Archive for May, 2014

Termis Chapter Meeting 2014 - Regenerative Medicine Engineering
Comecer will be exhibiting a new solution for regenerative medicine. 10 -- 13 June, Genova -- Italy, Booth no. 3 More information: http://www.comecer.com/events/termis-2014/

By: Comecer Group

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Termis Chapter Meeting 2014 - Regenerative Medicine Engineering - Video

Miami (PRWEB) May 30, 2014

GlobalStemCellsGroup.com will host the First International Symposium on Stem Cell Research in Buenos Aires, Argentina Oct. 2, 3 and 4. The symposium will provide an opportunity to showcase advancements in stem cell research and therapies on a global level and establish a dialogue among the worlds leading stem cell experts. Pioneers and luminaries in stem cell medicine will be featured speakers as well as accomplished guests prepared to share their knowledge and experience in their individual medical specialties.

Regenerative medicine as a field is still in its infancy, and Global Stem Cells Group President and CEO Benito Novas believes it is time to clear up old misconceptions and change outdated attitudes by educating people on the wide range of illnesses and injuries stem cell therapies are already treating and curing. The first step, Novas says, is establishing a dialogue between researchers and practitioners in order to move stem cell therapies from the lab to the physicians office.

Our objective is to open a dialogue among the worlds medical and scientific communities in order to advance stem cell technologies and translate them into point-of-care medical practices, Novas says. Our mission is to bring the benefits of stem cell therapies to the physicians office for the benefit and convenience of the patient, safely and in full compliance with the highest standard of care the world has to offer.

An interdisciplinary team of leading international stem cell experts will provide a full day of high-level scientific lectures aimed at medical professionals.

Among the growing list of speakers are some of the worlds most prominent authorities on stem cell medicine including:

The objective of Global Stem Cell Groups international symposium is to educate the public and the medical community, and at the same time establish a dialog between physicians, scientists, biotech companies and regulatory agencies in order to advance stem cell technologies so they can be used to benefit people who need them.

Global Stem Cells Group is also joining forces with some of the most prestigious regenerative medicine conferences in South America including:

Stem cell therapies are revolutionizing the anti-aging aesthetics industry while offering new hope for sufferers of serious chronic debilitating diseases

For more information on the Global Stem Cell Group First International Symposium on Stem Cells and Regenerative Medicine and the events lineup of speakers, visit the Global Stem Cells Symposium website, email bnovas(at)regenestem(dot)com, or call 305-224-1858.

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Global Stem Cells Group to Host the First International Symposium on Stem Cells and Regenerative Medicine in Buenos ...

PUBLIC RELEASE DATE:

30-May-2014

Contact: Liz Ahlberg eahlberg@illinois.edu 217-244-1073 University of Illinois at Urbana-Champaign

CHAMPAIGN, Ill. The gap between stem cell research and regenerative medicine just became a lot narrower, thanks to a new technique that coaxes stem cells, with potential to become any tissue type, to take the first step to specialization. It is the first time this critical step has been demonstrated in a laboratory.

University of Illinois researchers, in collaboration with scientists at Notre Dame University and the Huazhong University of Science and Technology in China, published their results in the journal Nature Communications.

"Everybody knows that for an embryo to form, somehow a single cell has a way to self-organize into multiple cells, but the in vivo microenvironment is not well understood," said study leader Ning Wang, a professor of mechanical science and engineering at the U. of I. "We want to know how they develop into organized structures and organs. It doesn't happen by random chance. There are biological rules that we don't yet understand."

During fetal development, all the specialized tissues and organs of the body form out of a small ball of stem cells. First, the ball of generalized cells separates into three different cell lines, called germ layers, which will become different systems of the body. This crucial first step has eluded researchers in the lab. No one has yet been able to induce the cells to form the three distinct germ layers, in the correct order endoderm on the inside, mesoderm in the middle and ectoderm on the outside. This represents a major hurdle in the application of stem cells to regenerative medicine, since researchers need to understand how tissues develop before they can reliably recreate the process.

