A cow in New Zealand has been genetically modified to produce hypoallergenic milk.

AgResearch

Two genetically engineered farm animals reported today illustrate how far from Frankensteins stitched-together monster animal biotechnology has come. One of those animals, a cow, secretes milk that lacks an allergy-inducing protein because researchers accurately blocked its production using the technique of RNA interference1. And in pigs, scientists have used an enzyme called a TALEN2 to scramble a gene that would normally help remove cholesterol.

RNA interference (RNAi) and TALENs are more accurate at targeting the gene in question than are earlier genetic engineering techniques. For years, researchers tried to remove the allergy-inducing milk protein beta-lactoglobulin from cow's milk, which can cause diarrhea and vomiting in some toddlers. They tried replacing the gene encoding beta-lactoglobulin with a defective form, but this proved nearly impossible because the techniques available to introduce foreign genes into animal genomes were not precise, and misplaced genes failed to express themselves correctly.

In 2006, scientists at AgResearch in Hamilton, New Zealand began to experiment with molecules that interfere with the messenger RNA go-between that enables translation of a gene into protein. In mice, they discovered a short chunk of RNA, called a microRNA, that targeted beta-lactoglobulin messenger RNA directly to prevent its translation. They inserted DNA encoding a version of this microRNA into the genome to create genetically modified cow embryos that they hoped would grow into cows without the allergen in their milk. Out of 100 embryos, one calf yielded beta-globulin-free milk. This isnt a quick process, says Stefan Wagner, a molecular biologist at AgResearch. That's why it has taken so long to succeed in making an allergen-free cow, he says.

Wagner says that TALENs, which were not readily available when he began his research, might speed up the process, and that the team plans to use them to eliminate beta-lactoglobulin. RNAi cannot eliminate the protein completely because some messenger RNA slips past the blockade, but each TALEN targets a specific DNA sequence in the genome and cuts it. As the body repairs the break, mutations are often introduced that render the targeted gene non-functional. The TALEN technology is staggeringly easy, quick, and leaves no mark in the genome, says Bruce Whitelaw, a molecular biologist at the Roslin Institute near Edinburgh in the United Kingdom, who contributed to the work in pigs. In essence, we are just mimicking an evolutionary process with precise, man-made editors.

His team used TALENs to disrupt genes encoding low-density lipoprotein (LDL) receptors. Without these receptor proteins to remove cholesterol-containing LDLs from the blood, LDLs build-up and lead to atherosclerosis. Pigs with this condition may be reliable models of human atheroscelerosis in biomedical research.

The TALEN-modified pig is not the first model of human heart disease (see Model pigs face a messy path), but the technique makes genetic engineering less costly and more efficient. Id be exaggerating if I said that pigs and cows can now be thought of as big mice, but we are moving in that direction, says Heiner Niemann, a bioengineer at the Institute of Farm Animal Genetics in Neustadt, Germany.

The excitement surrounding these technological advances is bittersweet, however. Originally, engineered animals were produced with the aim of making food safer, healthier and more abundant. Yet despite years of investment, almost no animal has been approved by regulatory agencies around the world. Wagner says he has not tasted the milk from his special cow because hes not permitted to under New Zealand law. We must restrict our research to scientific analysis, he says. The current climate for animal biotech is not very good, and therefore, we are nowhere near getting this to the consumer."

Originally posted here:
Animals engineered with pinpoint accuracy

Recommendation and review posted by Bethany Smith

Smoking is not the only cause of lung cancer.

"It's a heterogeneous group of people who get lung cancer these days," said Dr. Linda Garland, director of clinical research in thoracic oncology at The University of Arizona Cancer Center in Tucson.

Garland says she's seen a stigma attached to lung cancer, where people blame the patient and think it's something they brought on themselves by smoking. But that is not an accurate picture.

Secondhand smoke exposure, and exposure to uranium and radon, are all associated with causing lung cancer in nonsmokers, she said. And nonsmokers who live in very polluted cities get lung cancer at a higher rate than people who live in a very clean environment.

Other cases are attributed to genetics.

The good news for people whose lung cancer is related to genetic abnormalities is that there are oral drugs that have proven very effective in shrinking tumors.

"The interesting thing is we've come to find a lot of very important information about 'never smokers' ' lung cancer in that we now have defined three very specific genetic abnormalities and those drive the lung cancer," Garland said.

"These driver mutations or fusion genes create in a very simplistic way a very activated pathway that leads to proliferation, ability to metastasize, replication potential - all the things that define a cancer cell."

When a tumor is removed, it can be tested for the three genetic abnormalities and if one is found, the patient can be treated with one of two cancer medications that became available in the last 15 years. When the gene mutation is targeted with the right medication, very rapid, very significant tumor shrinkage can occur, Garland said.

"Sometimes it looks like you've got the electrical circuit to Los Angeles County and you take the main breaker and turn it off. It's very dramatic," she said. "People can get some very prolonged, excellent benefit from these pills."

Read this article:
Genetics, pollution contribute to lung cancer

Recommendation and review posted by Bethany Smith

LOS ANGELES, Oct.1, 2012 /PRNewswire/ --Response Genetics, Inc. (RGDX), a company focused on the development and commercialization of molecular diagnostic tests for cancer, announced today the addition of James Wynne as the company's Vice President, Sales & Marketing. In this newly created position, Mr. Wynne will be responsible for leading the company's ResponseDX strategic and operational sales and marketing activities including the expansion of the company's direct sales efforts and identifying new service offerings.

"With Jim's strong background in providing results driven and advanced skills in sales management, marketing and communications in the clinical laboratory diagnostics space, we believe he is ideally suited to lead our ResponseDX sales and marketing efforts," said Thomas A. Bologna, Chairman & Chief Executive Officer of Response Genetics. "Jim's track record of building a performance driven sales team along with his true appreciation for how to market clinical testing services to pathologists and oncologists will be a tremendous asset to us. We are looking forward to his contributions."

Mr. Wynne has spent the last 20 plus years in cancer diagnostics. He spent the first six years in pharmaceutical sales moving into leadership roles. He joined Impath in 1995 as a Territory Sales Manager before being promoted to Director of Sales for the western region. Under his leadership revenue grew exponentially. After nine successful years, Mr. Wynne was recruited to UCLA Medical Center as the Director of Sales for UCLA's pathology outreach program. Mr. Wynne joins Response Genetics from Clarient, Inc. where he started in 2004 when the company was known as Chromavision Medical Systems. Mr. Wynne recruited and developed the original Clarient sales team and worked with the marketing group to prioritize product development. During his tenure, he directly helped the sales team grow to an approximately $115 million revenue generating organization at the time of its acquisition by GE Healthcare. Mr. Wynne received a BA in Sociology from the University of California, Los Angeles and an MBA from Pepperdine University.

Mr. Wynne, commenting on his appointment, "I am extremely excited about joining Response Genetics for a number of reasons. It's a perfect fit for my background, interests and skills, and I am happy to be a part of the leadership team that Tom has assembled to transition Response Genetics into a top line, sales driven, high growth company."

About Response Genetics, Inc.

