Archive for the ‘Gene Therapy Research’ Category

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

Contact: Les Lang llang@med.unc.edu 919-966-9366 University of North Carolina School of Medicine

CHAPEL HILL, N.C. -- University of North Carolina at Chapel Hill researchers working as part of the International Cystic Fibrosis Consortium have discovered several regions of the genome that may predispose cystic fibrosis (CF) patients to develop an intestinal blockage while still in the uterus.

A report of this international study appears online April 1, 2012 in the journal Nature Genetics. It was the work of the North America CF Gene Modifier Consortium, which brought together dozens of investigators from the United States, Canada, and from France, to identify genetic variations that could be linked with meconium ileus (MI), an intestinal obstruction that usually requires emergency surgery for treatment, and can result in a substantially increased rate of serious health problems.

MI affects roughly 15-20 percent of all patients with CF, a genetic condition that causes scarring throughout the body, especially the lungs and pancreas. Though every CF patient carries mutations in both copies of the same gene coding for a protein called cystic fibrosis transmembrane conductance regulator, or CFTR symptoms can vary widely from patient to patient.

The genome-wide association study (GWAS) of more than 3,700 CF patients identified non-CFTR genetic variants in the cell membrane that separates the interior of cells from the outside environment. More specifically, the variants involved genes responsible for ion transport in the lower end of the small intestine.

"These variants involve cells in the small intestine that predispose CF patients to develop MI while still in the womb," said one of the senior study authors Michael Knowles, MD, professor of pulmonary and critical care medicine at UNC and a member of UNC's Cystic Fibrosis-Pulmonary Research and Treatment Center.

"The discovery provides new understanding of the pathogenic mechanisms underlying MI. In addition, it offers the possibility of developing therapies to intervene in utero," Knowles said. "Further, it provides molecular insight into the role of genetic variation in ion transporters in CF, which may be applicable to more commonly, and severely, involved organs such as the lungs."

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Other UNC study coauthors are Wanda K. O'Neal, Rhonda G. Pace, Jaclyn R. Stonebraker, Sally D. Wood, and Fred A. Wright. In the U.S., the study was funded by the National Heart, Lung and Blood Institute, the National Institute of Diabetes and Digestive and Kidney Diseases, and the U.S. Cystic Fibrosis Foundation.

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Gene variations linked to intestinal blockage in newborns with cystic fibrosis

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

Contact: Caroline Arbanas arbanasc@wustl.edu 314-286-0109 Washington University School of Medicine

Scientists at Washington University School of Medicine in St. Louis are using powerful DNA sequencing technology not only to identify mutations at the root of a patient's tumor considered key to personalizing cancer treatment but to map the genetic evolution of disease and monitor response to treatment.

"We're finding clinically relevant information in the tumor samples we're sequencing for discovery-oriented research studies," says Elaine Mardis, PhD, co-director of The Genome Institute at the School of Medicine. "Genome analysis can play a role at multiple time points during a patient's treatment, to identify 'driver' mutations in the tumor genome and to determine whether cells carrying those mutations have been eliminated by treatment."

This work is helping to guide the design of future cancer clinical trials in which treatment decisions are based on results of sequencing, says Mardis, who is speaking April 1 at the opening plenary session of the American Association for Cancer Research annual meeting in Chicago. She also is affiliated with the Siteman Cancer Center at the School of Medicine and Barnes-Jewish Hospital.

To date, Mardis and her colleagues have sequenced all the DNA the genome of tumor cells from more than 700 cancer patients. By comparing the genetic sequences in the tumor cells to healthy cells from the same patient, they can identify mutations underlying each patient's cancer.

Already, information gleaned through whole-genome sequencing is pushing researchers to reclassify tumors based on their genetic makeup rather than their location in the body. In patients with breast cancer, for example, Mardis and her colleagues have found numerous driver mutations in genes that have not previously been associated with breast tumors.

A number of these genes have been identified in prostate, colorectal, lung or skin cancer, as well as leukemia and other cancers. Drugs that target mutations in these genes, including imatinib, ruxolitinib and sunitinib, while not approved for breast cancer, are already on the market for other cancers.

"We are finding genetic mutations in multiple tumor types that could potentially be targeted with drugs that are already available," Mardis says.

She predicts, however, that it may require a paradigm change for oncologists to evaluate the potential benefits of individualized cancer therapy. While clinical trials typically involve randomly assigning patients to a particular treatment regimen, a personalized medicine approach calls for choosing drugs based on the underlying mutations in each patient's tumor.

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DNA sequencing lays foundation for personalized cancer treatment

Paulina Porizkova is the face of Avon Cosmetics latest breakthrough anti-aging miracle, Anew Genics.

Paulina who? To a generation more familiar with the likes of Gisele, Kate and Heidi, the name might not ring the loudest of bells. Ask any true-blue beauty and fashion hound, however, and she (or hegays will kill for their mastery of supermodel lore) will tell you that some two decades ago, even before Linda, Naomi, Elle and Christy became global first-name icons who hogged the same headlines as Hollywood stars, the Czech-born Porizkova was the fashion worlds model du jour, her Alpine cheekbones adorning every magazine cover from Vogue to Sports Illustrated and her $6-million dollar modeling contract with Este Lauder then the highest ever paid to a mannequin.

