Archive for the ‘Gene Therapy Research’ Category

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

bluebird bio, Inc. (BLUE) a clinical-stage company committed to developing potentially transformative gene therapies for severe genetic and orphan diseases, today announced that the first subject in its phase 2/3 childhood cerebral adrenoleukodystrophy (CCALD) study, Starbeam (ALD-102) has undergone infusion with bluebird bios Lenti-D drug product in an autologous hematopoietic stem cell transplantation.

Treating our first subject in this study reflects the recent advances in the field of gene therapy and is the culmination of years of collaborative effort between the team at Dana-Farber/Boston Childrens Cancer and Blood Disorders Center and our colleagues at Massachusetts General Hospital, INSERM in Paris, and bluebird bio, stated David A. Williams, MD, Chief of hematology/oncology at Boston Childrens Hospital and Associate Chairman of pediatric oncology at Dana-Farber Cancer Institute. Boys with CCALD face significant risks of mortality and morbidity with allogeneic stem cell transplantation, the current standard of care treatment, if an optimally matched donor cannot be identified. bluebirds autologous Lenti-D drug product has the potential to circumvent this challenge and address an important unmet medical need for patients with this devastating disease.

Successfully initiating treatment in the Starbeam study represents an important step towards improving outcomes for patients with CCALD and is a major milestone for bluebird and its lentiviral gene therapy platform, stated Dave Davidson, MD, bluebird bios Chief Medical Officer.

About the Starbeam study (ALD-102)

The phase 2/3 study is designed to evaluate the safety and efficacy of Lenti-D drug product in the treatment of subjects with childhood cerebral adrenoleukodystrophy, or CCALD, a rare, hereditary neurological disorder affecting young boys that is often fatal. The trial study is planned to enroll up to 15 boys who will be followed for 24 months following a transplant with bluebird bios lentiviral transduced stem cells, Lenti-D. During this 24 month period, patients will be assessed for the onset of major functional disabilities, and other key assessments of disease progression.

For more information please contact clinicaltrials@bluebirdbio.com.

About Childhood Cerebral Adrenoleukodystrophy (CCALD)

Childhood Cerebral Adrenoleukodystrophy is an X-linked disease caused by the aberrant expression of the ABCD1 gene in boys leading to the inability of patients to metabolize very long chain fatty acids in cells of the brain. The disease is characterized by progressive destruction of myelin, leading to severe loss of neurological function and eventual death. The worldwide incidence of adrenoleukodystrophy (ALD) is approximately one in 20,000 newborns. CCALD accounts for about 30-40% of patients diagnosed with ALD.

About bluebird bio, Inc.

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bluebird bio Announces First Patient Transplanted in Phase 2/3 Starbeam ALD-102 Study for the Treatment of CCALD

PUBLIC RELEASE DATE:

27-Oct-2013

Contact: Peggy Vaughn nianews3@mail.nih.gov 301-496-1752 NIH/National Institute on Aging

An international group of researchers has identified 11 new genes that offer important new insights into the disease pathways involved in Alzheimer's disease. The highly collaborative effort involved scanning the DNA of over 74,000 volunteersthe largest genetic analysis yet conducted in Alzheimer's researchto discover new genetic risk factors linked to late-onset Alzheimer's disease, the most common form of the disorder.

By confirming or suggesting new processes that may influence Alzheimer's disease developmentsuch as inflammation and synaptic functionthe findings point to possible targets for the development of drugs aimed directly at prevention or delaying disease progression.

Supported in part by the National Institute on Aging (NIA) and other components of the National Institutes of Health, the International Genomic Alzheimer's Project (IGAP) reported its findings online in Nature Genetics on Oct. 27, 2013. IGAP is comprised of four consortia in the United States and Europe which have been working together since 2011 on genome-wide association studies (GWAS) involving thousands of DNA samples and shared datasets. GWAS are aimed at detecting the subtle gene variants involved in Alzheimer's and defining how the molecular mechanisms influence disease onset and progression.

"Collaboration among researchers is key to discerning the genetic factors contributing to the risk of developing Alzheimer's disease," said Richard J. Hodes, M.D., director of the NIA. "We are tremendously encouraged by the speed and scientific rigor with which IGAP and other genetic consortia are advancing our understanding."

The search for late-onset Alzheimer's risk factor genes had taken considerable time, until the development of GWAS and other techniques. Until 2009, only one gene variant, Apolipoprotein E-e4 (APOE-e4), had been identified as a known risk factor. Since then, prior to today's discovery, the list of known gene risk factors had grown to include other playersPICALM, CLU, CR1, BIN1, MS4A, CD2AP, EPHA1, ABCA7, SORL1 and TREM2.