Response Genetics, Inc. (the "Company") is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic testing services for cancer. The Company's technologies enable extraction and analysis of genetic information from genes derived from tumor samples stored as formalin-fixed and paraffin-embedded specimens. The Company's principal customers include oncologists and pathologists. In addition to diagnostic testing services, the Company generates revenue from the sale of its proprietary analytical pharmacogenomic testing services of clinical trial specimens to the pharmaceutical industry. The Company's headquarters is located in Los Angeles, California. For more information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of the Company related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Company's plans, objectives, projections, expectations and intentions, such as the ability of the Company, to provide clinical testing services to the medical community, to continue to expand its sales force, to continue to build its digital pathology initiative, to attract and retain qualified management, to continue to provide clinical trial support to pharmaceutical clients, to enter into new collaborations with pharmaceutical clients, to enter into areas of companion diagnostics, to continue to execute on its business strategy and operations, to continue to analyze cancer samples and the potential for using the results of this research to develop diagnostic tests for cancer, the usefulness of genetic information to tailor treatment to patients, or to successfully file a registration statement with the Securities Exchange Commission ("SEC"), and other statements identified by words such as "project," "may," "could," "would," "should," "believe," "expect," "anticipate," "estimate," "intend," "plan" or similar expressions.

These statements are based upon the current beliefs and expectations of the Company's management and are subject to significant risks and uncertainties, including those detailed in the Company's filings with the SEC. Actual results, including, without limitation, actual sales results, if any, or the application of funds, may differ from those set forth in the forward-looking statements. These forward-looking statements involve certain risks and uncertainties that are subject to change based on various factors (many of which are beyond the Company's control). The Company undertakes no obligation to publicly update forward-looking statements, whether because of new information, future events or otherwise, except as required by law.

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Response Genetics, Inc. Announces Appointment of James Wynne as Vice President, Sales & Marketing

Recommendation and review posted by Bethany Smith

A beautiful, fresh face, Sabrina Cohen can stun you with her charm.

But she is far more. This 24-year-old, who has spent 10 years in a wheelchair as a result of a car accident, is battling to raise money for research and therapies that may eventually reverse paralysis and treat central nervous system impairments.

A native of Miami Beach, she is one of five leaders being honored by the Palm Beach-based Genetic Policy Institute at its eighth annual World Stem Cell Summit Dec. 4 at the Palm Beach County Convention Center in West Palm Beach. She is receiving the Inspirational Award.

This award brings a lot of meaning to my life and the path I have chosen to follow, she says of her founding of the nonprofit Sabrina Cohen Foundation.

This provides a platform for my foundation to inspire others and to share my hope for (stem cell) regeneration.

Other honorees include CBS 60 Minutes for its hard-hitting programs on unproven stem cell treatments; Susan Solomon, CEO of the New York Stem Cell Foundation; Alliance for Regenerative Medicine; and the Nebraska Coalition for Lifesaving Cures.

We recognize the dedicated individuals and organizations that positively impact the cause of stem-cell advancement aimed at finding cures and alleviating human suffering, said Bernard Siegel, executive director of GPI.

Through their positive actions, our honorees have moved the regenerative medicine needle, bringing closer the day when patients will be safely treated through these innovative technologies.

Previous Stem Cell Action awardees have included Maryland Governor Martin OMalley, Research!America, Juvenile Diabetes Research Foundation, Michael J. Fox, Robert Klein, Sherry Lansing, Palm Beacher A. Alfred Taubman and the National Association of Biology Teachers.

This year, panels will address advancing treatments for specific diseases and conditions including cancer, diabetes, HIV/AIDS, cardiovascular disease, spinal cord injury, paralysis, multiple sclerosis, ALS, Parkinsons, eye diseases and others.

Originally posted here:
Stem-cell advocacy ‘moved the needle’

Recommendation and review posted by simmons

NEW YORK, Oct. 1, 2012 /PRNewswire/ -- Reportlinker.com announces that a new market research report is available in its catalogue:

Translational Regenerative Medicine: Market Prospects 2012-2022

http://www.reportlinker.com/p0595030/Translational-Regenerative-Medicine-Market-Prospects-2012-2022.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=Blood_Supply,_Tissue_Banking_and_Transplantation

Report Details

New study shows you commercial potential of regenerative treatments

See what the future holds for translational regenerative medicine. Visiongain's updated report lets you assess forecasted sales at overall world market, submarket, product and regional level to 2022.

There you investigate the most lucrative areas in that research field, industry and market. Discover prospects for tissue-engineered products, stem cell treatments and gene therapy.

We pack our study with information and analysis to help your work and save you time:

Access to present and predicted trends, with commercial opportunities and prospects revealed

Data and discussions - including our revenue forecasts to 2022 - for your research, analyses and decision making

Read this article:
Translational Regenerative Medicine: Market Prospects 2012-2022

Recommendation and review posted by simmons

ScienceDaily (Oct. 1, 2012) A novel therapy in the early stages of development at Virginia Commonwealth University Massey Cancer Center shows promise in providing lasting protection against the progression of multiple myeloma following a stem cell transplant by making the cancer cells easier targets for the immune system.

Outlined in the British Journal of Hematology, the Phase II clinical trial was led by Amir Toor, M.D., hematologist-oncologist in the Bone Marrow Transplant Program and research member of the Developmental Therapeutics program at VCU Massey Cancer Center. The multi-phased therapy first treats patients with a combination of the drugs azacitidine and lenalidomide. Azacitidine forces the cancer cells to express proteins called cancer testis antigens (CTA) that immune system cells called T-cell lymphocytes recognize as foreign. The lenalidomide then boosts the production of T-cell lymphocytes. Using a process called autologous lymphocyte infusion (ALI), the T-cell lymphocytes are then extracted from the patient and given back to them after they undergo a stem cell transplant to restore the stem cells' normal function. Now able to recognize the cancer cells as foreign, the T-cell lymphocytes can potentially protect against a recurrence of multiple myeloma following the stem cell transplant.

"Every cell in the body expresses proteins on their surface that immune system cells scan like a barcode in order to determine whether the cells are normal or if they are foreign. Because multiple myeloma cells are spawned from bone marrow, immune system cells cannot distinguish them from normal healthy cells," says Toor. "Azacitidine essentially changes the barcode on the multiple myeloma cells, causing the immune system cells to attack them," says Toor.

The goal of the trial was to determine whether it was safe, and even possible, to administer the two drugs in combination with an ALI. In total, 14 patients successfully completed the investigational drug therapy. Thirteen of the participants successfully completed the investigational therapy and underwent a stem cell transplant. Four patients had a complete response, meaning no trace of multiple myeloma was detected, and five patients had a very good partial response in which the level of abnormal proteins in their blood decreased by 90 percent.

In order to determine whether the azacitidine caused an increased expression of CTA in the multiple myeloma cells, Toor collaborated with Masoud Manjili, D.V.M., Ph.D., assistant professor of microbiology and immunology at VCU Massey, to conduct laboratory analyses on bone marrow biopsies taken from trial participants before and after treatments. Each patient tested showed an over-expression of multiple CTA, indicating the treatment was successful at forcing the cancer cells to produce these "targets" for the immune system.

