Humans have been manipulating crop genetics for thousands of years, crossing and selecting plants that exhibit desirable traits. In the last century, breeders exposed crops to radiation and chemicals that induced random mutations. These and other lab methods gave fruits and vegetables new colors, made crops disease resistant and made grains easier to harvest. Most wheat, rice and barley are descendants of mutant varieties, as are many vegetables and fruits. Hello, Star Ruby grapefruit! In the early 1980s, scientists discovered how to insert genes from other species into plants. The process led to the 1994 commercialization of the first GMO, the Flavr Savr tomato. It was tasteless and was pulled from the market. No GMO meat is currently for sale, though not for lack of trying. AquaBounty Technologies has been trying for 19 years to win approval for salmon engineered to grow twice as fast as conventional salmon, with less feed. The 1995 application remains pending before the U.S. Food and Drug Administration, which has determined the fish is safe to consume. Advocates want it labeled.

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Engineered Food

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PUBLIC RELEASE DATE:

30-May-2014

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

New Rochelle, NY, May 30, 2014High throughput screening of compounds in live cells is a powerful approach for discovering new drugs, but the potential for cell toxicity must be considered. A novel technique that uses DNA-binding fluorescent dyes to evaluate the cytotoxicity of an experimental compound in real-time during screening, saving time and resources, is described in ASSAY and Drug Development Technologies, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the ASSAY and Drug Development Technologies website.

Lucius Chiaraviglio and James Kirby, Beth Israel Deaconess Medical Center, evaluated 19 fluorescent DNA-binding dyes and identified four dyes that were not harmful to cells and could not cross the cell membrane if a cell was viable. The authors demonstrated the ability to use these dyes to detect cell death during drug screening in the article "Evaluation of Impermeant, DNA-Binding Dye Fluorescence as a Real-Time Readout of Eukaryotic Cell Toxicity in a High Throughput Screening Format."

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About the Journal

Assay and Drug Development Technologies is an authoritative peer-reviewed journal published 10 times a year in print and online. It provides early-stage screening techniques and tools that enable identification and optimization of novel targets and lead compounds for new drug development. Complete tables of content and a complementary sample issue may be viewed on the ASSAY and Drug Development Technologies website.

About the Publisher

Mary Ann Liebert, Inc., publishers, is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many areas of science and biomedical research, including OMICS: A Journal of Integrative Biology and Genetic Testing and Molecular Biomarkers. 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 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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DNA-binding fluorescent dyes detect real-time cell toxicity during drug screening

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With a little genetic engineering, the vaccine that was key in helping eradicate smallpox more than 30 years ago could also be key in curing cancer, if a young Cleveland biotech has anything to say about it.

Western Oncolytics is developing a dual-mechanism therapy that combines oncolytic virus and gene therapy technologies with the hope of wiping out the ability of cancer cells to survive in the body.

CEO Kurt Rote is a first-time entrepreneur, but you wouldnt know it from talking to him. After getting a biomedical engineering degree from Duke and moving to Switzerland to get an MBA, he worked for a short time at a small biotech firm before deciding to risk everything to realize a personal dream of curing cancer.

In pursuit of bleeding-edge technology, he started making calls to university researchers.I went down a list of NIH grants and talked to as many of them as possible, he said. I wanted to go where the science led me.

Where it led him was to the office of Stephen H. Thorne at the University of Pittsburgh Cancer Center, who had been studying oncolytic viruses for years.

Oncolytic viruses are genetically modified to infect and kill cancer cells while simultaneously triggering an anti-tumor immune response. Their promise lies in being able to treat cancers with side effects that parallel those of a flu shot, rather than those from chemotherapy.

Although theyve been studied for decades, theyre just now advancing to the point where theyre being tested in large-scale human trials. Amgen recently completed a Phase 3 study in melanoma patients of an oncolytic virus it bought from Biovex in a 2011 deal worth up to $1 billion. The results of the trial were mixed, potentially limiting the commercial viability of the drug, but the trial serves as an important milestone for the field.

The therapy developed in Thornes lab employs similar concepts but is based on more advanced technology and has shown better tumor shrinkage and remission in animal testing, Rote said.

A number of different elements work together in the vaccine. It contains the vaccinia virus (used in the smallpox vaccine) with three gene modifications: the addition of two that signal T-cells to come to the tumor and reduce the number of immune suppressor cells in the tumor, respectively, and the deletion of a viral gene which leads to infected cells sending more signals to the immune system.

And, to avoid the immune system from being triggered immediately, before the virus reaches the tumor, scientists have modified its surface to delay the immune response.

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Virus that helped eradicate smallpox takes on cancer in startups dual-mechanism immunotherapy

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GoldLab Symposium 2014 - Lucy Shapiro
Lucy Shapiro, Ph.D., Professor and Director of the Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine spoke at GLS2014...

By: GOLDLABCOLORADO

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The Resilience Project seeks to find people who are unaffected by genetic mutations that would normally cause severe and fatal disorders

An example of a protein complex created by a mutated gene linked to Pfeiffer syndrome, one 125 diseases and conditions that The Resilient Project is looking at. The green amino acid is where the mutation has occurred. Credit: Yevgeniy Antipin and Eric Schadt

Cystic fibrosis is caused by mutations in a single gene. For people born with two mutated copies of that gene, the prognosis is often grim. They can suffer from a variety of ailments, including reduced lung function and digestive problems. Many dont live into adulthood. Mutations in single genes cause many other diseases such as Tay-Sachs disease or some types of muscular dystrophy; the prognoses for people born with these conditions are similarly bleak.