"It's very hard to generate tissues or organs, and the reason is that we don't know how they form in vivo," Wang said. "The problem, fundamentally, is that the biological process is not clear. What is the biological environment that controls this, so they can become more organized and specialized?"

Wang's team demonstrated that not only is it possible for mouse embryonic stem cells to form three distinct germ layers in the lab, but also that achieving the separation requires a careful combination of correct timing, chemical factors and mechanical environment. The team uses cell lines that fluoresce in different colors when they become part of a germ layer, which allows the researchers to monitor the process dynamically.

The researchers deposited the stem cells in a very soft gel matrix, attempting to recreate the properties of the womb. They found that several mechanical forces played a role in how the cells organized and differentiated the stiffness of the gel, the forces each cell exerts on its neighbors, and the matrix of proteins that the cells themselves deposit as a scaffolding to give the developing embryo structure.

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For the first time in the lab, researchers see stem cells take key step toward development

Patients do not have an automatic right to a compassionate therapy for which there is no scientific evidence of efficacy, according to a landmark ruling of the European Court of Human Rights in Strasbourg.

The 28 May ruling referred to the case of Nivio Durisotto, whose daughter suffers a degenerative brain disease. He wished her to be treated with a controversial stem cell-based therapy offered by the Stamina Foundation, based in Brescia, Italy.

But more generally, it will guide any judge facing requests from desperate patients for access to unproved therapies promoted from outside the regulated medical sector.

The judgement is yet another blow for the Stamina Foundation, whose president, Davide Vannoni, is now facing charges of fraudulently obtaining public money to support his therapy.

The Italian Medicines Agency had closed down the Stamina operations in August 2012 on safety grounds (see Leaked files slam stem-cell therapy). In March 2013, the government issued a decree allowing patients to continue Stamina treatment if they had already begun.

Then on 11 September, 2013 an expert committee appointed by the health ministry to examine the Stamina method concluded that there was no evidence to indicate that it might be efficacious (see Advisers declare Italian stem-cell therapy unscientific). The committee further warned that it could be dangerous.

With encouragement from Vannoni, some patients appealed to courts for the right to treatment with the Stamina method. Some judges ruled that the treatment should be given on compassionate grounds, while others including the judge in the Durisotto case ruled that compassionate therapy was not justified because there was no scientific evidence of efficacy.

Durisotto brought his appeal to the European Court of Human Rights on 28 September, 2013 a month after losing his case in Italy.

The European Court dismissed Durisottos claim, saying that the Italian courts ruling had pursued the legitimate aim of protecting health and was proportionate to that aim. It further said that the Italian courts decision had been properly reasoned and was not arbitrary, and that the therapeutic value of the Stamina method had, to date, not yet been proven scientifically. Because the case had been appropriately reasoned, it said, Durisottos daughter had not been discriminated against even if some other national courts had allowed the therapy for similar medical conditions.

Munich-based patent lawyer Clara Sattler de Sousa e Brito, an expert in biomedical laws, says that this clear ruling that scientific proof is necessary will help avoid the use of unproven therapies for so-called compassionate purposes in the future.

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Human rights court rules that evidence must support compassionate therapy

By: Stephanie Guadian EL PASO, Texas - Inaki Arruti is an El Paso boy battling leukemia and a shortage of blood and bone marrow donations from the Hispanic community. I recently shared his story with KFOX 14 viewers.

The story hit home for Janet Chavarria. She is an employee at Western Technical College and Inaki's cousin.

After being inspired by our story to take action, she and the school organized a two-day Be the Match blood and bone marrow drive. Those who agreed to register simply swabbed their cheeks. The DNA will be compared to patients for a possible match.

It's not just Inaki. There are more children out there you know that have this. There are more people that have this. So, if we are not helping out Inaki, there might be someone else. But hopefully, there will be a match, said Janet Chavarria.