IGAP's discovery reported today of 11 new genes strengthens evidence about the involvement of certain pathways in the disease, such as the role of the SORL1 gene in the abnormal accumulation of amyloid protein in the brain, , a hallmark of Alzheimer's disease. It also offers new gene risk factors that may influence several cell functions, to include the ability of microglial cells to respond to inflammation.

The researchers identified the new genes by analyzing previously studied and newly collected DNA data from 74,076 older volunteers with Alzheimer's and those free of the disorder from 15 countries. The new genes (HLA-DRB5/HLA0DRB1, PTK2B, SLC24A4-0RING3, DSG2, INPP5D, MEF2C, NME8, ZCWPW1, CELF1, FERMT2 and CASS4) add to a growing list of gene variants associated with onset and progression of late-onset Alzheimer's. Researchers will continue to explore the roles played by these genes, to include:

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NIH-supported study identifies 11 new Alzheimer's disease risk genes

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Newswise BOSTON A fine-grained scan of DNA in lung cancer cells has revealed a gene fusion a forced merger of two normally separate genes that spurs the cells to divide rapidly, scientists at Dana-Farber Cancer Institute and the University of Colorado Cancer Center report in a new paper in the journal Nature Medicine. Treating the cells with a compound that blocks a protein encoded by one of those genes NTRK1 caused the cells to die.

The finding suggests that the fusion of NTRK1 to other genes fuels the growth of some lung adenocarcinomas (a form of non-small cell lung cancer), and that drugs that target NTRK1s protein product could be effective in patients whose lung tumors harbor such fusions.

Treatment with targeted therapies is now superior to standard chemotherapy for many patients with lung cancers that harbor genetic changes including those with fusions involving the gene ALK, says Pasi A. Jnne, MD, PhD, of Dana-Farber, the senior co-author of the paper with Robert C. Doebele, MD, PhD, of CU Cancer Center. We know of several other genes that are fused in lung cancer and that offer attractive targets for new therapies. Our discovery places lung adenocarcinomas with NTRK1 fusions squarely within that group.

In the study, researchers performed next-generation DNA sequencing tests which read the individual elements of the genetic code over long stretches of chromosomes on tumor samples from 36 patients with lung adenocarcinomas whose tumors did not contain any previously known genetic alterations that could be found with standard clinical tests. In two of those samples both from women who had never smoked investigators found that a key region of the NTRK1 gene had become fused to normally distant genes (to the gene MPRIP in one patient; and the gene CD74 in the other).

NTRK1 holds the blueprint for a protein called TRKA, which dangles from the surface of cells and receives growth signals from other cells. The binding of NTRK1 to other genes causes TRKA to issue cell-growth orders on its own, without being prompted by outside signals.

In the laboratory, investigators mixed NTRK1-inhibiting agents into lung adenocarcinoma cells harboring NTRK1 fusions. The result was a dampening of TRKAs activity and the death of the cancer cells.

Investigators then designed a new test using fluorescence in situ hybridization (FISH) to detect NTRK1 fusions and tested an additional 56 tumor samples. In total, three of 91 tumor samples which had no other sign of cancer-causing genetic abnormalities, had fusions involving NTRK1.

These findings suggest that in a few percent of lung adenocarcinoma patients people in whose cancer cells we had previously been able to find no genetic abnormality tumor growth is driven by a fusion involving NTRK1, Jnne says. Given that lung cancer is a common cancer, even a few percent is significant and translates into a large number of patients. Our findings suggest that targeted therapies may be effective for this subset of lung cancer patients.

"This is still preclinical work," Doebele says, "but it's the first and maybe even second and third important steps toward picking off another subset of lung cancer with a treatment targeted to the disease's specific genetic weaknesses."