Some people who have a fateful mutation, however, live healthy lives without any apparent symptoms of illness. These rare individuals are the focus of The Resilience Project, a new initiative that aims to identify people unaffected by their problematic genes and figure out how they have avoided their dismal destinies. The hope is that by studying these people, researchers can find new approaches for treating these genetic diseases. The leaders of the project, Stephen Friend, president of Sage Bionetworks in Seattle, and Eric Schadt, professor of genomics at Icahn School of Medicine at Mount Sinai in New York City, describe it in the May 30 Science.

The new initiative seeks to enroll one million people over the age of 40 to search for such unexpected heroes, as project leaders call them. Those who enroll will receive a DNA kit, much like those that companies such as 23andMe use, which they then return with cheek swab samples. Unlike other commercial DNA companies, however, The Resilience Project is looking specifically at 162 genes that can cause what Friend and Schadt refer to as catastrophic diseases.

In the vast majority of cases, Schadt says, people will simply get a confirmation that they do not have two copies of any of the mutated alleles that would cause one of the 125 diseases the project is looking for. But they expect that about one in 15,000 people are living healthy lives with mutations that should cause severe illness. That estimate comes from a retrospective analysis of about 600,000 genomes collected by 23andMe and other companies. (In the general populace disease rates vary widely by type of affliction and region, from as many as one in every 2,000 births to one in every million births).

Assuming that figure is correct, Schadt says they expect to find between 50 and 100 people (out of the million they hope to enroll) who have thrived despite having these genetic mutations. Those people would then be invited to undergo further study that will hopefully yield new clues about ways to fight these disorders. However they were able to naturally resist the disease, Schadt says, that would then become the therapeutic angle you would then pursue to prevent the disease.

Schadt imagines a number of ways that people could avoid these disorders. One is genetic; its possible that these resilient people have mutations in other genes that protect them from the effects of the disease-causing mutations. In some cases, a mutation that disables a separate gene can actually have beneficial effects. If that is the case, Schadt says, those other genes would be good targets for pharmaceutical drugs, because it is much easier to knock out a working gene than to make up for a nonworking one. Synthetic molecules can be created to target and disable particular genes.

The unexpected heroes may also have been exposed to environmental factors that allowed them to escape their genetic fates. This effect would be much more difficult to tease out, Schadt says, because the environmental cues could involve anything from a persons diet to exposure to certain toxins. These factors would most likely show up as epigenetic changes, he says, in which the packaging of a persons DNA is altered.

Daniel MacArthur, a geneticist at Harvard Medical School and Massachusetts General Hospital, wrote in an e-mail that The Resilience Project is intriguing and extremely ambitious. He thinks that it will be useful for understanding the genetic basis of these ailments as well as for determining which healthy people in the world actually carry these problematic mutations. But he cautions that there will be major statistical challenges associated with moving from these heroes to fully understanding the genetic basis of disease resistance.

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Genetic Heroes May Be Key to Treating Debilitating Diseases

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PUBLIC RELEASE DATE:

30-May-2014

Contact: Diana Quattrone Diana.Quattrone@fccc.edu 215-815-7828 Fox Chase Cancer Center

CHICAGO, IL (May 30, 2014)Three genetic changes can predict whether a patient will benefit from chemotherapy before surgery to remove bladder cancer, according to new findings presented by Fox Chase Cancer Center researchers during the 50th Annual Meeting of the American Society of Clinical Oncology.

During the study, 36 patients with muscle-invasive bladder cancer received chemotherapy before surgery, consisting of an accelerated regimen of methotrexate, vinblastine, doxorubicin, and cisplatin (AMVAC). By the time surgery rolled around, 14 patients appeared cancer-free. All but one of these patients carried mutations in at least one of three specific genes; none of these mutations were present in any of the people who still harbored traces of cancer after AMVAC.

These results suggest that doctors may one day sequence patients' tumors for the presence of these three mutations, to determine who will likely benefit most from chemotherapy before surgery, said Elizabeth R. Plimack, MD, Attending Physician in the Department Medical Oncology at Fox Chase.

"The purpose of the study is to find ways to identify patients who are likely to respond to early chemotherapy," said Dr. Plimack. "For those patients who won't benefit from it, we can send them directly to surgery to save time. But if they carry at least one of these mutations, we can treat them knowing they are likely to respond," she noted.

To uncover a genetic pattern that predicted responses to AMVAC, Dr. Plimack and her colleagues in collaboration with Foundation Medicine sequenced 287 cancer-related genes in tissue samples taken before patients underwent chemotherapy. The analysis clearly landed on three genes, all associated with repairing damaged DNA, carried by all but one of the people who benefited from chemotherapy. To see such a clear distinction between the genetic profiles of responding and non-responding tumors is remarkable, Dr. Plimack added. "It is unusual to see statistics this good," she said.

Additionally, patients whose cancer disappeared after AMVAC tended to carry more mutations in their tumors than those with residual cancer at the time of surgery.

