetes project is given funding boost

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Dr. A.P.REYES~U.S. SENATOR-LEGALIZING STEM CELL THERAPY
I created this video with the YouTube Slideshow Creator (http://www.youtube.com/upload)

By: Arturo Reyes

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Dr. A.P.REYES~U.S. SENATOR-LEGALIZING STEM CELL THERAPY - Video

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PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Henry French henry.french@icr.ac.uk 020-715-35380 Institute of Cancer Research

Mutations in a gene that helps regulate when genes are switched on and off in cells have been found to cause rare cases of Wilms tumour, the most common kidney cancer occurring in children.

A study led by scientists at The Institute of Cancer Research, London, identified mutations in the CTR9 gene in six children with Wilms tumour.

Wilms tumour affects around one in 10,000 children and usually develops before the age of five years. Treatment of Wilms tumour is very successful, with 90 per cent of children being cured.

Usually Wilms tumour only affects one child in a family, but very occasionally more than one child in a family develops the cancer. When this happens it indicates that hereditary genetic factors are likely to be involved.

The researchers studied the genes of 35 families with more than one case of Wilms tumour, recruited to the study through a network of collaborators from across the world. In six children, from three different families, they found CTR9 mutations that stopped the gene working properly. No similar mutations were present in 1,000 individuals without Wilms tumour.

The research is published today (Thursday) in the journal Nature Communications and is part of the Factors Associated with Childhood Tumours Study, which is funded by the Wellcome Trust, and aims to identify genetic causes of childhood cancers. The study was also supported by Cancer Research UK.

CTR9 is part of a multi-protein complex, known as PAF1, which regulates when genes are switched on and off. The PAF1 complex has many essential diverse roles in controlling cellular processes and organ development in the embryo. Interestingly, mutations of another gene in the complex, CDC73, have previously been shown to cause cancer, particularly of the parathyroid gland, but also occasionally Wilms tumour.

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Mutations in a gene essential for cell regulation cause kidney cancer in children

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Sequencing the genomes of tumor cells has revealed thousands of mutations associated with cancer. One way to discover the role of these mutations is to breed a strain of mice that carry the genetic flaw -- but breeding such mice is an expensive, time-consuming process.

Now, MIT researchers have found an alternative: They have shown that a gene-editing system called CRISPR can introduce cancer-causing mutations into the livers of adult mice, enabling scientists to screen these mutations much more quickly.

In a study appearing in the Aug. 6 issue of Nature, the researchers generated liver tumors in adult mice by disrupting the tumor suppressor genes p53 and pten. They are now working on ways to deliver the necessary CRISPR components to other organs, allowing them to investigate mutations found in other types of cancer.

"The sequencing of human tumors has revealed hundreds of oncogenes and tumor suppressor genes in different combinations. The flexibility of this technology, as delivery gets better in the future, will give you a way to pretty rapidly test those combinations," says Institute Professor Phillip Sharp, an author of the paper.

Tyler Jacks, director of MIT's Koch Institute for Integrative Cancer Research and the David H. Koch Professor of Biology, is the paper's senior author. The lead authors are Koch Institute postdocs Wen Xue, Sidi Chen, and Hao Yin.

Gene disruption

CRISPR relies on cellular machinery that bacteria use to defend themselves from viral infection. Researchers have copied this bacterial system to create gene-editing complexes that include a DNA-cutting enzyme called Cas9 bound to a short RNA guide strand that is programmed to bind to a specific genome sequence, telling Cas9 where to make its cut.

In some cases, the researchers simply snip out part of a gene to disrupt its function; in others, they also introduce a DNA template strand that encodes a new sequence to replace the deleted DNA.

To investigate the potential usefulness of CRISPR for creating mouse models of cancer, the researchers first used it to knock out p53 and pten, which protect cells from becoming cancerous by regulating cell growth. Previous studies have shown that genetically engineered mice with mutations in both of those genes will develop cancer within a few months.

Studies of such genetically engineered mice have yielded many important discoveries, but the process, which requires introducing mutations into embryonic stem cells, can take more than a year and costs hundreds of thousands of dollars. "It's a very long process, and the more genes you're working with, the longer and more complicated it becomes," Jacks says.

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Gene-editing technique offers new way to model cancer

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Mutated versions of a gene called PALB2 can dramatically increase a woman's risk of breast cancer, a new study has found.

Women carrying the PALB2 mutation have a one in three chance of developing breast cancer by the age of 70, British researchers report in the Aug. 7 issue of the New England Journal of Medicine.

The risk is even higher for women with a family history of breast cancer, the investigators found.

"If a mutation carrier has a strong family history, the risk would go up to about six in 10 by age 70," said senior study author Marc Tischkowitz, a researcher with the department of medical genetics at the University of Cambridge.

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Those odds place PALB2 just behind the BRCA1 and BRCA2 genes as a top genetic risk factor for breast cancer, Tischkowitz said.