"We designed this therapy in a way that could be replicated, fairly inexpensively, at any facility equipped to perform a stem cell transplant," says Toor. "We plan to continue to explore the possibilities of immunotherapies in multiple myeloma patients in search for more effective therapies for this very hard-to-treat disease."

In addition to Manjili, Toor collaborated with John McCarty, M.D., director of the Bone Marrow Transplant Program at VCU Massey, and Harold Chung, M.D., William Clark, M.D., Catherine Roberts, Ph.D., and Allison Hazlett, also all from Massey's Bone Marrow Transplant Program; Kyle Payne, Maciej Kmieciak, Ph.D., from Massey and the Department of Microbiology and Immunology at VCU School of Medicine; Roy Sabo, Ph.D., from VCU Department of Biostatistics and the Developmental Therapeutics program at Massey; and David Williams, M.D., Ph.D., from the Department of Pathology at VCU School of Medicine, co-director of the Tissue and Data Acquisition and Analysis Core and research member of the Developmental Therapeutics program at Massey.

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Immune system harnessed to improve stem cell transplant outcomes

Recommendation and review posted by simmons

HOUSTON, Oct. 1, 2012 /PRNewswire/ --The Houston Stem Cell Summit will host an extraordinary lineup of keynote speakers who represent the most accomplished stem cell scientists, clinicians and entrepreneurs in the United States. Joining these distinguished speakers will be Governor of Texas, Rick Perry, consistent champion of adult stem cell therapies.

(Logo: http://photos.prnewswire.com/prnh/20120831/NY66463LOGO )

The Houston Stem Cell Summit will be held October 26 27 in its namesake city and will highlight the latest therapeutic research regarding the use of adult stem and progenitor cell therapies. The Summit will also provide a forum for entrepreneurs to discuss their latest efforts to commercialize stem cell therapies, and to debate and discuss FDA and other legal and regulatory issues impacting stem cell research and commercialization.

Opening Keynote Address October 26, 2012 Arnold I. Caplan, PhD, Professor of Biology and Professor of General Medical Sciences (Oncology) Case Western Reserve University

Dr. Caplan has helped shape the direction and focus of adult stem cell research and commercialization. Virtually every adult stem cell company and literally tens of thousands of research papers are based on Dr. Caplan's original and ground breaking research. Professor Caplan is considered to be the "father" of the mesenchymal stem cell and first described this progenitor cell in his landmark paper; "Mesenchymal stem cells", Journal of Orthopaedic Research 1991;9(5):641-650. Since that foundational study, Dr. Caplan has published over 360 manuscripts and articles in peer reviewed journals. Dr. Caplan has been Chief Scientific Officer at OrthoCyte Corporation since 2010. In addition, Dr. Caplan co-founded Cell Targeting Inc. and has served as President of Skeletech, Inc. as its founder. He is the recipient of several honors and awards from the orthopedic research community. Dr. Caplan holds a Ph. D. from Johns Hopkins University Medical School and a B.S. in chemistry from the Illinois Institute of Technology.

Summit Keynote Address October 26, 2012 Texas Governor Rick Perry

Governor Perry is the 47th and current Governor of Texas. Governor Perry has long championed the role of medical technologies in building the future of not only Texas, but also the United States. In many ways, his strong advocacy on behalf of research and advanced medical technologies is one of his strongest and as yet underappreciated legacies. In addition to his service to the state of Texas, Governor Perry has also served as Chairman of the Republican Governors Association in 2008 and again in 2011. Despite a rigorous schedule, particularly in the teeth of this election season, Governor Perry has graciously made time to speak and encourage the researchers, patients, companies and physicians who form the fabric and future of the stem cell therapy community.

Texas Medical Center Keynote Address, October 27, 2012 James T. Willerson, MD

Over the course of his career, Dr. James T. Willerson has served as a medical, scientific and administrative leader for each of the major institutions that are the foundation of the Texas Medical Center. Dr. Willerson is currently President and Medical Director, Director of Cardiology Research, and Co-Director of the Cullen Cardiovascular Research Laboratories at Texas Heart Institute (THI). Dr. Willerson was appointed President-Elect of THI in 2004 and became President and Medical Director in 2008. He is also an adjunct professor of Medicine at Baylor College of Medicine and at The University of Texas MD Anderson Cancer Center. He is the former chief of Cardiology at St. Luke's Episcopal Hospital and the former chief of Medical Services at Memorial Hermann Hospital.

Dr. Willerson has served as a visiting professor and invited lecturer at more than 170 institutions.

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Houston Stem Cell Summit Announces Extraordinary Lineup of Keynote Speakers

Recommendation and review posted by simmons

For more than 40 years, Lesley Kelly of Glasgow, Scotland, lived with third-degree burns that stretched over 60 percent of her body.

Kelly was 2 years old when she fell into a bathtub filled with hot water that scorched most of the right side of her body. She lost full range of motion around many of her joints.

"When you have bad scarring, the buildup is very thick and has no elasticity," said Kelly, 45, whose right elbow was most affected by the buildup of scar tissue. "The problem with thermal burn scarring [is that] it's hard to get the range of motion."

Kelly underwent numerous reparative surgeries through the years, but the scar tissue continued to grow back. The procedures did not lessen the look of her scars.

In 2011, Kelly underwent a new, experimental procedure that used stem cells from her own fat tissue to repair the buildup around her right elbow.

Surgeons cleaned the scar buildup around the elbow and used liposuction to pull fat from off Kelly's waist. They separated the fat cells from the stem and regenerative cells, which were then injected into the wound on Kelly's arm. The procedure took less than two hours.

Within months, Kelly was able to regain 40 degrees of motion that she had lost more than 40 years ago.

"If this technology was available earlier in my life, my scars would not have been as bad," said Kelly.

There are an estimated 50,000 to 70,000 burn cases each year in the U.S., according to the American Burn Association.

The stem cell therapy, approved in the U.K. to treat soft tissue wounds, is now gaining traction in the U.S.

See the rest here:
Experimental Stem Cell Therapy May Help Burn Victims

Recommendation and review posted by simmons

Lesley Kelly, 45, underwent stem cell therapy to repair scar tissue buildup in her right arm. (Cytori Therapeutics, Inc.)

By Lara Salahi, ABC News For more than 40 years, Lesley Kelly of Glasgow, Scotland, lived with third-degree burns that stretched over 60 percent of her body.

Kelly was 2 years old when she fell into a bathtub filled with hot water that scorched most of the right side of her body. She lost full range of motion around many of her joints.

"When you have bad scarring, the buildup is very thick and has no elasticity," said Kelly, 45, whose right elbow was most affected by the buildup of scar tissue. "The problem with thermal burn scarring [is that] it's hard to get the range of motion."

Kelly underwent numerous reparative surgeries through the years, but the scar tissue continued to grow back. The procedures did not lessen the look of her scars.

In 2011, Kelly underwent a new, experimental procedure that used stem cells from her own fat tissue to repair the buildup around her right elbow.

Surgeons cleaned the scar buildup around the elbow and used liposuction to pull fat from off Kelly's waist. They separated the fat cells from the stem and regenerative cells, which were then injected into the wound on Kelly's arm. The procedure took less than two hours.