Porizkova is now 46, ancient by modelling standards, but in Avons recently rolled out Anew Genics ad campaign, she looks as stunning as ever. The beauty brand is not caught up in some trendy retro mode in hiring Porizkova for its latest product. Here, the medium is unmistakably the message, for the seemingly ageless Porizkova is hawking what Avon says is a skincare breakthrough serum that helps you look up to 10 years younger.

One look at its spectacular-looking poster girl, just four years shy of 50, and the product makes it point.

Pioneer status

The Anew Genics line, beginning with the Treatment Concentrate that is now available in the Philippines exclusively through Avon representatives (at P1,799), is the latest iteration of the beauty companys flagship anti-aging brand, Anew, which celebrates its 20th anniversary this year. Launched in 1992, the brand has become a worldwide $1-billion bestseller, with some 11,000 units of Anew reportedly sold every hour.

Avon claims pioneer status in the skincare industry as the first to mass-market alpha hydroxy acidnow a standard part of many anti-aging productsas the main ingredient of its Anew line. The brand has regularly introduced variants through the yearsamong them Anew Clinical, Anew Rejuvenate, Anew Reversalist, Anew Ultimate, Anew Platinum and Anew Solar Advanceto incorporate the latest skincare innovations its scientists and researchers have come up with.

Anew Genics, says Dr. Xiaochun Luo, chief scientific officer and group vice president for Avons global research and development, is another groundbreaking product that women will definitely be excited to try. Our international team of researchers and product developers invested 10 years in developing this product to make younger and reenergized skin accessible to women.

Come-on

Look up to 10 years younger! is Anew Genics come-onmade possible, says Xiaochun, by a patented YouthGen technology thats supposed to stimulate the activity of a youth gene in the body, which in turn leads to younger-looking skin.

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Harnessing the youth gene to fight skin aging

Rice University and IBM today have announced a partnership to build the first award-winning IBM Blue Gene supercomputer in Texas. Rice also announced a related collaboration agreement with the University of Sao Paulo in Brazil to initiate the shared administration and use of the Blue Gene supercomputer, which allows both institutions to share the benefits of the new computing resource.

Rice faculty will use the Blue Gene to further their own research and to collaborate with academic and industry partners on a broad range of science and engineering questions related to energy, geophysics, basic life sciences, cancer research, personalized medicine and more.

The collaborative agreement securing Brazil's share of time on Rice's Blue Gene was signed in Sao Paulo March 27 by a delegation that included Rice President David Leebron and USP President Joo Grandino Rodas. Leebron is traveling with a delegation led by Houston Mayor Annise Parker. The delegation includes Rice Provost George McLendon, Greater Houston Partnership (GHP) President and CEO Jeff Moseley and other GHP members.

"Collaboration and partnership have a unique place in Rice's history as a pre-eminent research university, and it is fitting that Rice begins its second century with two innovative partnerships that highlight the university's commitments to expanding our international reach, strengthening our research and building stronger ties with our home city," Leebron said.

USP is Brazil's largest institution of higher education and research, and Rodas said the agreement represents an important bond between Rice and USP. "The joint utilization of the supercomputer by Rice University and USP, much more than a simple sharing of high-tech equipment, means the strength of an effective partnership between both universities," he said.

Mayor Parker, a 1978 Rice alumna, said, "When I was at Rice, it looked inward. Today it looks outward through this agreement. It strengthens not only Rice University but also the city of Houston."

Rice's new P series Blue Gene supercomputer, which has yet to be named, is slated to become operational in May. It is based on IBM's POWER processor technology, which was developed in part at the company's Austin, Texas labs. Rice and IBM shared the cost of the system.

"High-performance computers like the IBM Blue Gene/P are critical in virtually every discipline of science and engineering, and we are grateful for IBM's help in bringing this resource to Rice," McLendon said. "For individual faculty, the supercomputer will open the door to new areas of research. The Blue Gene also opens doors for Rice as the university seeks to establish institutional relationships both in our home city and with critical international partners like USP."

Unlike the typical desktop or laptop computer, which have a single microprocessor, supercomputers typically contain thousands of processors. This makes them ideal for scientists who study complex problems, because jobs can be divided among all the processors and run in a matter of seconds rather than weeks or months. Supercomputers are used to simulate things that cannot be reproduced in a laboratory -- like Earth's climate or the collision of galaxies -- and to examine vast databases like those used to map underground oil reservoirs or to develop personalized medical treatments.

USP officials said they expect their faculty to use the supercomputer for research ranging from astronomy and weather prediction to particle physics and biotechnology.