It makes sense that the three key genes are associated with DNA repair, said Dr. Plimack. Patients who carry these mutations will likely have more mutations because their cells cannot easily repair cellular damage, so when cancer starts, mutations quickly accumulate. But since cisplatin works by further damaging DNA, these same tumors are more likely to succumb to its effects, since they lack mechanisms to sidestep chemotherapy. "These patients may have developed cancer because a damaged cell couldn't repair itself, but once they have cancer, the defective DNA repair machinery makes the tumor more likely to respond to chemotherapy because the cells can't repair the additional damage caused by cisplatin," said Dr. Plimack.

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Genetic profile predicts which bladder cancer patients will benefit from early chemotherapy

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Rh blood types and population genetics
he Rh (Rhesus) blood group system (including the Rh factor) is one of thirty-three current human blood group systems. It is the most important blood group system after ABO. At present, the...

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Gene Therapy Section Formed Within the Alliance for Regenerative Medicine
WASHINGTON, DC and SALT LAKE CITY, UT, United States, via eTeligis Inc., 05/20/2014 - - The Alliance for Regenerative Medicine and the American Society of Gene Cell Therapy Partner to Support...

By: Eteligis.com

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Gene Therapy Section Formed Within the Alliance for Regenerative Medicine - Video

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Personalized Medicine Using Gene Based Assays in Transplantation
Visit: http://www.uctv.tv/) Genomic monitoring of transplant patients. Series: "UCSF Transplant Update" [Health and Medicine] [Show ID: 28302]

By: University of California Television (UCTV)

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Returning To Work After a Spinal Cord Injury
In this video I talk briefly about returning to work after I suffered a spinal cord injury.

By: Paralyzed Living

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Phil Reyes, one of the Parkinson's patients in Summit 4 Stem Cell, urges California's stem cell agency to support its research.

A potentially groundbreaking trial to treat spinal cord injuries with tissue grown from human embryonic stem cells will resume, after being funded by the California's stem cell agency.

The California Institute for Regenerative Medicine's governing committee approved without opposition a $14.3 million award to Asterias Biotherapeutics of Menlo Park. Asterias is taking over from Geron, which stopped clinical trials in November, 2011. Geron, also of Menlo Park, said it discontinued the trials for business reasons. Asterias is a subsidiary of Alameda-based BioTime.

Patients will be given transplants of neural tissue grown from the embryonic stem cells. The hope is that the cells will repair the severed connections, restoring movement and sensation below the injury site.

CIRM also unanimously approved a $5.6 million grant for another potential breakthrough: a clinical trial by Sangamo Biosciences of Richmond, Calif, to cure HIV infection with gene therapy. The trial is now in Phase II. Immune cells are taken from the patient and given a mutant form of a gene that HIV uses to get inside the cells. The mutated gene resists infection. The genetically altered cells are then given back to the patient.

Approval of both grants had been expected, as staff reports had recommended their approval. The agency met in San Diego.

In addition CIRM's Independent Citizens Oversight Committee funded $16.2 million in grants to bring three stem cell researchers to California. That vote was more contentious, with some committee members arguing that it made no sense to bring more scientists to California without a specific need. In addition, they argued that CIRM's main emphasis needs to be on funding clinical trials.

Member Jeff Sheehy said that bringing the scientists to California doesn't create more scientific capacity. However, a vote to deny funding failed, and a subsequent vote to approve funding passed.

CIRM is projected to run out of its $3 billion in bond funding by 2017, and supporters of the public agency are considering asking California voters for more money.

Also appearing at the CIRM meeting were advocates of funding a stem cell-based therapy for Parkinson's disease. The therapy, which may be approved in 2015 for a clinical trial, uses artificial embryonic stem cells called induced pluripotent stem cells grown from the patient's own skin cells. The group, Summit 4 Stem Cell, plans to ask for funding to help with the trial in the near future.

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Spinal cord, HIV stem cell treatments funded

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30.05.2014 - (idw) Veterinrmedizinische Universitt Wien

Janus kinases (JAKs) are proteins that can promote the growth of cancer cells. The protein JAK2 is of special therapeutic significance: its inactivation is believed to destroy cancer cells. However, the effect of JAK2 inhibition on healthy blood stem cells is so far unknown. Scientists at the Vetmeduni Vienna show that the loss of JAK2 in the mouse causes healthy blood stem cells to disappear while cancer cells preserve their growth potential. Future studies will address the question as to whether these data can be passed on to treatment in humans. The results were published in the journal Leukemia. As a new therapeutic approach, Janus kinases are currently in the limelight of cancer research. The focus of interest is the protein JAK2. By inhibiting this protein one tries to cure chronic bone marrow diseases, such as myelofibrosis and chronic myeloid leukemia (CML).

Loss of JAK2 is advantageous for leukemia cells

Scientists working with Veronika Sexl at the Institute of Pharmacology and Toxicology may initiate a transformation of thought in regard of JAK2 inhibition. To simulate the human disease as accurately as possible, the scientists used a mouse leukemia model. In an experiment, mice received blood cancer cells as well as healthy hematopoietic stem cells in which JAK2 had been removed. "In mice, the absence of JAK2 accelerated the course of leukemia drastically," the scientists concluded.

The loss of JAK2 caused healthy hematopoietic stem cells to disappear in mice. "Leukemic cells, on the other hand, remained entirely unaffected; they do not need JAK2. This led to an imbalance in which the number of leukemia cells was very predominant, and eventually caused the acceleration of leukemia," says Eva Grundschober, one of the lead authors.