The co-lead authors of the study are Aria Vaishnavi, BS, of the University of Colorado School of Medicine and Marzia Capelletti, PhD, of Dana-Farber. Co-authors include Anh Le, BA, Severine Kako, Sakshi Mahale, MS, Kurtis Davies, PhD, Dara Aisner, MD, PhD, Amanda Pilling, PhD Eamon Berge, MD, and Marileila Varella-Garcia, PhD, of the University of Colorado School of Medicine; Mohit Butaney, Dalia Ercan, and Peter Hammerman, MD, PhD, of Dana-Farber; Levi Garraway, MD, PhD, of Dana-Farber and the Broad Institute of MIT and Harvard; Gregory Kryukov, PhD, of the Broad Institute; Jhingook Kim, MD, of Samsung Medical Center, Seoul, Korea; Hidefumi Sasaki, MD, of Nagoya City University, Nagoya, Japan; Seung-il Park, MD, PhD, of Asan Medical Center, Seoul, Korea; Julia Haas, PhD, and Steven Andrews, PhD, of Array BioPharma; Doron Lipson, PhD, Philip Stephens, PhD, and Vince Miller, MD, of Foundation Medicine.

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Study Finds New Genetic Error in Some Lung Cancers

AURORA, Colo. (PRWEB) October 27, 2013

A study lead by scientists at University of Colorado Cancer Center and Dana-Farber Cancer Institute in Boston has uncovered a new sub-type of lung cancer. The study revealed a gene fusion - a forced merger of two normally separate genes that spurs the cells to divide rapidly causing non-small cell lung cancer. The study is published in the journal Nature Medicine.

Scientists from CU Cancer Center and Dana-Farber collaborated on the finding. The group went a step beyond identifying the gene mutation, NTRK1, that drives some lung cancers. The scientists also showed the abnormal cells can be targeted by several drugs.

Whether a drug is already is in clinical trials, or already approved for another cancer, or just sitting on the pharma shelf somewhere, many drugs exist that turn off these candidate genes," said Robert C. Doebele, MD, PhD, the studys senior author and investigator at the CU Cancer Center.

Doebele found Array BioPharma in Boulder, Colo. happened to have several compounds specific to NTRK1. The group showed that mutated NRTK1 genes in cells treated with drug candidate ARRY-470 and others was effectively turned off. The drug blocks a protein causing cancer cells to die.

This is still preclinical work," Doebele says, "but it's the first and maybe even second and third important steps toward picking off another subset of lung cancer with a treatment targeted to the disease's specific genetic weaknesses."

Foundation Medicine, Inc. performed next-generation DNA sequencing tests which read the individual elements of the genetic code over long stretches of chromosomes on tumor samples from 36 patients with lung adenocarcinomas whose tumors did not contain any previously known genetic alterations that could be found with standard clinical tests. In two of those samples both from women who had never smoked investigators found that a key region of the NTRK1 gene had become fused to normally distant genes (to the gene MPRIP in one patient; and the gene CD74 in the other).

NTRK1 holds the blueprint for a protein called TRKA, which dangles from the surface of cells and receives growth signals from other cells. The joining of NTRK1 to other genes causes TRKA to issue cell-growth orders on its own, without being prompted by outside signals.

In the laboratory, investigators mixed NTRK1-inhibiting agents into lung adenocarcinoma cells harboring NTRK1 fusions. The result was a dampening of TRKAs activity and the death of the cancer cells.

Leila Varella-Garcia, PhD, at CU Cancer Center then designed a new test using fluorescence in situ hybridization (FISH) to detect NTRK1 fusions and tested an additional 56 tumor samples. Three of 91 tumor samples, which had no other sign of cancer-causing genetic abnormalities, had fusions involving NTRK1.

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New Genetic Error in Some Lung Cancers Identified by CU Scientists

Newswise PHILADELPHIA - The largest international Alzheimer's disease genetics collaboration to date has found 11 new genetic areas of interest that contribute to late onset Alzheimer's Disease (LOAD), doubling the number of potential genetics-based therapeutic targets to interrogate. The study, published in Nature Genetics, provides a broader view of genetic factors contributing to the disease and expands the scope of disease understanding to include new areas including the immune system, where a genetic overlap with other neurodegenerative diseases such as multiple sclerosis and Parkinson's disease was identified.

"Human genetic studies are being used with increased frequency to validate new drug targets in many diseases. Here we greatly increased the list of possible drug target candidates for Alzheimers disease, finding as many new significant genes in this one study as have been found in the last 15 years combined," said co-senior author Gerard Schellenberg, PhD, director of the Alzheimers Disease Genetics Consortium (ADGC) and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "This international effort has given us new clues into the steps leading to and accelerating Alzheimer's disease. We can add these new genetic clues to what we already know and try to piece together the mechanism of this complex disease."