Within months, Kelly was able to regain 40 degrees of motion that she had lost more than 40 years ago.

"If this technology was available earlier in my life, my scars would not have been as bad," said Kelly.

There are an estimated 50,000 to 70,000 burn cases each year in the U.S., according to the American Burn Association.

Go here to read the rest:
New Therapy May Help Burn Victims

Recommendation and review posted by simmons

SAN FRANCISCO, CA--(Marketwire - Oct 1, 2012) - The life sciences sector continued to outperform the broader markets in September, but developments during the month were notable for highlighting the acceleration of the transformation of healthcare through personalized medicine, Burrill & Company says.

"Our healthcare system is dysfunctional and has largely been unchanged through human history in its episodic approach that focuses on treating the symptoms of illness," says G. Steven Burrill, CEO of Burrill & Company, a diversified global financial services firm. "Although personalized medicine's transformation of healthcare is an evolutionary rather than a revolutionary process, the events of the past month point to a rapid acceleration of efforts to make medicine personalized, predictive, and pre-emptive and promises to bend the cost-curve of healthcare in a meaningful way."

The University of Texas MD Anderson Cancer Center's announced an ambitious $3 billion Cancer Moon Shots Program, which seeks to develop new diagnostics, devices, drugs, and policies to detect, prevent, and treat cancer by capitalizing on the convergence of low-cost sequencing, artificial intelligence, and other emerging technologies.

September also saw a number of developments on the sequencing front. Chinese sequencing giant BGI-Shenzhen announced a $117.6 million acquisition of the struggling next-generation sequencing company Complete Genomics. Mountain View, California-based Complete Genomics, which has been working to provide whole genome sequencing through a service-based business model, announced a restructuring in June that included a shift in focus to the development of clinical applications for its whole genome sequencing service. BGI-Shenzhen provides deep pockets that should accelerate the clinical applications of Complete Genomic's technology.

Complete Genomics' larger competitors also announced developments that should accelerate the clinical utility of genomic sequencing. Life Technologies began shipping its low-cost Ion Proton sequencing system. The company said the chip-based system cost about a third of genome scale sequencing systems that rely on light to read a genome. The device sits on a desktop and can sequence exomes and transcriptomes in two to four hours at a cost of $1,000 per run. Life Technologies next expects to release a second-generation chip for the system around the end of the first quarter of 2013 that will be able to sequence the human genome in a few hours for $1,000.

At the same time, the genetic sequencing tools company Illumina and the non-profit healthcare system Partners Healthcare announced an agreement to provide geneticists and pathologists networking tools and infrastructure to report and interpret data from genetic sequencing. By pairing Illumina's expertise in sequencing with Partners Healthcare's understanding of what's needed for clinical utility, the two hope to leverage each other's strengths to deliver a comprehensive sequencing and clinical reporting solution.

Others are also taking steps to apply new personalized medicine approaches to clinical care. The Big Data analytics company GNS Healthcare in September announced a new program with the healthcare insurance company Aetna to use GNS' supercomputing capabilities to help identify Aetna members at risk for heart and metabolic disorders that can result in stroke, heart attack or diabetes, earlier than it does today. GNS will develop data-driven models that will define a person's risk for developing metabolic syndrome using Aetna claims data as well as health records. A separate agreement between GNS and the contract research organization Covance seeks to improve drug development by using GNS' modeling to predict the safety and efficacy of a drug candidate against different patient characteristics.

On the research side, September also saw major advances in understanding the genetics underlying disease. The Encode Project, an ambitious international effort to characterize and publish all of the functional elements in the human genome, found that the 80 percent of DNA once thought of as "junk" actually plays a critical role in regulating genes and can also play a part in the onset of disease. Researchers identified more than 4,000 switches involved in gene regulation. The findings not only create a new understanding of the role of some 80 percent of DNA once thought to serve no functional role, but also provide a new source of potential targets for drugs, and new insight into how genes are regulated and how people become ill.

Separately, a collaborative effort funded by the National Cancer Institute and the National Human Genome Research Institute, using data generated as part of The Cancer Genome Atlas, has provided a new understanding of the four major subtypes of breast cancer and finds shared genetic features between the form of breast cancer known as "Basal-like" or "Triple Negative" breast cancer and serious ovarian cancer. The findings will lead to researchers comparing treatments and outcomes for patients with the two forms of cancer and could lead to new therapeutic approaches.

"With new research findings we are reminded about how much we still don't know, but also of the rapid progress we are making," says Burrill. "We are seeing real examples of personalized medicine moving from idea to practice in meaningful ways."

Read more:
Personalized Medicine's Transformation of Healthcare Accelerates

Recommendation and review posted by sam

NEW YORK, Oct. 1, 2012 /PRNewswire/ -- Reportlinker.com announces that a new market research report is available in its catalogue:

Translational Regenerative Medicine: Market Prospects 2012-2022

http://www.reportlinker.com/p0595030/Translational-Regenerative-Medicine-Market-Prospects-2012-2022.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=Blood_Supply,_Tissue_Banking_and_Transplantation

Report Details

New study shows you commercial potential of regenerative treatments

See what the future holds for translational regenerative medicine. Visiongain's updated report lets you assess forecasted sales at overall world market, submarket, product and regional level to 2022.

There you investigate the most lucrative areas in that research field, industry and market. Discover prospects for tissue-engineered products, stem cell treatments and gene therapy.

We pack our study with information and analysis to help your work and save you time:

Access to present and predicted trends, with commercial opportunities and prospects revealed

Data and discussions - including our revenue forecasts to 2022 - for your research, analyses and decision making

See original here:
Translational Regenerative Medicine: Market Prospects 2012-2022

Recommendation and review posted by sam

Public release date: 1-Oct-2012 [ | E-mail | Share ]

Contact: Elizabeth Streich estreich@columbia.edu 212-305-3689 Columbia University Medical Center

An experimental treatment for blindness, developed from a patient's skin cells, improved the vision of blind mice in a study conducted by Columbia ophthalmologists and stem cell researchers.

The findings suggest that induced pluripotent stem (iPS) cells which are derived from adult human skin cells but have embryonic properties could soon be used to restore vision in people with macular degeneration and other diseases that affect the eye's retina.

"With eye diseases, I think we're getting close to a scenario where a patient's own skin cells are used to replace retina cells destroyed by disease or degeneration," says the study's principal investigator, Stephen Tsang, MD, PhD, associate professor of ophthalmology and pathology & cell biology. "It's often said that iPS transplantation will be important in the practice of medicine in some distant future, but our paper suggests the future is almost here."

The advent of human iPS cells in 2007 was greeted with excitement from scientists who hailed the development as a way to avoid the ethical complications of embryonic stem cells and create patient-specific stem cells. Like embryonic stem cells, iPS cells can develop into any type of cell. Thousands of different iPS cell lines from patients and healthy donors have been created in the last few years, but they are almost always used in research or drug screening.

No iPS cells have been transplanted into people, but many ophthalmologists say the eye is the ideal testing ground for iPS therapies.