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Rice, IBM partner to build Texas’ first Blue Gene supercomputer

OMAHA, Neb.--(BUSINESS WIRE)--

Transgenomic, Inc. (OTCBB: TBIO.OB - News) today announced that Jeana DaRe, Ph.D., Assistant CLIA Laboratory Director at Transgenomic, presented clinical findings from patients tested for nuclear mitochondrial disorders using Transgenomics NuclearMitome Test on Thursday, March 29, at the 2012 Annual Meeting of the American College of Medical Genetics (ACMG) in Charlotte, North Carolina. The discussion, titled Clinical re-sequencing of over 410 genes to diagnose mitochondrial disorders included details of both the technical performance of the NuclearMitome Test as well as the wide variety of clinically revealing results discovered through its use. The NuclearMitome Test employs next-generation sequencing technology to identify mutations in 448 genes, and represents the most comprehensive genetic test available for mitochondrial disorders.

In her presentation, Dr. DaRe highlighted two case studies. In both cases, patients achieved a definitive diagnosis through the identification of genetic mutations far outside the normal spectrum of genetic testing. These results concluded the patients diagnostic odysseys, which had encompassed wide-ranging genetic and non-genetic tests as well as consultation with various medical specialties, all of which had failed to pinpoint the underlying disease. These results are a typical occurrence in patients sent for NuclearMitome testing.

The NuclearMitome Test is a cutting-edge technology that is reshaping the process for accurately diagnosing and effectively treating patients with mitochondrial disorders, said Craig Tuttle, CEO of Transgenomic. Since its launch in June 2011, clinicians have embraced this test as a way to simultaneously assay the hundreds of genes relevant to mitochondrial-based developmental disorders and achieve otherwise impossible diagnoses. The NuclearMitome test is rapidly becoming an important asset for the medical and patient communities and for Transgenomic.

About Mitochondrial Diseases

Mitochondrial diseases are the most common metabolic diseases of childhood with an estimated frequency of 1 in 2000 births. They are characterized by multi-organ involvement, particularly neuromuscular symptoms, and often follow a rapidly progressive course. The variability in clinical presentation makes diagnosis tremendously challenging, as it traditionally relies on often-inconclusive enzymatic analyses that do not pinpoint the underlying molecular defect. Knowledge of the specific cause of disease can be important for developing personalized treatment strategies.

About Transgenomic, Inc.

Transgenomic, Inc. (www.transgenomic.com) is a global biotechnology company advancing personalized medicine in cancer and inherited diseases through its proprietary molecular technologies and world-class clinical and research services. The company has three complementary business divisions: Transgenomic Pharmacogenomic Services is a contract research laboratory that specializes in supporting all phases of pre-clinical and clinical trials for oncology drugs in development. Transgenomic Clinical Laboratories specializes in molecular diagnostics for cardiology, neurology, mitochondrial disorders, and oncology. Transgenomic Diagnostic Tools produces equipment, reagents, and other consumables that empower clinical and research applications in molecular testing and cytogenetics. Transgenomic believes there is significant opportunity for continued growth across all three businesses by leveraging their synergistic capabilities, technologies, and expertise. The company actively develops and acquires new technology and other intellectual property that strengthen its leadership in personalized medicine.

Forward-Looking Statements

Certain statements in this press release constitute forward-looking statements of Transgenomic within the meaning of the Private Securities Litigation Reform Act of 1995, which involve known and unknown risks, uncertainties and other factors that may cause actual results to be materially different from any future results, performance or achievements expressed or implied by such statements. Forward-looking statements include, but are not limited to, those with respect to management's current views and estimates of future economic circumstances, industry conditions, company performance and financial results, including the ability of the Company to grow its involvement in the diagnostic products and services markets. The known risks, uncertainties and other factors affecting these forward-looking statements are described from time to time in Transgenomic's filings with the Securities and Exchange Commission. Any change in such factors, risks and uncertainties may cause the actual results, events and performance to differ materially from those referred to in such statements. Accordingly, the Company claims the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995 with respect to all statements contained in this press release. All information in this press release is as of the date of the release and Transgenomic does not undertake any duty to update this information, including any forward-looking statements, unless required by law.

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Transgenomic, Inc. Announces Presentation of Results from 448-Gene NuclearMitome Test in 78 Patients at the 2012 ...

HOUSTON, March 30, 2012 /PRNewswire/ --Rice University and IBM (NYSE: IBM) today announced a partnership to build the first award-winning IBM Blue Gene supercomputer in Texas. Rice also announced a related collaboration agreement with the University of Sao Paulo (USP) in Brazil to initiate the shared administration and use of the Blue Gene supercomputer, which allows both institutions to share the benefits of the new computing resource.

(Logo: http://photos.prnewswire.com/prnh/20090416/IBMLOGO )

Rice faculty will use the Blue Gene to further their own research and to collaborate with academic and industry partners on a broad range of science and engineering questions related to energy, geophysics, basic life sciences, cancer research, personalized medicine and more.

The collaborative agreement securing Brazil's share of time on Rice's Blue Gene was signed in Sao Paulo March 27 by a delegation that included Rice President David Leebron and USP President Joao Grandino Rodas. Leebron is traveling with a delegation led by Houston Mayor Annise Parker. The delegation includes Rice Provost George McLendon, Greater Houston Partnership (GHP) President and CEO Jeff Moseley and other GHP members.