Pooling resources through the International Genomics of Alzheimers Project (IGAP), the collaborative team collected 74,076 patients and controls from 15 countries. After a two stage meta-analysis, the group found some genes which confirmed known biological pathway of Alzheimer's disease, including the role of the amyloid pathway (SORL1 , CASS4) and tau (CASS4, FERMT2). Newly discovered genes involved in the immune response and inflammation (HLA-DRB5/DRB1, INPP5D, MEF2C) reinforced a pathway implied by previous work (on CR1, TREM2). Additional genes related to cell migration (PTK2B), lipid transport and endocytosis (SORL1) were also confirmed. And new hypotheses emerged related to hippocampal synaptic function (MEF2C , PTK2B), the cytoskeleton and axonal transport (CELF1, NME8, CASS4) as well as myeloid and microglial cell functions (INPP5D).

One of the more significant new associations was found in the HLA-DRB5 - DRB1 region, one of the most complex parts of the genome, which plays a role in the immune system and inflammatory response. It has also been associated with multiple sclerosis and Parkinson's disease, suggesting that the diseases where abnormal proteins accumulate in the brain may have a common mechanism involved, and possibly have a common drug target, Dr. Schellenberg noted.

"We know that healthy cells are very good at clearing out debris, thanks in part to the immune response system, but in these neurodegenerative diseases where the brain has an inflammatory response to bad proteins and starts forming plaques and tangle clumps, perhaps the immune response can get out of hand and do damage," said Dr. Schellenberg. "Through this powerful international group as well as our own US collaborations, we'll expand the data set even further to look for rare variants and continue our analysis to find more opportunities to better understand the disease and find viable therapeutic targets. Large-scale sequencing will certainly play a part in the next phase of our genetics studies."

Started in 2011, IGAP includes the contributions from the European Alzheimers Disease Initiative (EADI) in France led by Philippe Amouyel, MD, PhD, at the Institute Pasteur de Lille and Lille University; the Genetic and Environmental Risk in Alzheimers Disease (GERAD) from the United Kingdom led by Julie Williams, PhD, at Cardiff University; the neurology subgroup of the Cohorts for Heart and Aging in Genomic Epidemiology (CHARGE) led by Sudha Seshadri, MD, at Boston University School of Medicine; the Alzheimers Disease Genetics Consortium (ADGC) from the United States led by Gerard Schellenberg, PhD, Perelman School of Medicine at the University of Pennsylvania; as well as ADGC teams from the University of Miami, Vanderbilt University, Boston University and Columbia University in the United States, among others.

The National Institute on Aging provided funding for the ADGC (U01 AG032984, R01 AG033193), and the Alzheimer's Association provided crucial support to make this international collaboration possible.

# # #

Penn Medicineis one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania(founded in 1765 as the nation's first medical school) and theUniversity of Pennsylvania Health System, which together form a $4.3 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according toU.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.

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International Group Finds 11 New Alzheimer's Genes to Target for Drug Discovery, Adding New Clues Into Complex Disease ...

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PUBLIC RELEASE DATE:

27-Oct-2013

Contact: Kim Menard kim.menard@uphs.upenn.edu 215-662-6183 University of Pennsylvania School of Medicine

PHILADELPHIA - The largest international Alzheimer's disease genetics collaboration to date has found 11 new genetic areas of interest that contribute to late onset Alzheimer's Disease (LOAD), doubling the number of potential genetics-based therapeutic targets to interrogate. The study, published in Nature Genetics, provides a broader view of genetic factors contributing to the disease and expands the scope of disease understanding to include new areas including the immune system, where a genetic overlap with other neurodegenerative diseases such as multiple sclerosis and Parkinson's disease was identified.

"Human genetic studies are being used with increased frequency to validate new drug targets in many diseases. Here we greatly increased the list of possible drug target candidates for Alzheimer's disease, finding as many new significant genes in this one study as have been found in the last 15 years combined," said co-senior author Gerard Schellenberg, PhD, director of the Alzheimer's Disease Genetics Consortium (ADGC) and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "This international effort has given us new clues into the steps leading to and accelerating Alzheimer's disease. We can add these new genetic clues to what we already know and try to piece together the mechanism of this complex disease."

Pooling resources through the International Genomics of Alzheimer's Project (IGAP), the collaborative team collected 74,076 patients and controls from 15 countries. After a two stage meta-analysis, the group found some genes which confirmed known biological pathway of Alzheimer's disease, including the role of the amyloid pathway (SORL1 , CASS4) and tau (CASS4, FERMT2). Newly discovered genes involved in the immune response and inflammation (HLA-DRB5/DRB1, INPP5D, MEF2C) reinforced a pathway implied by previous work (on CR1, TREM2). Additional genes related to cell migration (PTK2B), lipid transport and endocytosis (SORL1) were also confirmed. And new hypotheses emerged related to hippocampal synaptic function (MEF2C , PTK2B), the cytoskeleton and axonal transport (CELF1, NME8, CASS4) as well as myeloid and microglial cell functions (INPP5D).