"The eye is a transparent and accessible part of the central nervous system, and that's a big advantage. We can put cells into the eye and monitor them every day with routine non-invasive clinical exams," Tsang says. "And in the event of serious complications, removing the eye is not a life-threatening event."

In Tsang's new preclinical iPS study, human iPS cells derived from the skin cells of a 53-year-old donor were first transformed with a cocktail of growth factors into cells in the retina that lie underneath the eye's light-sensing cells.

The primary job of the retina cells is to nourish the light-sensing cells and protect the fragile cells from excess light, heat, and cellular debris. If the retina cells die which happens in macular degeneration and retinitis pigmentosa the photoreceptor cells degenerate and the patient loses vision. Macular degeneration is a leading cause of vision loss in the elderly, and it is estimated that 30 percent of people will have some form of macular degeneration by age 75. Macular degeneration currently affects 7 million Americans and its incidence is expected to double by 2020.

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Stem cells improve visual function in blind mice

Recommendation and review posted by Bethany Smith

HOUSTON, Oct. 1, 2012 /PRNewswire/ --The Houston Stem Cell Summit will host an extraordinary lineup of keynote speakers who represent the most accomplished stem cell scientists, clinicians and entrepreneurs in the United States. Joining these distinguished speakers will be Governor of Texas, Rick Perry, consistent champion of adult stem cell therapies.

(Logo: http://photos.prnewswire.com/prnh/20120831/NY66463LOGO )

The Houston Stem Cell Summit will be held October 26 27 in its namesake city and will highlight the latest therapeutic research regarding the use of adult stem and progenitor cell therapies. The Summit will also provide a forum for entrepreneurs to discuss their latest efforts to commercialize stem cell therapies, and to debate and discuss FDA and other legal and regulatory issues impacting stem cell research and commercialization.

Opening Keynote Address October 26, 2012 Arnold I. Caplan, PhD, Professor of Biology and Professor of General Medical Sciences (Oncology) Case Western Reserve University

Dr. Caplan has helped shape the direction and focus of adult stem cell research and commercialization. Virtually every adult stem cell company and literally tens of thousands of research papers are based on Dr. Caplan's original and ground breaking research. Professor Caplan is considered to be the "father" of the mesenchymal stem cell and first described this progenitor cell in his landmark paper; "Mesenchymal stem cells", Journal of Orthopaedic Research 1991;9(5):641-650. Since that foundational study, Dr. Caplan has published over 360 manuscripts and articles in peer reviewed journals. Dr. Caplan has been Chief Scientific Officer at OrthoCyte Corporation since 2010. In addition, Dr. Caplan co-founded Cell Targeting Inc. and has served as President of Skeletech, Inc. as its founder. He is the recipient of several honors and awards from the orthopedic research community. Dr. Caplan holds a Ph. D. from Johns Hopkins University Medical School and a B.S. in chemistry from the Illinois Institute of Technology.

Summit Keynote Address October 26, 2012 Texas Governor Rick Perry

Governor Perry is the 47th and current Governor of Texas. Governor Perry has long championed the role of medical technologies in building the future of not only Texas, but also the United States. In many ways, his strong advocacy on behalf of research and advanced medical technologies is one of his strongest and as yet underappreciated legacies. In addition to his service to the state of Texas, Governor Perry has also served as Chairman of the Republican Governors Association in 2008 and again in 2011. Despite a rigorous schedule, particularly in the teeth of this election season, Governor Perry has graciously made time to speak and encourage the researchers, patients, companies and physicians who form the fabric and future of the stem cell therapy community.

Texas Medical Center Keynote Address, October 27, 2012 James T. Willerson, MD

Over the course of his career, Dr. James T. Willerson has served as a medical, scientific and administrative leader for each of the major institutions that are the foundation of the Texas Medical Center. Dr. Willerson is currently President and Medical Director, Director of Cardiology Research, and Co-Director of the Cullen Cardiovascular Research Laboratories at Texas Heart Institute (THI). Dr. Willerson was appointed President-Elect of THI in 2004 and became President and Medical Director in 2008. He is also an adjunct professor of Medicine at Baylor College of Medicine and at The University of Texas MD Anderson Cancer Center. He is the former chief of Cardiology at St. Luke's Episcopal Hospital and the former chief of Medical Services at Memorial Hermann Hospital.

Dr. Willerson has served as a visiting professor and invited lecturer at more than 170 institutions.

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Houston Stem Cell Summit Announces Extraordinary Lineup of Keynote Speakers

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For more than 40 years, Lesley Kelly of Glasgow, Scotland, lived with third-degree burns that stretched over 60 percent of her body.

Kelly was 2 years old when she fell into a bathtub filled with hot water that scorched most of the right side of her body. She lost full range of motion around many of her joints.

"When you have bad scarring, the buildup is very thick and has no elasticity," said Kelly, 45, whose right elbow was most affected by the buildup of scar tissue. "The problem with thermal burn scarring [is that] it's hard to get the range of motion."

Kelly underwent numerous reparative surgeries through the years, but the scar tissue continued to grow back. The procedures did not lessen the look of her scars.

In 2011, Kelly underwent a new, experimental procedure that used stem cells from her own fat tissue to repair the buildup around her right elbow.

Surgeons cleaned the scar buildup around the elbow and used liposuction to pull fat from off Kelly's waist. They separated the fat cells from the stem and regenerative cells, which were then injected into the wound on Kelly's arm. The procedure took less than two hours.

Within months, Kelly was able to regain 40 degrees of motion that she had lost more than 40 years ago.

"If this technology was available earlier in my life, my scars would not have been as bad," said Kelly.

There are an estimated 50,000 to 70,000 burn cases each year in the U.S., according to the American Burn Association.

The stem cell therapy, approved in the U.K. to treat soft tissue wounds, is now gaining traction in the U.S.

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Experimental Stem Cell Therapy May Help Burn Victims

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Lesley Kelly, 45, underwent stem cell therapy to repair scar tissue buildup in her right arm. (Cytori Therapeutics, Inc.)

By Lara Salahi, ABC News For more than 40 years, Lesley Kelly of Glasgow, Scotland, lived with third-degree burns that stretched over 60 percent of her body.

Kelly was 2 years old when she fell into a bathtub filled with hot water that scorched most of the right side of her body. She lost full range of motion around many of her joints.

"When you have bad scarring, the buildup is very thick and has no elasticity," said Kelly, 45, whose right elbow was most affected by the buildup of scar tissue. "The problem with thermal burn scarring [is that] it's hard to get the range of motion."

Kelly underwent numerous reparative surgeries through the years, but the scar tissue continued to grow back. The procedures did not lessen the look of her scars.

In 2011, Kelly underwent a new, experimental procedure that used stem cells from her own fat tissue to repair the buildup around her right elbow.

Surgeons cleaned the scar buildup around the elbow and used liposuction to pull fat from off Kelly's waist. They separated the fat cells from the stem and regenerative cells, which were then injected into the wound on Kelly's arm. The procedure took less than two hours.

Within months, Kelly was able to regain 40 degrees of motion that she had lost more than 40 years ago.

"If this technology was available earlier in my life, my scars would not have been as bad," said Kelly.