"The oncogene BCR-ABL, which was present in mice with leukemia, does not appear to require JAK2 for its activity. However, JAK2 is essential for healthy cells," explains Andrea Hlbl-Kovacic, the other lead author.

A closer investigation of healthy stem cells supports this hypothesis. In the absence of JAK2, healthy stem cells cannot survive and reproduce blood cells. As the next step, the following question will be raised in Sexl's laboratory: how does JAK2 mediate its life-sustaining effect on healthy stem cells? What portions of the JAK2 protein are required for this purpose and are these affected by current therapies?

The article Acceleration of Bcr-Abl+ leukemia induced by deletion of JAK2, by Eva Grundschober, Andrea Hlb-Kovacic, Neha Bhagwat, Boris Kovacic, Ruth Scheicher, Eva Eckelhart, Karoline Kollmann, Matthew Keller, Florian Grebien, Kay-Uwe Wagner, Ross L. Levine and Veronika Sexl was published today in the journal Leukemia. doi:10.1038/leu.2014.152 http://www.nature.com/leu/journal/vaop/naam/abs/leu2014152a.html

About the University of Veterinary Medicine, Vienna The University of Veterinary Medicine, Vienna in Austria is one of the leading academic and research institutions in the field of Veterinary Sciences in Europe. About 1,200 employees and 2,300 students work on the campus in the north of Vienna which also houses five university clinics and various research sites. Outside of Vienna the university operates Teaching and Research Farms. http://www.vetmeduni.ac.at

Scientific Contact: Prof. Veronika Sexl

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One cell's meat is another cell's poison

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A Harvard-led team is the first to demonstrate the ability to use low-power light to trigger stem cells inside the body to regenerate tissue, an advance they reported in Science Translational Medicine. The research, led by Wyss Institute Core Faculty member David Mooney, Ph.D., lays the foundation for a host of clinical applications in restorative dentistry and regenerative medicine more broadly, such as wound healing, bone regeneration, and more.

The team used a low-power laser to trigger human dental stem cells to form dentin, the hard tissue that is similar to bone and makes up the bulk of teeth. What's more, they outlined the precise molecular mechanism involved, and demonstrated its prowess using multiple laboratory and animal models.

A number of biologically active molecules, such as regulatory proteins called growth factors, can trigger stem cells to differentiate into different cell types. Current regeneration efforts require scientists to isolate stem cells from the body, manipulate them in a laboratory, and return them to the bodyefforts that face a host of regulatory and technical hurdles to their clinical translation. But Mooney's approach is different and, he hopes, easier to get into the hands of practicing clinicians.

"Our treatment modality does not introduce anything new to the body, and lasers are routinely used in medicine and dentistry, so the barriers to clinical translation are low," said Mooney, who is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences (SEAS). "It would be a substantial advance in the field if we can regenerate teeth rather than replace them."

The team first turned to lead author and dentist Praveen Arany, D.D.S., Ph.D., who is now an Assistant Clinical Investigator at the National Institutes of Health (NIH). At the time of the research, he was a Harvard graduate student and then postdoctoral fellow affiliated with SEAS and the Wyss Institute.

Arany took rodents to the laboratory version of a dentist's office to drill holes in their molars, treat the tooth pulp that contains adult dental stem cells with low-dose laser treatments, applied temporary caps, and kept the animals comfortable and healthy. After about 12 weeks, high-resolution x-ray imaging and microscopy confirmed that the laser treatments triggered the enhanced dentin formation.

"It was definitely my first time doing rodent dentistry," said Arany, who faced several technical challenges in performing oral surgery on such a small scale. The dentin was strikingly similar in composition to normal dentin, but did have slightly different morphological organization. Moreover, the typical reparative dentin bridge seen in human teeth was not as readily apparent in the minute rodent teeth, owing to the technical challenges with the procedure.

"This is one of those rare cases where it would be easier to do this work on a human," Mooney said.

Next the team performed a series of culture-based experiments to unveil the precise molecular mechanism responsible for the regenerative effects of the laser treatment. It turns out that a ubiquitous regulatory cell protein called transforming growth factor beta-1 (TGF-1) played a pivotal role in triggering the dental stem cells to grow into dentin. TGF-1 exists in latent form until activated by any number of molecules.

Here is the chemical domino effect the team confirmed: In a dose-dependent manner, the laser first induced reactive oxygen species (ROS), which are chemically active molecules containing oxygen that play an important role in cellular function. The ROS activated the latent TGF-1complex which, in turn, differentiated the stem cells into dentin.

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Researchers Use Light To Coax Stem Cells To Repair Teeth

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Open wide, this won't hurt a bit. That might actually be true if the dentist's drill is replaced by a promising low-powered laser that can prompt stem cells to make damaged hard tissue in teeth grow back. Such minimally invasive treatment could one day offer an easy way to repair or regrow our pearly whites.

When a tooth is chipped or damaged, dentists replace it with ceramic or some other inert material, but these deteriorate over time.

To find something better, researchers have begun to look to regenerative medicine and in particular to stem cells to promote tissue repair. Most potential stem cell therapies require the addition of growth factors or chemicals to coax dormant stem cells to differentiate into the required cell type. These chemicals would be applied either directly to the recipient's body, or to stem cells that have been removed from the body and cultured in a dish for implantation.