"Collaboration and partnership have a unique place in Rice's history as a pre-eminent research university, and it is fitting that Rice begins its second century with two innovative partnerships that highlight the university's commitments to expanding our international reach, strengthening our research and building stronger ties with our home city," Leebron said.

USP is Brazil's largest institution of higher education and research, and Rodas said the agreement represents an important bond between Rice and USP. "The joint utilization of the supercomputer by Rice University and USP, much more than a simple sharing of high-tech equipment, means the strength of an effective partnership between both universities," he said.

Mayor Parker, a 1978 Rice alumna, said, "When I was at Rice, it looked inward. Today it looks outward through this agreement. It strengthens not only Rice University but also the city of Houston."

Rice's new Blue Gene supercomputer, which has yet to be named, is slated to become operational in May. It is based on IBM's POWER processor technology, which was developed in part at the company's Austin, Texas labs. Rice and IBM shared the cost of the system.

"High-performance computers like the IBM Blue Gene/P are critical in virtually every discipline of science and engineering, and we are grateful for IBM's help in bringing this resource to Rice," McLendon said. "For individual faculty, the supercomputer will open the door to new areas of research. The Blue Gene also opens doors for Rice as the university seeks to establish institutional relationships both in our home city and with critical international partners like USP."

Unlike the typical desktop or laptop computer, which have a single microprocessor, supercomputers typically contain thousands of processors. This makes them ideal for scientists who study complex problems, because jobs can be divided among all the processors and run in a matter of seconds rather than weeks or months. Supercomputers are used to simulate things that cannot be reproduced in a laboratory -- like Earth's climate or the collision of galaxies -- and to examine vast databases like those used to map underground oil reservoirs or to develop personalized medical treatments.

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Rice University, IBM Partner to Bring First Blue Gene Supercomputer to Texas

A forum critical of UC Berkeleys plans to ramp up genetic engineering research at a planned massive new second campus of Lawrence Berkeley National Laboratory in Richmond drew a capacity crowd to the David Brower Center Thursday night.

One speaker after another ripped into the potential consequences of the universitys grandiose plans, including the human and environmental devastation certain to be wrought on Africa and Latin America.

We will be posting several articles on the gathering, but we will begin with a focus on some of the ways the labs end products could impact other lands targeted by the labs emphasis on using genetic engineering to transform living plants into fuel.

A resonant voice from Nigeria

Environmental activist Nnimmo Bassey, executive director of Environmental Rights Action in Nigeria and chair of Friends of the Earth International, ripped into comments made a day earlier by Jay Keasling, UC Berkeley professor, founder of three genetic engineering companies, and head of the Department of Energy-funded Joint BioEnergy Institute [JBEI], which is slated to relocate to the new Richmond campus.

In an article in the San Francisco Chronicle, Keasling had dismissed criticisms by Bassey and others that any successful program to use genetically altered microbes to create fuel from plant matter would wreak ecological and human devastation in Africa, Latin America, and Asia:

Thast so-called wasteland is somebodys land, Bassey said. The worlds pastoralists thrive on lands marginal or unsuitable for farming. People do live in the Sahara desert. People do live in the Kalahari Desert. People do live in the desert here in the United States.

The one sure result of a global land grab is conflict, he said. A second is the introduction of genetically modified organisms [GMOs] into more nations where theyve been previously banned.

Bassey, whose words flow in resonant, almost musical bass tones, is a winner of the 2010 Right Livelihood Award, often called the Alternate Nobel Prize because it is awarded by the Swedish legislature the day before the Nobels are handed out in the same city, Stockholm. The prize is given for working on practical and exemplary solutions to the most urgent challenges facing the world today.

Much of Basseys work has centered on the devastation wrought on his country by oil companies like Chevron, which has sunk its claws and talons into Richmond, and, like Shell, BP, and other oil companies is moving into agrofuels.

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Stakeholders weigh in on UC Berkeley GMO complex

30-03-2012 11:44 Personalized medicine is becoming an increasingly important aspect of cancer treatment. Levi Garraway, MD, PhD, of Dana-Farber Cancer Institute and the Broad Institute, describes a new database of nearly 1000 cancer cell lines, across numerous tumor types, that will be used to help predict the effectiveness of cancer drugs based on a tumor's genetic profile.

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Levi Garraway on cancer cell genetic profile catalogs | Dana-Farber Cancer Institute - Video

Editor's Choice Academic Journal Main Category: Cardiovascular / Cardiology Also Included In: Heart Disease;Genetics Article Date: 30 Mar 2012 - 8:00 PDT

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Following PCI, the standard care for patients commonly consists of aspirin and clopidogrel to reduce the risk of blood clot formation, however, this dual antiplatelet therapy results in many patients becoming vulnerable to major adverse cardiovascular events.