One of the more significant new associations was found in the HLA-DRB5 - DRB1 region, one of the most complex parts of the genome, which plays a role in the immune system and inflammatory response. It has also been associated with multiple sclerosis and Parkinson's disease, suggesting that the diseases where abnormal proteins accumulate in the brain may have a common mechanism involved, and possibly have a common drug target, Dr. Schellenberg noted.

"We know that healthy cells are very good at clearing out debris, thanks in part to the immune response system, but in these neurodegenerative diseases where the brain has an inflammatory response to bad proteins and starts forming plaques and tangle clumps, perhaps the immune response can get out of hand and do damage," said Dr. Schellenberg. "Through this powerful international group as well as our own US collaborations, we'll expand the data set even further to look for rare variants and continue our analysis to find more opportunities to better understand the disease and find viable therapeutic targets. Large-scale sequencing will certainly play a part in the next phase of our genetics studies."

###

Started in 2011, IGAP includes the contributions from the European Alzheimer's Disease Initiative (EADI) in France led by Philippe Amouyel, MD, PhD, at the Institute Pasteur de Lille and Lille University; the Genetic and Environmental Risk in Alzheimer's Disease (GERAD) from the United Kingdom led by Julie Williams, PhD, at Cardiff University; the neurology subgroup of the Cohorts for Heart and Aging in Genomic Epidemiology (CHARGE) led by Sudha Seshadri, MD, at Boston University School of Medicine; the Alzheimer's Disease Genetics Consortium (ADGC) from the United States led by Gerard Schellenberg, PhD, Perelman School of Medicine at the University of Pennsylvania; as well as ADGC teams from the University of Miami, Vanderbilt University, Boston University and Columbia University in the United States, among others.

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International group finds 11 new Alzheimer's genes to target for drug discovery

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Next spring, students at local high schools will dive into the study of the marine bacterium Kytococcus sedentarius, thanks to a $1.1 million National Science Foundation grant to UB.

Stephen Koury and his colleagues in the School of Medicine and Biomedical Sciences, received the grant to educate regional high school teachers and recruit high school students to pursue careers in STEM (science, technology, engineering and mathematics) fields. The new program focuses on bioinformatics, an interdisciplinary field that uses software tools to store, retrieve, organize and analyze biologic information. Bioinformatics is a field of rapid growth that provides tools for better health care through improvement in prevention, detection, diagnosis and treatment of diseases.

Koury, research assistant professor in the Department of Biotechnical and Clinical Laboratory Sciences, notes that new jobs on the Buffalo Niagara Medical Campus likely will require training in biotechnology and bioinformatics; the new program will provide a pipeline for educator and student recruitment, training and mentorship in STEM fields at the high school level.

For us to be successful, we need to create the environment where children not only want to get involved, but want to stay in Buffalo, says Norma Nowak, professor of biochemistry, director of science and technology at UBs New York State Center of Excellence in Bioinformatics and Life Sciences, and associate professor of oncology at Roswell Park Cancer Institute. This needs to be the spark that lights the fire.

Over the next three years, the grant will allow 450 high school students and 90 teachers to conduct and present scientific research in bioinformatics. The program will involve educators and students from 13 counties, including Niagara, Erie, Chautauqua, Cattaraugus, Wyoming, Genesee, Orleans, Monroe, Livingston, Allegany, Ontario, Wayne and Steuben.

The educational program will begin with a two-week workshop at UB, where high school teachers will receive training in microbial genome annotation. The teachers then will pass on their new skills to selected students in their schools, with support from UB faculty and staff.

During the first semester, students will be introduced to basic aspects of genetics and genomics. They also will receive career mentoring through a partnership with the New York State Area Health Education Center System (AHEC), a unit of UBs Department of Family Medicine that addresses health care workforce needs.

The second semester will focus on conducting Web-based research in microbial annotation through a program called IMG-ACT, a bioinformatics tool kit available through the U.S. Department of Energys Joint Genome Institute. The program will end with a capstone symposium at which students will present the results of their research to university faculty, researchers and employers in the biosciences fields.