But such treatments have yet to make it into the doctor's clinic because the approach needs to be precisely controlled so that the stem cells don't differentiate uncontrollably.

Praveen Arany at the National Institute of Dental and Craniofacial Research in Bethesda, Maryland, and his colleagues wondered whether they could use stem cells to heal teeth, but bypass the addition of chemicals by harnessing the body's existing mechanisms.

"Everything we need is in the existing tooth structure the adult stem cells, the growth factors, and exactly the right conditions," says Arany.

So they tried laser light, because it can promote regeneration in heart, skin, lung, and nerve tissues.

To mimic an injury, Arany's team used a drill to remove a piece of dentin the hard, calcified tissue beneath a tooth's enamel that doesn't normally regrow from the tooth of a rat. They then shone a non-ionising, low-power laser on the exposed tooth structure and the soft tissue underneath it. This allowed the light to reach the dental stem cells deep inside the pulp of the tooth.

Twelve weeks after a single 5-minute treatment, new dentin had formed in the cavity. Similar dentin production was seen in mice and in cultured human dental stem cells.

It not quite the end of the dentist's intervention though, they would still need to cap the tooth to protect it, because the stem cells that produce enamel are not present in adults.

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Forget the dentist's drill, use lasers to heal teeth

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Ranking among the X-Men probably isn't all that it's cracked up to be, but who wouldn't want their uncanny ability to regenerate lost bone or tissue? New research into tooth repair and stem cell biology, from a cross-institution team led by David Mooney of Harvard's Wyss Institute, may bring such regeneration one step closer to reality or at the very least, give us hope that we can throw away those nasty dentures.

The researchers employed a low-power laser to trigger human dental stem cells to form dentin, a hard bone-like tissue that is one of four major components of teeth (the others being enamel, pulp, and cementum). This kind of low-level light therapy has previously been used to remove or stimulate hair growth and to rejuvenate skin cells, but the mechanisms were not well understood, results varied, and evidence of its efficacy was largely anecdotal.

The new work is the first to document the molecular mechanism involved, thus laying the foundations for controlled treatment protocols in not only restorative dentistry but also avenues like bone regeneration and wound healing. "The scientific community is actively exploring a host of approaches to using stem cells for tissue regeneration efforts," said Wyss Institute Founding Director Don Ingber. "Dave [Mooney] and his team have added an innovative, noninvasive, and remarkably simple but powerful tool to the toolbox."

To test the team's hypothesis, Praveen Arany, an assistant clinical investigator at the National Institutes of Health, drilled holes in the molars of rats and mice, then treated them with low-dose lasers and temporary caps. Around 12 weeks later, tests confirmed that the laser treatments triggered enhanced dentin formation.

Performing dentistry on rat teeth takes extreme precision and is actually harder than the same procedure on human teeth (Image: ames Weaver, Harvard's Wyss Institute)

Further experiments were conducted on microbial cultures in the laboratory, where they found that a regulatory cell protein called transforming growth factor beta-1 (TGF-1) was activated in a chemical domino effect that in turn caused the stem cells to form dentin. The good news there is that TGF-1 is more or less ubiquitous, with key roles in many biological processes such as immune response, wound healing, development, and malignancies.

This means we could one day see the technique used to do far more than help repair teeth. But first it needs to clear planned human clinical trials, so for now you'll have to make do with dentures, canes and all manner of other prosthetics while the likes of Wolverine prance around with self-healing bodies.

A paper on the research was recently published in the journal Science Translational Medicine.

Source: Wyss Institute at Harvard

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Low-power laser triggers stem cells to repair teeth

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PUBLIC RELEASE DATE:

29-May-2014

Contact: George Hunka ghunka@aftau.org 212-742-9070 American Friends of Tel Aviv University

About one in eight women in the United States will contract breast cancer in her lifetime. Now new research from Tel Aviv University-affiliated researchers, in collaboration with Johns Hopkins University, has provided another tool to help women, clinicians, and scientists searching for a cure to the one of the most widespread yet incurable diseases on the planet.

Dr. Ella Evron and Dr. Ayelet Avraham of the TAU-affiliated Assaf Harofeh Medical Center, together with Prof. Saraswati Sukumar of Johns Hopkins, have found that "gene regulation," the process that shuts off certain parts of a cell's DNA code or blueprint in healthy breast tissue cells, may also play a critical role in the development of breast cancer. Their research, published in PLOS ONE, focused on one particular gene TRIM29 selected from a pool of 100 genes with regulatory patterns specific to normal breast tissue, to prove the link between breast-specific genes and the pathology of cancer.

"We found that normal tissue affects the cancer that grows in that organ in other words, the specific pattern of gene regulation in the normal breast affects breast cancer, the characteristics of the disease, and its clinical behavior," said Dr. Avraham, a biologist and a researcher in the lab. "We hope that this study will lead to a better understanding of the cancer predisposition of mammary tissues and point to new targets for cancer intervention."

Searching for the right gene

In the study, normal tissue samples taken from conventional breast reduction surgeries were examined in a laboratory. The researchers isolated the milk ducts and purified the breast-tissue cells to create a cell culture, which was then tested for different gene regulation profiles.

While all cell types share the same genetic code (DNA), certain genes are specifically "expressed" or "silenced" in each cell type. Consequently, the unique gene expression patterns in every tissue dictate its structure and function. Various "gatekeeper" mechanisms either allow or block gene expression in our cells. One such mechanism is "DNA methylation," which shuts off or silences parts of the genetic code to form a specific pattern that identifies each tissue type.