This persistent vulnerability is linked to elevated on-treatment platelet reactivity, which can lead to a sudden blockage in the stents that can cause heart attacks or death. The characteristics of elevated on-treatment platelet reactivity are inadequate inhibition of the platelet PsY12 receptor following clopidogrel treatment.

According to scientists, numerous clinical variables have been implicated, however, the strongest predictor is the loss-of-function CYP2C19*2 allele (rs4244285), which is a common genetic variant that occurs in almost 30% of western Europeans and in about 50% of Asians.

Two unique P2Y12 inhibitors are prasugrel and ticagrelor, which compared with clopidogrel provide a more potent platelet inhibition. Although both drugs reduce major adverse cardiovascular events following acute coronary syndrome, they are also linked to higher complications in terms of bleeding. The researchers point out that retrospective genetic studies demonstrated that both, prasugrel and ticagrelor remained unaffected by the CYP2C19*2 allele. According to the authors, personalization of dual antiplatelet therapy after PCI could successfully minimize major adverse cardiovascular and adverse bleeding events if CYP2C19*2 carrier status could be identified in the future.

Spartan Biosciences in Ottawa, ON, Canada, has developed Spartan RX CYP2C19 as a point-of-care genetic test for the CYP2C19*2 allele that is performed with a buccal swab, which enables health-care personnel with no previous training in genetic laboratory techniques to undertake genotyping at the patient's bedside.

The researchers decided to evaluate the clinical feasibility and pharmacodynamic efficacy of personalized dual antiplatelet therapy in patients who receive PCI treatment for acute coronary syndrome and stable coronary artery disease.

The standard care for these patients is a medical regimen of aspirin and clopidogrel, however, the new genetic test means that physicians can personalize the patient's therapy and select whether they should opt to administer a more potent anti-platelet drug like prasugrel to those patients who have a high risk of failing treatment with clopidogrel.

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Using Antiplatelet Therapy After Coronary Interventions - Study

By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) Interleukin Genetics today reported that its fourth-quarter revenues increased 13 percent, driven by a partnership with Amway.

The Waltham, Mass.-based genetic test maker had total revenues of $575,339 for the three-month period ended Dec. 31, compared to $510,767 for the fourth quarter of 2010. It said that its revenue came primarily from the sale of its Inherent Health genetic tests through the Amway global sales channel. That partnership dates back to October 2009.

Interleukin's net loss for the quarter was $1.4 million, or $.04 per share, compared to a net loss of $1.2 million, or $.03 per share, for Q4 2010.

Its R&D spending increased to $387,106 from $354,051 year over year, while its SG&A spending declined to $1.1 million from $1.3 million.

For full-year 2012, Interleukin's revenues climbed around 45 percent to $2.9 million from $2 million in 2011.

"Our genetic testing revenue has grown by more than forty percent this year over last year as we added new partnerships for distribution of our tests," Interleukin Genetics CEO Lewis Bender said in a statement. "In addition, our collaboration with Stanford University continued with an extension study whose results showed that the genetic patterns identified by our Weight Management Test can help individuals lose more weight when diets are selected based on genotype."

The firm also is developing a genetic test for periodontal disease risk.

Interleukin posted a net loss of $5 million, or $.14 per share, compared to a net loss of $6 million, or $.17 per share, for 2010.

Its R&D spending for the year was $1.4 million, flat with 2010, and its SG&A expenses declined to $4.7 million from $5.5 million.

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Interleukin Genetics' Revenues Rise

AMSTERDAM, The Netherlands, March 30, 2012 /PRNewswire/ --

Amsterdam Molecular Therapeutics (Euronext: AMT - News), a leader in the field of human gene therapy, announced that the Extraordinary General Meeting (EGM) of shareholders was held in Amsterdam, the Netherlands, today in accordance with the EGM Notice of February 17, 2012. At the EGM, shareholders approved all the resolutions proposed for the substantial corporate restructuring and financing transaction, which will result in the assets and certain liabilities being acquired by a newly formed private company, uniQure BV, and the AMT legal entity being liquidated.

The shareholders in uniQure previously included a condition to the transaction that meant an additional 1.0 million of investment was to be secured by AMT prior to completion. This condition has been waived. Completion of the uniQure transaction is expected to occur in early April 2012. Further details on timing on the uniQure transaction are set out on the company's website.

The resolutions put to the EGM convened in accordance with the Notice were passed by a majority in excess of 99 percent. The detailed voting information and results pursuant to Section 2:120 paragraph 5 of the Dutch Civil Code will be posted on the website http://www.amtbiopharma.com.

About Amsterdam Molecular Therapeutics

AMT is a world leader in the development ofhuman gene based therapies.AMT has a product pipeline of gene therapy products in development for hemophilia B, acute intermittent porphyria, Parkinson's disease and SanfilippoB. Using adeno-associated viral (AAV) derived vectors as the delivery vehicle of choice for therapeutic genes, the company has been able to design and validate probably the world's first stable and scalable AAV manufacturing platform.This proprietary platform can be applied to a large number of rare(orphan) diseases caused by one faulty gene and allows AMT to pursue its strategy of focusing on this sector of the industry. The assets of AMT are subject to a proposed acquisition by uniQure BV. AMT was founded in 1998 and is based in Amsterdam. Further information can be found at http://www.amtbiopharma.com.