According to Be the Match, a national marrow donor program, Hispanics have only a 72 percent chance of finding a donor, compared with 93 percent for white patients. Anita Gonzales is a Be the Match employee working in El Paso.

We are blessed with another country right next to us. But everything they blow into the air. Unfortunately, it comes into El Paso and we breathe it. It's in the particles in the air, the ground that we walk on, the food that we eat. So, anyone can get leukemia. It's not inherited, said Gonzales.

Today -- the most common way of collecting stem cells is done by filtering them from a person's blood. The procedure is considered painless and similar to donating blood. The donation could one day save of the life of someone like Inaki.

Nearly 300 people signed up to be potential matches at the two day blood and bone marrow drive at Western Technical College. If you would like to find out how you can sign up to be a donor, check outbethematch.org

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Drive held to save El Paso boy and other children in need of donations

Beverly Hills, California (PRWEB) May 29, 2014

The Beverly Hills Orthopedic Institute is now providing several types of stem cell procedures for healing ligament injuries and meniscal tears of the knee. The stem cell therapies are often able to repair the injuries, provide pain relief and help patients avoid the need for surgery. For more information and scheduling, call (310) 438-5343.

Injuries to the knee may occur from sports injuries, auto accidents or result from degenerative arthritis. Conventional treatments typically work well for pain relief, however, they do not repair the damaged soft tissue. Therefore, conventional treatments result in healing that is incomplete and may still lead to the need for the surgery.

At Beverly Hills Orthopedic Institute, Double Board Certified Los Angeles Orthopedic Surgeon Dr. Raj has been a pioneer in stem cell procedures for the knee. He is an expert in several types of stem cell therapies for knee injuries including amniotic derived or bone marrow derived stem cell injections.

The regenerative medicine procedures are performed as an outpatient and maintain exceptionally low risk. The amniotic-derived stem cell material is processed at an FDA regulated lab, while the bone marrow-derived stem cell therapy involves a short harvesting procedure from the patient himself. Both types of procedures have been shown in small studies to have excellent clinical results for knee conditions.

Along with treating all types of knee injuries with stem cell therapy, Beverly Hills orthopedic surgeon Dr. Raj also treats shoulder, hip ankle and spinal conditions with regenerative medicine as well. Treatments are provided for amateur and professional athletes, weekend warriors, executives, grandparents, students and more.

For those who desire to explore stem cell procedures for helping repair knee injuries and avoiding surgery, call the Beverly Hills Orthopedic Institute at (310) 438-5343.

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Beverly Hills Orthopedic Institute Now Offering Stem Cell Procedures for Meniscal Tears and Ligament Injuries of the ...

PUBLIC RELEASE DATE:

30-May-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center

STANFORD, Calif. For many scientists, the clinical promise of stem cells has been dampened by very real concerns that the immune system will reject the transplanted cells before they could render any long-term benefit. Previous research in mice has suggested that even stem cells produced from the subject's own tissue, called iPS cells, can trigger an immune attack.

Now researchers at the Stanford University School of Medicine have found that coaxing iPS cells in the laboratory to become more-specialized progeny cells (a cellular process called differentiation) before transplantation into mice allows them to be tolerated by the body's immune system.

"Induced pluripotent stem cells have tremendous potential as a source for personalized cellular therapeutics for organ repair," said Joseph Wu, MD, PhD, director of the Stanford Cardiovascular Institute. "This study shows that undifferentiated iPS cells are rejected by the immune system upon transplantation in the same recipient, but that fully differentiating these cells allows for acceptance and tolerance by the immune system without the need for immunosuppression."

The findings are described in a paper to be published online May 30 in Nature Communications. Wu is senior author of the paper. Postdoctoral scholars Patricia Almeida, PhD, and Nigel Kooreman, MD, and assistant professor of medicine Everett Meyer, MD, PhD, share lead authorship.