The researchers compared the DNA methylation profiles of thousands of genes in breast, colon, lung, and endometrial tissues, selecting one gene, TRIM29, for further analysis. They found that the TRIM29 gene bore a unique DNA regulation in normal and cancerous breast tissues as opposed to other organ tissues.

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How breast cancer 'expresses itself'

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Newswise LA JOLLARonald M. Evans, director of the Gene Expression Laboratory at Salk and Howard Hughes Medical Institute investigator, is one of three scientists chosen to receive $5 million in research funding as part of The Lustgarten Foundation's new "Distinguished Scholars" program, which recognizes individuals who have made outstanding achievements in research to focus their efforts on finding a cure for pancreatic cancer.

The Lustgarten Foundation, the nation's largest private funder of pancreatic cancer research, established the new Distinguished Scholars initiative to identify and fund the best minds in research today to engage in pancreatic cancer research. The three scientists will each receive $5 million in research funding over the next five years. The grantees were selected by The Lustgarten Foundation's Scientific Advisory Board due to their historical accomplishments of breakthrough research.

"I am deeply honored by The Lustgarten Foundation's support and belief that this research will pave the road to a cure," says Evans. "We are excited to tackle the challenge and know that this funding will help us pioneer new advances toward understanding and treating this devastating disease."

"The Foundation's Scientific Advisory Board has selected these outstanding scientists because each one is a leader in their field with the greatest potential for developing an early detection test and more effective therapies for the nation's most lethal cancer," says Kerri Kaplan, executive director of The Lustgarten Foundation. "Together, we will pursue our mutual goals of improving survival rates for people with pancreatic cancer and eradicating this deadly disease."

Douglas Fearon, of Cold Spring Harbor Laboratory and Weill Cornell Medical College, and Bert Vogelstein, of Johns Hopkins Kimmel Cancer Center, will also both receive funding as part of the new program.

Evans, who is also the holder of the March of Dimes Chair in Molecular and Developmental Biology, focuses on hormones and how they communicate signals within the body. Several of the hormone signals Evans discovered are primary targets in the treatment of breast cancer, prostate cancer, pancreatic cancer and leukemia, as well as osteoporosis and asthma. Most recently he has been studying the use of Vitamin D in the treatment of pancreatic cancer in the laboratory. As a Lustgarten Foundation Distinguished Scholar, he will expand these studies to conduct clinical trials in pancreatic cancer patients using Vitamin D therapies.

About The Lustgarten Foundation and Pancreatic Cancer: Pancreatic cancer is swift and silent, often undetected until it's too late. More than 39,000 people will die from it this year. The overall five-year survival rate for pancreatic cancer is six percent and most with advanced cancer die within a year. There are no early detection tests, no effective long-term treatments and, unless the cancer is surgically removed in its earliest stages, no cure. It is the fourth-leading cause of cancer deaths in the United States.

The Lustgarten Foundation is America's largest private foundation dedicated to funding pancreatic cancer research. Based in Bethpage, New York, the Foundation supports focused research to find a cure for pancreatic cancer, facilitates dialogue within the medical and scientific community, and educates the public about the disease through awareness campaigns and fundraising events. The Foundation has provided millions of research dollars and assembled the best scientific minds with the hope that one day, a cure can be found. Cablevision Systems Corporation, a leading media and telecommunications company, underwrites The Lustgarten Foundation's administrative costs, so 100 percent of every dollar donated to the Foundation goes directly to pancreatic cancer research. Additional information about The Lustgarten Foundation is available at http://www.lustgarten.org.

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Salk Professor Named Grantee in New Pancreatic Cancer Research Program

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PUBLIC RELEASE DATE:

29-May-2014

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

New Rochelle, NY, May 29, 2014Women have accounted for half the students in U.S. medical schools for nearly two decades, but as professors, deans, and department chairs in medical schools their numbers still lag far behind those of men. Why long-held gender stereotypes are keeping women from achieving career advancement in academic medicine and what can be done to change the institutional culture are explored in an article in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website.

In "Stuck in the Out-Group: Jennifer Can't Grow Up, Jane's Invisible, and Janet's Over the Hill," Anna Kaatz, PhD, MPH and Molly Carnes, MD, MS, University of Wisconsin-Madison, present examples of three women at different stages of their careers to illustrate the ways in which gender stereotypes can influence people's judgment and negatively affect women in social interactions, causing them to be in the out-group and lose out on opportunities for professional advancement.

"Challenging cultural stereotypes about women and men is a critical step toward achieving gender equity in academic medicine," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

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About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website. Journal of Women's Health is the official journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

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Gender stereotypes keep women in the out-group

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WEDNESDAY, May 28, 2014 (HealthDay News) -- A team of international researchers has identified nearly 85 percent of proteins in the human body.

Proteins are the substances that provide structure, function and regulation of the body's tissues and organs. Human genes contain instructions (encoding) that direct the production of proteins, according to the U.S. National Institutes of Health.

In addition to finding the majority of the body's proteins, the researchers also identified 193 new proteins on the human genome. The proteins were found in areas of DNA that were believed to be "noncoding," or regions that do not encode proteins.