There are an estimated 50,000 to 70,000 burn cases each year in the U.S., according to the American Burn Association.

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New Therapy May Help Burn Victims

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Public release date: 1-Oct-2012 [ | E-mail | Share ]

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine

Working with mice, Johns Hopkins researchers say they have developed a gene-based therapy to stop the rodent equivalent of the autoimmune disease myasthenia gravis by specifically targeting the destructive immune response the disorder triggers in the body.

The technique, the result of more than 10 years of work, holds promise for a highly specific therapy for the progressively debilitating muscle-weakening human disorder, one that avoids the need for long-term, systemic immunosuppressant drugs that control the disease but may create unwanted side effects.

The research, if replicated in humans, could be a big leap in treating not only myasthenia gravis, but also other autoimmune disorders, the researchers say.

"To treat autoimmune diseases, we normally give drugs that suppress not only the specific antibodies and cells we want to inhibit, but that also broadly interfere with other functions of the immune system," says Daniel B. Drachman, M.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and leader of the study published this month in the Journal of Neuroimmunology. "Our goal was to suppress only the abnormal response, without damaging the remainder of the immune system, and that's what we did in these mice."

A healthy immune system has the amazing ability to distinguish between the body's own cells, recognized as "self," and foreign proteins and other substances including germs and tumors to fight infections, cancer and other diseases. The body's immune defenses normally coexist peacefully with cells that carry distinctive "self" marker molecules. But when immune defenders encounter foreign molecules, they quickly launch an attack. Autoimmune disorders occur when the immune system makes a mistake, in which it confuses "self" with something foreign, and then launches an attack by immune cells and/or antibodies to seek out and damage the body's own cells.

Drachman, one of the world's leading authorities on myasthenia gravis and other neurologic autoimmune disorders, and his colleagues say they have found a way to create a "guided missile" approach as opposed to the "carpet bombing" of overall immunosuppression. Essentially, Drachman says, the method eliminates the cells of the immune system that are involved in the attack against self and leaves other cells alone.

The research team created the guided missiles by genetically engineering dendritic cells, which are the immune cells that specialize in presenting antigens to the immune system's T-cells. They extracted dendritic cells from mice with myasthenia gravis, purified them and inserted genes which direct these dendritic cells to target the auto-aggressive immune cells, and destroy them using a "warhead" known as Fas ligand. Then they injected back into the mice the genetically engineered cells, which homed in on the immune system's faulty T-cells. The newly introduced "guided missiles" then sought out and bound themselves to those T-cells, causing apoptosis, or cellular suicide, which halted the autoimmune attack before it could gain traction.

"This way, the autoantibodies were specifically reduced, a key step in treating myasthenia gravis," Drachman says.

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Researchers halt autoimmune disease myasthenia gravis in mice

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October 1, 2012

redOrbit Staff & Wire Reports Your Universe Online

A team of researchers, led by members of the University of Cincinnati (UC) and Cincinnati Childrens Hospital Medical Center, have reportedly discovered a new genetic mutation that leads to deafness and hearing loss associated with a relatively rare condition.

In a September 30 press release, lead investigator and UC assistant professor of ophthalmology Zubair Ahmed explain that he and his colleagues were able to pinpoint the gene which caused deafness in Usher syndrome type 1 as well as deafness that is not associated with the syndrome through the genetic analysis of 57 humans from Pakistan and Turkey.

The culprit, according to Ahmed, is a protein known as CIB2. Mutations in the protein, which binds to calcium inside cells, has been discovered to be linked to deafness both in Usher syndrome and cases of non-syndromic hearing loss.

He noted that these mutations were found to be the primary genetic cause of non-syndromic hearing loss in Pakistan, and that during their research, he and his colleagues discovered a second CIB2 mutation that has been linked to deafness among people of Turkish heritage.

In animal models, CIB2 is found in the mechanosensory stereocilia of the inner ear hair cells, which respond to fluid motion and allow hearing and balance, and in retinal photoreceptor cells, which convert light into electrical signals in the eye, making it possible to see, Saima Riazuddin, assistant professor in UCs department of otolaryngology and co-lead investigator on the study, added in a statement.

Ahmed, Riazuddin, and company found that CIB2 tended to be stained brighter at the tips of shorter rows of the cellular apical modifications known as stereocilia than nearby longer rows, where it could be involved in the calcium signaling process which regulates how the ear converts mechanical energy into the type of energy recognizable by a persons brain as sound.

With this knowledge, we are one step closer to understanding the mechanism of mechano-electrical transduction and possibly finding a genetic target to prevent non-syndromic deafness as well as that associated with Usher syndrome type 1, Ahmed explained.

Their work appears in the Sept. 30 advance online edition of the journal Nature Genetics. Researchers from the National Institute on Deafness and other Communication Disorders (NIDCD), the Baylor College of Medicine and the University of Kentucky were also involved in the study, which was funded by the NIDCD, the National Science Foundation (NSF), and the Research to Prevent Blindness Foundation.

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New Gene Associated With Hearing Loss Discovered

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By Daily Mail Reporter

PUBLISHED: 03:02 EST, 1 October 2012 | UPDATED: 03:05 EST, 1 October 2012

A gene that causes 1,000 babies to be born deaf in Britain each year has been discovered by scientists.

It is hoped the breakthrough will lead to new treatments for profound deafness.

Research published online in Nature Genetics shows babies born deaf have mutated versions of a protein called CIB2.

Two deaf children use sign language: Scientists hope their latest genetic discovery will help with developing new treatments

The gene binds to calcium within a cell and is behind a condition known as Usher syndrome type 1 that causes deafness and 'non-syndromic' hearing loss, the study shows.

Dr Zubair Ahmed, of the University of Cincinnati, said: 'In this study, researchers were able to pinpoint the gene which caused deafness in Usher syndrome type 1 as well as deafness that is not associated with the syndrome through the genetic analysis of 57 humans from Pakistan and Turkey.'

He said these findings could help researchers develop new therapeutic targets for those at risk for this syndrome.

Usher syndrome is a genetic defect that causes deafness, night-blindness and a loss of peripheral vision through the progressive degeneration of the retina.

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Deafness gene discovery could lead to new treatments

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Washington, October 1 (ANI): Researchers have discovered a new genetic mutation responsible for deafness and hearing loss associated with Usher syndrome type 1.

These findings could help researchers develop new therapeutic targets for those at risk for this syndrome.

For the study, researchers at the University of Cincinnati (UC) and Cincinnati Children's Hospital Medical Center work together with the National Institute on Deafness and other Communication Disorders (NIDCD), Baylor College of Medicine and the University of Kentucky.

Usher syndrome is a genetic defect that causes deafness, night-blindness and a loss of peripheral vision through the progressive degeneration of the retina.

"In this study, researchers were able to pinpoint the gene which caused deafness in Usher syndrome type 1 as well as deafness that is not associated with the syndrome through the genetic analysis of 57 humans from Pakistan and Turkey," said Zubair Ahmed, PhD, assistant professor of ophthalmology who conducts research at Cincinnati Children's and is the lead investigator on this study.