For many local students, this will be their first real-world taste of scientific experimentation. And since its an unscripted project, students will learn to rely on themselves, rather than the specific direction of instructors.

We cant say for sure what they should find, says Koury. They will actually be doing a research project, and by the time they are done, they will probably be the expert on the particular gene sequence they have studied. It will give them that joy of discovery.

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Genome project fosters bioinformatics education in high schools

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Cancer Genetics, Inc. (NASDAQ: CGIX)
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Meena Thirunavu, MD, Discusses Breast Cancer Genetics on KMSP Fox 9 News
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#1 New Cause of Diabetes: How Toxins Can Trigger Type 1 and Type 2 Diabetes Genetics Dr. Dan Pompa
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RPE65: A Journey in Gene Therapy

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MISGAV, Israel & SAN FRANCISCO--(BUSINESS WIRE)--

Medgenics, Inc. (NYSE MKT:MDGN and AIM:MEDU, MEDG), developer of a novel technology for the sustained production and delivery of therapeutic proteins in patients using their own tissue, announces that new, positive data on the Companys second-generation viral vectors were highlighted in a poster presentation at the European Society of Gene and Cell Therapy Congress. The poster in its entirety can be viewed at http://www.medgenics.com.

Entitled Second generation EPODURE Biopump markedly extends duration of EPO delivery in mice could prolong therapeutic effect in patients, the poster was presented yesterday by Reem Miari, MSc and Dr. Nir Shapir of Medgenics, and study authors. This new study showed that the Companys second-generation gene therapy vectors provided substantial improvements in levels and durability of therapeutic protein secretion in vitro and in vivo. In addition, the new vectors incorporated improvements in surgical technique, including co-administration of Depo-Medrol (methylprednisolone acetate) on implantation. More specifically, when Depo-Medrol was applied to second generation vectors, animals serum hEPO levels remained 40-50 fold higher for over 100 days post implantation when compared to first generation vector with no Depo-Medrol.

The Company plans to initiate human trials with a Biopump containing the second generation viral vector and new implantation protocol in the first half of 2014.

These new data are compelling and provide additional evidence of our success in advancing the Biopump technology while improving performance and handling, said Dr. Garry Neil, Global Head R&D at Medgenics. The second-generation viral vectors show potential to substantially increase the duration of the protein secretion of the Biopump with enhanced surgical techniques. These advances can be clinically meaningful, particularly for patients on chronic protein therapy. Based on these results we plan to accelerate our development work, and will advance the second-generation vectors into human clinical trials.

We are delighted to have these preliminary data on our second-generation Biopump presented at this prestigious scientific meeting, said Michael Cola, President and Chief Executive Officer of Medgenics. The Biopump technology platform, which produces therapeutic proteins in the body using a small tissue explant from the patients own skin, holds significant clinical opportunity in a variety of indications. We are very encouraged by these data as the enhanced viral vectors may improve the surgical procedure and prolong the therapeutic effect in patients.

About Medgenics

Medgenics is developing and commercializing Biopump, a proprietary tissue-based platform technology for the sustained production and delivery of therapeutic proteins using the patient's own tissue for the treatment of a range of chronic diseases including anemia, hepatitis, among others. For more information, please visit http://www.medgenics.com.

Forward-looking Statements

This release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934 and as that term is defined in the Private Securities Litigation Reform Act of 1995, which include all statements other than statements of historical fact, including (without limitation) those regarding the company's financial position, its development and business strategy, its product candidates and the plans and objectives of management for future operations. The company intends that such forward-looking statements be subject to the safe harbors created by such laws. Forward-looking statements are sometimes identified by their use of the terms and phrases such as "estimate," "project," "intend," "forecast," "anticipate," "plan," "planning, "expect," "believe," "will," "will likely," "should," "could," "would," "may" or the negative of such terms and other comparable terminology. All such forward-looking statements are based on current expectations and are subject to risks and uncertainties. Should any of these risks or uncertainties materialize, or should any of the company's assumptions prove incorrect, actual results may differ materially from those included within these forward-looking statements. Accordingly, no undue reliance should be placed on these forward-looking statements, which speak only as of the date made. The company expressly disclaims any obligation or undertaking to disseminate any updates or revisions to any forward-looking statements contained herein to reflect any change in the company's expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based. As a result of these factors, the events described in the forward-looking statements contained in this release may not occur.

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Medgenics Reports Positive Data with Second-Generation Viral Vectors at European Society of Gene and Cell Therapy ...