About uniQure

uniQure BV is a private company created specifically to acquire specific assets and liabilities of Amsterdam Molecular Therapeutics (AMT). The company is funded by Forbion Capital Partners, an existing investor in AMT. uniQure will act as the new holding company for the gene therapy business currently carried out by AMT.

Certain statements in this press release are "forward-looking statements" including those that refer to management's plans and expectations for future operations, prospects and financial condition. Words such as "strategy," "expects," "plans," "anticipates," "believes," "will," "continues," "estimates," "intends," "projects," "goals," "targets" and other words of similar meaning are intended to identify such forward-looking statements. Such statements are based on the current expectations of the management of AMT only. Undue reliance should not be placed on these statements because, by their nature, they are subject to known and unknown risks and can be affected by factors that are beyond the control of AMT. Actual results could differ materially from current expectations due to a number of factors and uncertainties affecting AMT's business. AMT expressly disclaims any intent or obligation to update any forward-looking statements herein except as required by law.

Continued here:
Amsterdam Molecular Therapeutics Announces Results of Extraordinary General Meeting

U.S. researchers say they have developed a lifesaving genetic screening program for families at high risk of contracting colorectal cancer.

Dr. Samir Gupta, assistant professor of internal medicine at the University of Texas Southwestern in Dallas, who is also head of the high-risk colorectal cancer clinic, said colorectal cancer is the second-leading killer after lung cancer -- and while hereditary colorectal cancer is rare, its family impact can be widespread.

Cancer tends to develop rapidly in those with Lynch syndrome, one of the more common inherited conditions. Lynch syndrome accounts for 3 percent to 5 percent of all colon cancers, and often is undiagnosed until the disease is advanced.

Families that have Lynch syndrome usually have more cases of colon cancer than would typically be expected, and at an earlier ages, than in the general population.

Gupta said doctors screen the tumors of colorectal cancer patients younger than age 70 and uterine cancer patients younger than age 55 to determine whether there is a high risk of a genetic cancer predisposition. If so, patients are encouraged to bring in as many family members as possible for testing, Gupta said.

"If we can bring in family members, we have a chance to catch their colon cancer early and even prevent it," Gupta said in a statement.

Patients with Lynch syndrome have an 80 percent risk of contracting colorectal cancer and as much as a 60 percent risk for uterine cancer, and higher than average risks for other cancer types, Gupta added.

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Genetic Screening For Colorectal Cancer

Published: March. 29, 2012 at 11:18 PM

DALLAS, March 29 (UPI) -- U.S. researchers say they have developed a lifesaving genetic screening program for families at high risk of contracting colorectal cancer.

Dr. Samir Gupta, assistant professor of internal medicine at the University of Texas Southwestern in Dallas, who is also head of the high-risk colorectal cancer clinic, said colorectal cancer is the second-leading killer after lung cancer -- and while hereditary colorectal cancer is rare, its family impact can be widespread.

Cancer tends to develop rapidly in those with Lynch syndrome, one of the more common inherited conditions. Lynch syndrome accounts for 3 percent to 5 percent of all colon cancers, and often is undiagnosed until the disease is advanced.

Families that have Lynch syndrome usually have more cases of colon cancer than would typically be expected, and at an earlier ages, than in the general population.

Gupta said doctors screen the tumors of colorectal cancer patients younger than age 70 and uterine cancer patients younger than age 55 to determine whether there is a high risk of a genetic cancer predisposition. If so, patients are encouraged to bring in as many family members as possible for testing, Gupta said.

"If we can bring in family members, we have a chance to catch their colon cancer early and even prevent it," Gupta said in a statement.

Patients with Lynch syndrome have an 80 percent risk of contracting colorectal cancer and as much as a 60 percent risk for uterine cancer, and higher than average risks for other cancer types, Gupta added.

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Genetic screenings detect at-risk families

NEW YORK, March 29, 2012 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE Amex:NBS) ("NeoStem" or "the Company"), a leader in the cell therapy industry, announced today the pricing of an underwritten public offering of 15,000,000 units at $0.40 per unit. Each unit consists of one share of common stock and a warrant to purchase one share of common stock with a per share exercise price of $0.51. Maxim Group LLC acted as sole bookrunner. The Company expects to receive $6,000,000 in gross proceeds, prior to deducting underwriting discounts and commissions and offering expenses payable by the Company. These funds will be used for working capital purposes, including research and development of cell therapeutic product candidates, expansion of business units, strategic transactions and other general corporate purposes. The Company has granted the underwriters a 45-day option to purchase up to an additional 2,250,000 units to cover over-allotments.

The financing is expected to close on or about April 3, 2012, subject to the satisfaction of customary closing conditions.