Ahmed stated that a protein, called CIB2, which binds to calcium within a cell, is associated with deafness in Usher syndrome type 1 and non-syndromic hearing loss.

"To date, mutations affecting CIB2 are the most common and prevalent genetic cause of non-syndromic hearing loss in Pakistan. However, we have also found another mutation of the protein that contributes to deafness in Turkish populations," he said.

"In animal models, CIB2 is found in the mechanosensory stereocilia of the inner ear-hair cells, which respond to fluid motion and allow hearing and balance, and in retinal photoreceptor cells, which convert light into electrical signals in the eye, making it possible to see," explained Saima Riazuddin, PhD, assistant professor in UC's department of otolaryngology who conducts research at Cincinnati Children's and is co-lead investigator on the study.

Researchers found that CIB2 staining is often brighter at shorter row stereocilia tips than the neighboring stereocilia of a longer row, where it may be involved in calcium signaling that regulates mechano-electrical transduction, a process by which the ear converts mechanical energy-or energy of motion-into a form of energy that the brain can recognize as sound.

"With this knowledge, we are one step closer to understanding the mechanism of mechano-electrical transduction and possibly finding a genetic target to prevent non-syndromic deafness as well as that associated with Usher syndrome type 1," Ahmed said.

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Gene that causes deafness pinpointed

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Editor's Note: Charles Gersbach can be reached at (919) 684-1129 or charles.gersbach@duke.edu. Lauren Polstein can be reached at (919) 688-9100 or Lauren.polstein@duke.edu. A photograph of the researchers is available, as well as an example of the gene expression.

Durham, NC - Using blue light, Duke University bioengineers have developed a system for ordering genes to produce proteins, an advance they said could prove invaluable in clinical settings as well as in basic science laboratories.

This new approach could greatly improve the ability of researchers and physicians to control gene expression, which is the process by which genes give instructions for the production of proteins key to all living cells.

"We can now, with our method, make gene expression reversible, repeatable, tunable, and specific to different regions of a gene," said Lauren Polstein, a graduate student working in the laboratory of Charles Gersbach, assistant professor of biomedical engineering at Duke's Pratt School of Engineering. "Current methods of getting genes to express can achieve some of those characteristics, but not all at once."

The new system can also control where the genes are expressed in three dimensions, which becomes especially important for researchers attempting to bioengineer living tissues.

"The light-based strategy allows us to regulate gene expression for biotechnology and medical applications, as well as for gaining a better understanding of gene function, interactions between cells, and how tissues develop into particular shapes," Polstein said.

The results of the Duke experiments were published online in the Journal of the American Chemical Society (http://tinyurl.com/brt3plh). The research was supported by a Faculty Early Career Development Award from the National Science Foundation and a Director's New Innovator Award from the National Institutes of Health.

The Duke system, which has been dubbed LITEZ (Light Induced Transcription using Engineered Zinc finger proteins), combines proteins from two diverse sources. The light-sensitive proteins are derived from a common flowering plant (Arabidopsis thaliana).

"We hijacked the specific proteins in plants that allows them to sense the length of the day," Gersbach said.

The second protein is in a class of so-called zinc finger proteins, which can be readily engineered to attach to specific regions of a gene. They are ubiquitous in biomedical research.

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Duke Blue Light Controls Gene Expression

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Washington, Oct 1 (IANS) Going deaf? Blame a genetic mutation, linked with Usher syndrome type 1, says the latest finding, which could help develop more effective ways of treating this syndrome.

Usher syndrome is a genetic defect that causes deafness, night-blindness and a loss of peripheral vision through the progressive degeneration of the retina.

Researchers from the University of Cincinnati and Cincinnati Children's Hospital Medical Centre, partnered the study with the National Institute on Deafness and other Communication Disorders (NIDCD), Baylor College of Medicine and the University of Kentucky, the journal Nature Genetics reports.

"Researchers were able to pinpoint the gene which caused deafness in Usher syndrome type 1 as well as deafness that is not associated with the syndrome through the genetic analysis of 57 humans from Pakistan and Turkey," says Zubair Ahmed, assistant professor of ophthalmology from Cincinnati Children's and the study's lead investigator.

Ahmed says that a protein, called CIB2, which binds to calcium within a cell, is associated with deafness in Usher syndrome type 1 and non-syndromic hearing loss. "To date, mutations affecting CIB2 are the most common and prevalent genetic cause of non-syndromic hearing loss in Pakistan," he says, according to a Cincinnati statement.

"With this knowledge, we are one step closer to understanding the mechanism of mechano-electrical transduction and possibly finding a genetic target to prevent non-syndromic deafness as well as that associated with Usher syndrome type 1," Ahmed says.

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Genetic defect plays role in hearing loss too

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Public release date: 30-Sep-2012 [ | E-mail | Share ]

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Vibration-induced white finger disease (VWF) is caused by continued use of vibrating hand held machinery (high frequency vibration >50 Hz), and affects tens of thousands of people. New research published in BioMed Central's open access journal Clinical Epigenetics finds that people with a genetic polymorphism (A2191G) in sirtuin1 (SIRT1), a protein involved in the regulation of endothelial NOS (eNOS), are more likely to suffer from vibration-induced white finger disease.

VWF (also known as hand arm vibration syndrome (HAVS)) is a secondary form of Raynaud's disease involving the blood vessels and nerves of arms, fingers and hands. Affected fingers feel stiff and cold and loose sensation for the duration of the attack, which can be very painful. Loss of sensation can make it difficult to carry out manual activities. Initially attacks are triggered by cold temperatures but as the disease progresses attacks can occur at any time.

Little is known about what causes the restriction in blood flow, however researchers from Germany investigated the role of SIRT 1 by looking at polymorphisms (naturally occurring variations in DNA sequence) in people affected by VWF.

SIRT1 regulates activation of other genes by controlling how tightly DNA is wound in the nucleus. Tightly wound DNA cannot be 'read' and consequently cannot be used to make new protein. SIRT1 is known to regulate vasodilation by targeting eNOS, a nitric oxide synthase within the cells lining the inside of blood vessels, which regulates smooth muscle contraction, and hence the diameter of the vessel, and the amount of blood that can flow through it.

Of 113 polymorphisms tested, in the gene coding for SIRT1, only four actually affected the protein, the rest were non-coding or false positives. Of these four, only one was different between people with VWF and unaffected controls. A single nucleotide at position 2191 can either be an A or a G. In the unaffected population 99.7% had the A, but amongst the patients with VWF, almost a third had the G.

Dr Susanne Voelter-Mahlknecht from the University of Tuebingen, who led this study, explained, "While this does not mean that only people with the G version of the gene for SIRT1 will get VWF, it can be used to identify a set of people who would be at risk of VWF if they used vibrating hand held tools. Testing for this variant before starting to work with vibrating machinery could prevent years of pain and disability."

###

Media contact

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The genetics of white finger disease

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Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-634-7302 Genetics Society of America

BETHESDA, MD October 1, 2012 With flu season around the corner, getting a seasonal vaccine might be one of the best ways to prevent people from getting sick. These vaccines only work, however, if their developers have accurately predicted which strains of the virus are likely to be active in the coming season because vaccines must be developed in advance of the upcoming flu season. Recently, a team of scientists from Germany and the United Kingdom have improved the prediction methods used to determine which strains of the flu virus to include in the current season's vaccine. The research describing this advance is published in the October 2012 issue of GENETICS (http://www.genetics.org).