In a world teeming with microbial threats, the immune system is a necessary watchdog. Immune cells patrol the body looking not just for foreign invaders, but also for diseased or cancerous cells to eradicate. The researchers speculate that the act of reprogramming adult cells to pluripotency may induce the expression of cell-surface molecules the immune system has not seen since the animal (or person) was an early embryo. These molecules, or antigens, could look foreign to the immune system of a mature organism.

Previous studies have suggested that differentiation of iPS cells could reduce their tendency to inflame the immune system after transplantation, but this study is the first to closely examine, at the molecular and cellular level, why that might be the case.

"We've demonstrated definitively that, once the cells are differentiated, the immune response to iPS-derived cells is indistinguishable from its response to unmodified tissue derived from elsewhere in the body," said Kooreman.

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Coaxing iPS cells to become more specialized prior to transplantation cuts rejection risk

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Newswise A study of 338 patients with coronary artery disease has identified a gene expression profile associated with an elevated risk of cardiovascular death. Used with other indicators such as biochemical markers and family history, the profile based on a simple blood test may help identify patients who could benefit from personalized treatment and counseling designed to address risk factors.

Researchers found the risk signature by comparing gene expression profiles in 31 study subjects who died of cardiovascular causes against the profiles of living members of the study group. Twenty-five of the 31 deaths occurred in the group with the high-risk profile, though coronary deaths were also recorded among the lower risk members of the study group. All of the patients studied had coronary artery disease (CAD), and about one in five had suffered a heart attack prior to the study.

Researchers from the Georgia Institute of Technology, Emory University and Princeton University participated in the study, which obtained gene expression profiles from blood samples taken from patients undergoing cardiac catheterization at Emory University clinics in Atlanta. The results are scheduled to be published in the open-access journal Genome Medicine on May 29, 2014.

We envision that with our gene expression-based marker, plus some biochemical markers, genotype information and family history, we could produce a tiered evaluation of peoples risks of adverse coronary events, said Gregory Gibson, director of the Center for Integrative Genomics at Georgia Tech and one of the studys senior authors. This could lead to a personalized medicine approach for people recovering from heart attack or coronary artery bypass grafting.

Coronary artery disease is the leading cause of death for both men and women in the United States. Manifested in the narrowing of blood vessels through the buildup of plaque, CAD sets the stage for heart attacks and long-term heart failure.

As many as half of Americans over the age of 50 suffer from CAD to some extent, so the researchers wondered if they could single out those with the highest risk of death. From a cohort of more than 3,000 persons known as the Emory Cardiovascular Biobank (EmCD), they selected two groups of patients for extensive gene expression analysis based on blood samples.

After following the patients for as long as five years, the researchers examined gene expression patterns in a total of 31 persons from the study group who had suffered coronary deaths. Comparing these patterns against those of other study subjects revealed a pattern in which genes affecting inflammation were up-regulated, while genes affecting T-lymphocytes were down-regulated.

The patients studied ranged in age from 51 to 73, were mostly Caucasian, and 65 percent male. Seventy percent of the subjects had significant CAD, and 18 percent were experiencing an acute myocardial infarction when blood samples were taken. Gene expression was analyzed using microarrays and two different normalization procedures to control for technical and biological covariates. Whole genome genotyping was used to support comparative genome-wide association studies of gene expression. Two phases of the study were conducted independently with the two different groups, and produced similar results.

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Gene Expression Signature Identifies Patients at Higher Risk for Cardiovascular Death

College Prep English at EIE May 29, 2014
Oratory practice: discussion of genetic engineering.

By: Abacus Ed

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College Prep English at EIE May 29, 2014 - Video

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

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

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

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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GoldLab Symposium 2014 - Lucy Shapiro - Video

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

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

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...

By: GeneticsLessons

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Rh blood types and population genetics - Video

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

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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Personalized Medicine Using Gene Based Assays in Transplantation - Video

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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Returning To Work After a Spinal Cord Injury - Video

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

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

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

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

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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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'