Finding proteins in areas with genes that weren't believed to code means the human genome could be more complex than previously believed, the researchers concluded.

"This was the most exciting part of this study, finding further complexities in the genome. The fact that 193 of the proteins came from DNA sequences predicted to be noncoding means that we don't fully understand how cells read DNA, because clearly those sequences do code for proteins," Dr. Akhilesh Pandey, a professor at the McKusick-Nathans Institute of Genetic Medicine and of biological chemistry, pathology and oncology at Johns Hopkins University in Baltimore, said in a news release.

More than 10 years ago, researchers identified all of the nearly 25,000 genes in human DNA. Known as the Human Genome Project, the research provided scientists with genetic information that helped them figure out how changes in certain genes could trigger some diseases.

The current researchers set out to create an initial catalog of all the proteins in the human body, or the human "proteome." The team identified proteins originating from more than 17,000 genes, which is about 84 percent of all of the genes in the human genome predicted to encode proteins.

Cataloging human proteins and where they can be found in the body may provide scientists even more insight than a catalog of all the genes in the human genome, the researchers pointed out. They explained that the characteristics of an organism depend on its genes. These genes, however, provide directions for making proteins, which are the building blocks of all cells in the body.

"You can think of the human body as a huge library where each protein is a book," explained Pandey, who is also the founder and director of the Institute of Bioinformatics in Bangalore, India. "The difficulty is that we don't have a comprehensive catalog that gives us the titles of the available books and where to find them. We think we now have a good first draft of that comprehensive catalog."

In attempting to catalog all of the proteins in the body, the team of researchers from Johns Hopkins and the Institute of Bioinformatics conducted a broad examination of the proteins in the human body from 30 tissue samples.

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Researchers Identify New Genetic Building Blocks

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Genetic testing can predict illnesses, but many don't want to know

Luke Hilger has been anticipating his 18th birthday for years, but not just for the usual reasons. Hilger has known since he was 12 years old that Huntingtons Disease runs in his family. Hes watched his mother steadily decline during the past five years, in the grip of what many in medicine believe to be among the bodys cruelest illnesses.

Huntingtons usually strikes people in their 40s. It causes nerve cells in the brain to break down. Sufferers lose control of their muscles and begin to twitch uncontrollably. Then they lose their ability to think. Eventually they develop depression and dementia. There is no cure.

There is a genetic test that will tell Hilger if he is destined to get Huntingtons. For the past five years, anxious about the possibility that he would suffer the same fate as his mother, Hilger was certain he wanted to take the test. But physicians, citing ethical considerations, told him he would have to wait until he was 18.

Hilger, who lives with his parents outside Salem, turns 18 in four months. He has attended national conferences for families of Huntingtons victims. He has looked for physical signs that he might be among those who get an early onset version of Huntingtons. And he has made a choice. He no longer wants to know his fate.

The idea was, I had to know, Hilger says. I had to know because its going to help me sleep at night.

But now, Hilger says, hes figured out that for him, the stress of not knowing is more bearable than if he takes the test and discovers he will suffer as he has seen his mother suffer.

Three weeks ago, scientists announced a promising new blood test that experts say within 10 years should be available to predict who is going to get dementia-causing Alzheimers disease. Physicians can use a brain scan to detect amyloid plaque buildup that has been associated with Alzheimers. Though the amyloid test is far from refined as a predictive tool, neurologists such as Eran Klein at Oregon Health & Science University say they are getting more inquiries from patients who want the test. Patients want to know if they are going to get Alzheimers, even though the disease has no cure and there is little therapy to ease its brain-decaying symptoms.

Hilger and Kleins fate-seeking patients are not medical oddities. They are, scientists and bioethicists say, a first wave that eventually could grow into a tsunami. As genetic testing and brain scanning become more widely used and better understood, most of us will have opportunities to know ahead of time what diseases we are likely to contract. The question is, will we want to? Only about one in five people with family histories of Huntingtons choose to take the genetic test that preoccupies Hilger.

Theres this technological paradigm that more information is always better, Klein says. But sometimes more information just complicates.

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Is there a disease in your future?

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TED

Stephen Friend spoke at TED 2014 in Vancouver.

In many cases, genetic factors can explain why some people get sick, or why people are predisposed to an illness. But most of the time, knowing about a genetic predisposition for certain diseases hasn't shown us how to prevent or cure that illness.

So maybe looking at sick people is the wrong approach.

Instead, we need to find the people who are genetically predisposed to these diseases but don't get sick, say biochemist Stephen Friend, president of Sage Bionetworks, and Eric Schadt, director of the Icahn Institute for Genomics at Mount Sinai School of Medicine.

Friend and Schadt are the principle investigators for the Resilience Project, an initiative that's trying to study those rare people who have the same genetic factors that normally cause disease but who are somehow protected by either genetic mutations or environmental factors.

In a TED 2014 talkreleased online today, Friend calls these people "unexpected heroes" most people don't know they have these hidden protective traits that could perhaps help others.

It turns out, he explains, that there are precedents for finding people like this and creating therapies based on the factors that make them unique.

In 1980s and 1990s, doctors realized that a very small number of people with high levels of HIV never developed AIDS, he explains. They had certain genetic mutations that prevented them from getting sick. Now, treatments for AIDS are being developed based on those mutations.