This offering is being made by means of a prospectus supplement and accompanying prospectus. Copies of the final prospectus supplement and accompanying prospectus relating to this offering may be obtained from the Securities and Exchange Commission's website at http://www.sec.gov or from Maxim Group LLC, 405 Lexington Avenue, New York, NY 10174 or via telephone at (212) 895-3685.

A shelf registration statement relating to the offering was previously filed with the Securities and Exchange Commission and became effective on June 13, 2011. This press release is neither an offer to sell nor a solicitation of an offer to buy any of the Company's securities. No offer, solicitation or sale will be made in any jurisdiction in which such offer, solicitation or sale is unlawful.

Further information regarding the offering is contained in the Company's Current Report on Form 8-K to be filed with the Securities and Exchange Commission and which may be accessed at http://www.sec.gov.

About NeoStem, Inc.

NeoStem, Inc. ("we," "NeoStem" or the "Company") continues to develop and build on its core capabilities in cell therapy to capitalize on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a large role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. Our January 2011 acquisition of Progenitor Cell Therapy, LLC ("PCT") provides NeoStem with a foundation in both manufacturing and regulatory affairs expertise. We believe this expertise, coupled with our existing research capabilities and collaborations, will allow us to achieve our mission of becoming a premier cell therapy company. Our PCT subsidiary's manufacturing base is one of the few current Good Manufacturing Practices ("cGMP") facilities available for contracting in the burgeoning cell therapy industry. Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011, is developing a cell therapy for the treatment of cardiovascular disease. Amorcyte's lead compound, AMR-001, represents NeoStem's most clinically advanced therapeutic and has commenced enrollment for a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. We also expect to begin a Phase 1 clinical trial by 2013 to investigate AMR-001's utility in arresting the progression of congestive heart failure and the associated comorbidities of that disease. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is engaged in collaboration with Becton-Dickinson that is exploring the earlier stage clinical development of a T-cell therapy for autoimmune conditions. In addition, our pre-clinical assets include our VSELTM Technology platform as well as our MSC (mesenchymal stem cells) product candidate for regenerative medicine.

For more information on NeoStem, please visit http://www.neostem.com.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward looking statements include statements herein with respect to the successful execution of the Company's business and medical strategy, including with respect to the development of AMR-001 and other cell therapies and its divestiture of its interest in Suzhou Erye Pharmaceutical Co., Ltd. about which no assurance can be given. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors. Factors that could cause future results to materially differ from the recent results or those projected in forward-looking statements include the "Risk Factors" described in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 19, 2012 and in the Company's periodic filings with the Securities and Exchange Commission. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem Announces Pricing of Public Offering for $6,000,000 in Gross Proceeds

28-03-2012 18:37 Plot: Dream Sequence: Melfina had been kidnapped. Taken by Hazanko, a mystic cult leader, bound and determined to use her powers to forward his own ambitions. But, before he can do anymore to her, Gene arrives to her rescue. Gene tries to finish him off quickly with one shot from his caster, but Caster Shell #4 proves insufficient in dealing with Hazanko. Melfina tries to get him to flee, fearing for her friend's life. But Gene remains determined to save her. With one final shot, Gene fires Caster Shell #13 at Hazanko, who responds with a magic attack of his own, resulting in an explosion that ends up killing Hazanko, but also mortally wounds Gene. Before blacking out, he sees Melfina's distraught face, pleading with him to not die... Jim is cooking "Breakfast" for Gene before he goes off to perform in his show. Gene, still hung over from one of his many nights of frivolity, groggily gets ready. Jim notes that Gene was rather restless during his sleep, and mentions that bad dreams can sometimes be caused by feelings of regret. He doesn't say it out loud, but he knows what's bothering Gene. All the better, as far as Jim was concerned. He hadn't yet fully forgiven Gene over what he had done. After his show was over, Gene spends some time alone, thinking back to Melfina. His thoughts are accompanied by a song Melfina used to sing, to help lift Gene and Jim's spirits. She had come to them, seeking protection from Hazanko. She was a healer, an exceptionally talented one, and ...

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[CM] Regrets of the Past (Gene Starwind) - Video

29-03-2012 09:34 The mission of Mary Crowley Cancer Research Centers is to expand treatment options for all cancer patients through investigational vaccine, gene and cellular therapies. At Mary Crowley Cancer Research Centers, there is a belief that a paradigm shift is occurring in cancer care, in which personalized molecular medicine will eventually transform the way patients are treated.