Women who carry a mutated form of either of the BRCA genes have a 45 percent to 65 percent risk of breast cancer by age 70, according to the U.S. National Cancer Institute.

Researchers first identified the PALB2 gene in 2006, and it was further associated with breast cancer in a study published in 2007, Tischkowitz said.

This new study provides the first solid evidence regarding the breast cancer risk associated with PALB2, said Dr. Roger Greenberg, an associate professor of cancer biology with the Abramson Family Cancer Research Institute at the University of Pennsylvania School of Medicine in Philadelphia.

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New breast cancer gene mutation raises risk dramatically

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PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

Numerous risk factors are believed to contribute to the development of autoimmune disorders such as multiple sclerosis, and new research is focusing on the role that bacteria in the gastrointestinal tract as well as other cell stress-related chemical signals could have in stimulating inflammation in the central nervous system and activating immunostimulatory cytokines. Two comprehensive Review articles are part of a focus on "Cytokines in Neuroinflammation and Immunity" in a special issue of Journal of Interferon & Cytokine Research (JICR), a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The articles are available free on the JICR website.

Kiel Telesford and Lloyd Kasper, Geisel School of Medicine at Dartmouth University (Lebanon, NH) and Javier Ochoa-Repraz, University of California-Santa Barbara, describe three key characteristics of the gut microbiome related to immune cell activity and cytokine production that may be relevant to susceptibility to and treatment of autoimmune disorders such as multiple sclerosis. In the article "Gut Commensalism, Cytokines, and Central Nervous System Demyelination," the authors note that our understanding of the biology of the gut microbiome and the immunoregulatory potential of bacteria and parasites in the gut is still in its infancy.

In the Review article "Interferons, Signal Transduction Pathways, and the Central Nervous System," Shreeram Nallar and Dhan Kalvakolanu, University of Maryland School of Medicine, Baltimore, explore in detail the latest research pointing to the role of cytokines, and in particular interferons, in contributing to the development of diseases affecting the central nervous system. The authors discuss the potential effects of either an excess or lack of interferons, the inflammatory effects of cytokines, and new therapeutic research strategies.

"The communications between the microbial community in the gut and the host immune system is turning out to be remarkably complex and is likely to impact on many aspects of both health and disease," says Editor-in-Chief Thomas A. Hamilton, PhD, Chairman, Department of Immunology, Cleveland Clinic Foundation, Ohio.

###

About the Journal

Journal of Interferon & Cytokine Research (JICR), led by Editors-in-Chief Ganes C. Sen, PhD, Chairman, Department of Molecular Genetics, Cleveland Clinic Foundation, Ohio, and Thomas A. Hamilton, PhD, is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that covers all aspects of interferons and cytokines from basic science to clinical applications. JICR, celebrating 35 years of publication in 2015, is an official journal of the International Cytokine & Interferon Society. Complete tables of content and a sample issue may be viewed on the JICR website.

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Is the gut microbiome a potential cause and therapeutic target for autoimmune diseases like multiple sclerosis?

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PUBLIC RELEASE DATE:

7-Aug-2014

Contact: Glenna Picton picton@bcm.edu 713-798-4710 Baylor College of Medicine

HOUSTON (Aug. 7, 2014) Researchers from the Lester and Sue Smith Breast Center at Baylor College of Medicine have uncovered new information about the genetic alterations that may contribute to the development of a subtype breast cancer typically associated with more aggressive forms of the disease and higher recurrence rates.

The study, led by Dr. Xiaosong Wang, assistant professor of medicine hematology and oncology and of molecular and cellular biology at Baylor, published today in Nature Communications and focused on the more aggressive molecular subtype of the estrogen-receptor positive breast cancer known as luminal B breast cancer.

"While expressing the estrogen receptor, the luminal B breast cancers usually have higher tumor grade, larger tumor size, and poor prognosis, with most cases difficult to treat by endocrine therapy," said Wang, the lead and corresponding author on the report. "We wanted to gain a deeper understanding about the genetic alterations underlying this particular form of breast cancer, because we do not know about what malfunctions potentially cause this form to be more aggressive."

In the study, Wang and colleagues identified a particular gene fusion on the estrogen receptor itself (hybrid gene formed from two previously separate genes) that was preferentially present in a subset of samples of tumors that were luminal B and ER-positive.

The fusion was a result of rearrangements in the estrogen receptor gene called ESR1 and another neighboring gene called CCDC170, Wang said.

The findings were based in part from data available through the National Human Genome Research Initiative's Cancer Genome Atlas project.

Rearrangement in the genes causes the disruption of the transfer of information. "In a majority of cases this fusion seems to be generated by a tandem duplication of the genetic material spanning the ESR1 and CCDC170 genes," said Wang.

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Study shines new light on genetic alterations of aggressive breast cancer subtype

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