Along the same lines, most individuals who have high lipid levels, meaning fatty acids and cholesterol, develop heart disease. But there are some who don't. This can sometimes be explained by genetic mutations or protective environmental factors. Once these are better understood, they may provide new strategies for fighting heart disease.

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How Healthy People Who Should Be Sick Could Revolutionize Medicine

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Genetic Researching: Gene Therapy
Bio Video.

By: Ali Banach

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Genetic Researching: Gene Therapy - Video

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PUBLIC RELEASE DATE:

28-May-2014

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

Tampa, Fla. (May 28, 2014) To be suitable for medical transplantation, one idea is that human embryonic stem cells (hESCs) need to remain "undifferentiated" i.e. they are not changing into other cell types. In determining the best way to culture hESCs so that they remain undifferentiated and also grow, proliferate and survive, researchers have used blood cell "feeder-layer" cultures using animal-derived feeder cells, often from mice (mouse embryonic fibroblasts [MEFs]). This approach has, however, been associated with a variety of contamination problems, including pathogen and viral transmission.

To avoid contamination problems, a Brazilian research team has investigated the use of human menstrual blood-derived mesenchymal cells (MBMCs) as feeder layers and found that "MBMCs can replace animal-derived feeder systems in human embryonic stem cell culture systems and support their growth in an undifferentiated stage."

The study will be published in a future issue of Cell Medicine, but is currently freely available on-line as an unedited early e-pub at: http://www.ingentaconnect.com/content/cog/cm/pre-prints/content-CM1019silvadosSantos.

"Human embryonic stem cells present a continuous proliferation in an undifferentiated state, resulting in an unlimited amount of cells with the potential to differentiate toward any type of cell in the human body," said study corresponding author Dr. Regina Coeli dos Santos Goldenberg of the Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro. "These characteristics make hESCs good candidates for cell based therapies."

Feeder-layers for hESCs comprised of MEFs have been efficiently used for decades but, because of the clinical drawbacks, the authors subsequently experimented with human menstrual blood cells as a potential replacement for animal-derived feeder-layers, not only for negating the contamination issues, but also because human menstrual blood is so accessible. MBMCs are without ethical encumbrances and shortages, nor are they difficult to access - a problem with other human cells, such as umbilical cord blood cells, adult bone marrow cells or placenta cells.

"Menstrual blood is derived from uterine tissues," explained the researchers. "These cells are widely available 12 times a year from women of child-bearing age. The cells are easily obtained, possess the capability of long-term proliferation and are clinically compatible with hESCs-derived cells."

The researchers found that their culture system using MBMCs as a feeder-layer for hESCs are the "closest and more suitable alternative to animal-free conditions for growing hESCs" and a "good candidate for large-expansion of cells for clinical application." They also found no difference in growth factor expression when comparing the use of growth factors in both the standard feeder system using animal cells and the feeder system they tested using hESCs.

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Brazilian researchers find human menstrual blood-derived cells 'feed' embryonic stem cells

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Discredited stem-cell treatment loses in Strasbourg

(ANSA) - Strasbourg, May 28 - The European Court of Human Rights on Wednesday ruled that an Italian ban on a controversial stem-cell therapy was legitimate. The case centered around a woman suffering from a degenerative brain disease since birth who argued her rights had been violated by the State denying her Stamina treatment. The process involves extracting bone-marrow stem cells from a patient, turning them into neurons by exposing them to retinoic acid for two hours, and injecting them back into the patient. But its credibility has long been suspect, and last fall the health ministry ruled that the Stamina Foundation would no longer be allowed to test the treatment on humans. The foundation was also stripped of its non-profit status after a study found its treatment was "ignorant of stem-cell biology". Recent investigations have shown risks of the treatment range from nausea to cancer, and as many as one quarter of all patients treated have experienced "adverse effects". The head of the foundation, Davide Vannoni, may face indictment.

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European rights court says Stamina ban legit

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Arany PR et al.

This image shows the structure of the tooth cells as they begin the regeneration process.

Using lasers to regenerate and grow body parts sounds like science fiction, but researchers have just demonstrated that it might be a tranformative tool in medicine or at least dentistry in the future.

A Harvard-led team just successfully used low-powered lasers to activate stem cells and stimulate the growth of teeth in rats and human dental tissue in a lab. The results were published today in the journal Science Translational Medicine.

Stem cells exist throughout the body, and they fascinate scientists because they have the ability to become different types of cells which means they have the potential to repair or replace damaged or worn out tissue. Figuring out new ways to make them useful has long been a goal of medical researchers.

Using lasers to make stem cells do their work is particularly appealing, since it's a minimally invasive technique, only requiring light once the damaged area is exposed. Scientists have theorized in the past that this was possible, since lasers have been shown to stimulate growth for unknown reasons, but this is the first time that the process has been demonstrated and observed.

The ability to naturally regrow dental tissue could transform dentistry, making it possible to regrow teeth instead of replacing them with a substitute like porcelain. But even more amazingly, once it's better understood, this same technique could potentially be used to heal wounds and regenerate bone, skin, and muscle.

The research is in its earliest stages and has not yet been tested on humans, so it's far too soon to say whether these futuristic techniques will ever make it to your local hospital. The treatment possibilities raised by these experiments, however, are exciting to contemplate.

Arany PR et al.

This is the exposed rat molar that received the laser treatment, causing it to start to grow back.

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Scientists Can Regrow Teeth With Lasers

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