"Seasonal influenza kills about half a million people per year, but improved vaccines can curb this number," said Michael Lssig, Ph.D., a researcher involved in the work from the Institute for Theoretical Physics at the University of Cologne in Kln, Germany. "Although this study is some distance from direct applications, it is a necessary step toward improved prediction methods. We hope that it helps yield better vaccines against influenza," Lssig added.

To make this advance, scientists analyzed the DNA sequences of thousands of influenza strains isolated from patients worldwide, dating to 1968. By analyzing this dataset, researchers were able to determine which strains were most successful at expanding into the entire population, and which mutations were least successful in spreading. Using a new statistical method, the researchers found that many more mutations than we thought initially succeed in replicating and surviving. These mutations compete; some make it into the entire population, others die out. This analysis of the virus enables prediction of trends which can help vaccine developers understand the rules of flu virus evolution. This knowledge, in turn, can be used to predict which strains of the virus are most likely to spread through a human population.

"Every year, new concerns emerge about 'super flus' that have the potential to kill many people," said Mark Johnston, Editor-in-Chief of the journal GENETICS. "This research itself will not stop any people from getting sick, but it could give us a heads up to particularly dangerous strains that might be on the horizon. With that information, we may be able to develop increasingly effective vaccines."

###

FUNDING: This work was partially supported by the Wellcome Trust [080711/ Z/06] (N.S.) and by Deutsche Forschungsgemeinschaft grant SFB 680 (to M.L.). This work was also supported in part by the National Science Foundation under grant PHY05-51164 during a visit to the Kavli Institute of Theoretical Physics (University of California, Santa Barbara).

CITATION: Natalja Strelkowa and Michael Lssig Clonal Interference in the Evolution of Influenza Genetics October 2012 192:671-682

ABOUT GENETICS: Since 1916, GENETICS (http://www.genetics.org/) has covered high quality, original research on a range of topics bearing on inheritance, including population and evolutionary genetics, complex traits, developmental and behavioral genetics, cellular genetics, gene expression, genome integrity and transmission, and genome and systems biology. GENETICS, a peer-reviewed, peer-edited journal of the Genetics Society of America is one of the world's most cited journals in genetics and heredity.

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Evolutionary analysis improves ability to predict the spread of flu

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ScienceDaily (Sep. 28, 2012) Vibration-induced white finger disease (VWF) is caused by continued use of vibrating hand held machinery (high frequency vibration >50 Hz), and affects tens of thousands of people. New research published in BioMed Central's open access journal Clinical Epigenetics finds that people with a genetic polymorphism (A2191G) in sirtuin1 (SIRT1), a protein involved in the regulation of endothelial NOS (eNOS), are more likely to suffer from vibration-induced white finger disease.

VWF (also known as hand arm vibration syndrome (HAVS)) is a secondary form of Raynaud's disease involving the blood vessels and nerves of arms, fingers and hands. Affected fingers feel stiff and cold and loose sensation for the duration of the attack, which can be very painful. Loss of sensation can make it difficult to carry out manual activities. Initially attacks are triggered by cold temperatures but as the disease progresses attacks can occur at any time.

Little is known about what causes the restriction in blood flow, however researchers from Germany investigated the role of SIRT 1 by looking at polymorphisms (naturally occurring variations in DNA sequence) in people affected by VWF.

SIRT1 regulates activation of other genes by controlling how tightly DNA is wound in the nucleus. Tightly wound DNA cannot be 'read' and consequently cannot be used to make new protein. SIRT1 is known to regulate vasodilation by targeting eNOS, a nitric oxide synthase within the cells lining the inside of blood vessels, which regulates smooth muscle contraction, and hence the diameter of the vessel, and the amount of blood that can flow through it.

Of 113 polymorphisms tested, in the gene coding for SIRT1, only four actually affected the protein, the rest were non-coding or false positives. Of these four, only one was different between people with VWF and unaffected controls. A single nucleotide at position 2191 can either be an A or a G. In the unaffected population 99.7% had the A, but amongst the patients with VWF, almost a third had the G.

Dr Susanne Voelter-Mahlknecht from the University of Tuebingen, who led this study, explained, "While this does not mean that only people with the G version of the gene for SIRT1 will get VWF, it can be used to identify a set of people who would be at risk of VWF if they used vibrating hand held tools. Testing for this variant before starting to work with vibrating machinery could prevent years of pain and disability.

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The above story is reprinted from materials provided by BioMed Central Limited.

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CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), and Seattle Genetics, Inc. (SGEN), today announced preliminary data from one arm of a three arm phase I, open-label, multicenter study designed to determine the safety and activity of sequential and combination treatment approaches of brentuximab vedotin with CHOP1 or CH-P chemotherapy in newly diagnosed patients with CD30-positive mature T- and NK- cell lymphomas. Data were presented from one arm, which evaluates brentuximab vedotin in sequence with CHOP in patients with newly diagnosed systemic anaplastic large cell lymphoma (sALCL), a subtype of mature T- and NK cell lymphomas. The data were reported during an oral presentation at the ESMO 2012 Congress (European Society for Medical Oncology) being held September 28 October 2, 2012 in Vienna, Austria.

Brentuximab vedotin is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of sALCL. Data from the other arms of the study evaluating administration of brentuximab vedotin with CH-P are expected to be presented during 2012.

The preliminary data from the sequential treatment arm of this phase I study show that side effects were manageable and there are also some encouraging data on activity, said Michelle Fanale, M.D., University of Texas MD Anderson Cancer Center, Houston, TX. We look forward to reporting additional data from the combination arms of the study at an upcoming medical congress.

Sequential Therapy with Brentuximab Vedotin in Newly Diagnosed Patients with Systemic Anaplastic Large Cell Lymphoma

The oral presentation featured data from Arm 1 of the study, which evaluated treatment with 1.8milligrams per kilogram of single-agent brentuximab vedotin for two cycles prior to sixcycles of CHOP. Patients who achieved a complete remission (CR) or partial remission (PR) following CHOP were eligible to continue single-agent brentuximab vedotin for up to eight cycles. The primary endpoints for Arm 1 are safety and tolerability. The secondary endpoint is investigator assessment of response using the Revised Response Criteria for Malignant Lymphoma (Cheson 2007). The median age of enrolled patients was 62years (range, 23-81). Among the 13 patients with newly diagnosed sALCL, ten had anaplastic lymphoma kinase (ALK)-negative disease and three had ALK-positive disease.

The companies plan to initiate a phase III clinical trial in patients with mature T-cell lymphomas evaluating brentuximab vedotin in combination with CH-P compared to CHOP in late 2012 to early 2013.

Data, presented by Dr. Fanale, included:

Details of the oral presentation are as follows:

Data on brentuximab vedotin was also described in the following poster session:

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Millennium and Seattle Genetics Highlight Data from ADCETRIS® (Brentuximab Vedotin) Trial in Patients with Newly ...

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