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Mary Crowley Cancer Research Centers' Mission - Video

29-03-2012 12:24 More LXBN TV interviews at: lxbn.lexblog.com While talk this week of course focuses on the oral arguments in the Affordable Care Act case, the Supreme Court last week ruled in a very important and influential intellectual property case. In Mayo Collaborative Services v. Prometheus Laboratories, Inc., the court ruled that the patent Prometheus had obtained for correlations between blood test results and patient health is not eligible for a patent because it incorporates laws of nature. Not only does this have a big impact on the medical community, but also another major case—the Myriad "gene patenting" case. To explain the background of Mayo v. Prometheus, whether or not these types of patents slow medical research and what this means for the Myriad case, we bring in Foley & Lardner Partner Antoinette Konski, who has covered this case exceptionally on the Personalized Medicine Bulletin-- http://www.personalizedmedicinebulletin.com

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Mayo v. Prometheus and Its Impact on Myriad "Gene Patenting" Case—Antoinette Konski - Video

Public release date: 29-Mar-2012 [ | E-mail | Share ]

Contact: Rebecca Scott rebeccas@unimelb.edu.au 61-383-440-181 University of Melbourne

An international team of researchers led by the University of Melbourne has used new technology to fast track the discovery of a breast cancer risk gene and could assist in the discovery of other cancer genes.

Professor Melissa Southey of the Genetic Epidemiology Laboratory, Department of Pathology at the University of Melbourne, who led the study, said it was a significant discovery and the first breast cancer risk gene to be discovered using the latest genetic sequencing technology.

"The mutations in the newly identified gene XRCC2, although rare, explain another proportion of breast cancers that run in families where there is no known genetic cause and that particularly occur at an early age," she said.

"We identified this gene quite quickly using genetic technology called massively parallel sequencing, which enables sequencing of large amounts of human DNA at high speed.'

"Due to these results and our methodology we believe that further risk genes will be identified at a faster rate than before and potentially for other cancers such as colorectal and prostate cancers," she said.

Professor Southey said the discovery could help manage the risk of breast cancer for families with a strong history of the disease and no known genetic cause.

"This discovery will assist some families to determine individual risk and which family members are at high risk of contracting the disease," Professor Southey said.

"Unaffected relatives of people with a mutation in this gene could also be offered predictive testing, subsequent genetic counselling and ongoing clinical management on the basis of their mutation status.'

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Breast cancer risk gene discovery fast tracked by new technology

ScienceDaily (Mar. 29, 2012) Mutations in a gene called XRCC2 cause increased breast cancer risk, according to a study published March 29 in the American Journal of Human Genetics. The study looked at families that have a history of the disease but do not have mutations in the currently known breast cancer susceptibility genes.

Sean Tavtigian, Ph.D., a Huntsman Cancer Institute (HCI) investigator and associate professor in the Department of Oncological Sciences at the University of Utah (U of U) is one of three co-principal investigators on the study, along with David Goldgar, Ph.D., professor in the Department of Dermatology at the U of U and an HCI investigator, and Melissa Southey, Ph.D., professor in the Department of Pathology at the University of Melbourne, Australia.

"We have added to the list of genes that harbour mutations causing breast cancer," said Tavtigian. "This knowledge will improve breast cancer diagnostics and add years to patients' lives. More important, relatives who have not been affected by the disease but carry the mutations will benefit even more. They can find out they are at risk before they have cancer and take action to reduce their risk or catch the cancer early."

XRCC2 may also provide a new target for chemotherapy. "A type of drug called a PARP inhibitor appears to kill tumor cells that have gene mutations in a particular DNA repair pathway. XRCC2 is in this pathway, as are BRCA1 and BRCA2. It's reasonably likely that a breast cancer patient who has a mutation in XRCC2 will respond well to treatment with PARP inhibitors," said Tavtigian.

According to Tavtigian, many breast cancer cases appear in families with a weak history of the disease. Only about 30 percent of the familial risk for breast cancer can be explained by a combination of mutations to and common sequence variation in the known breast cancer susceptibility genes. "So far most of the clinical diagnostic effort has been directed toward the very strong family history set of breast cancer cases and their close relatives," he said. "Our research looks at a population with a weaker family history, and as it turns out, a very rare gene mutation."

The researchers used a technology called exome capture massively parallel sequencing (exome sequencing), which shows the exact order of the nucleotides (the four building blocks of DNA) in all of the protein coding genes in the human genome. The ability of this technology to analyze the DNA of all of the genes in the genome in a single experiment, according to Tavtigian, makes it an amazingly powerful tool for genetic research. "We focused on the genes involved in a particular type of DNA repair, because most known breast cancer genes have been found there. That focused analysis allowed us to identify XRCC2 as a breast cancer susceptibility gene in individuals with a family history of breast cancer," says Tavtigian. "From the exome sequencing data, we found two different types of XRCC2 mutations that occur in breast cancer patients."

He explains that one type of mutation causes the gene to create an incomplete version of the protein. The resulting protein is usually dysfunctional. The other type occurs when a single amino acid in the protein is changed.

"It's a subtle change to the protein, but the resulting change in function could range anywhere from innocuous to even worse dysfunction than the incomplete protein causes," says Tavtigian. "Our sequence analyses suggest that we may have found the full spectrum of results in our study."

Further research is underway. "A worldwide effort has already been launched to figure out what fraction of breast cancer is due to mutations in this gene and how high the risk conferred by these mutations actually is," he says.

The article lists 30 co-authors from HCI, the U of U, and other research organizations based in North America, Australia, and Europe. The study was supported by funding from the National Institutes of Health (R01CA155767 and R01CA121245) plus several other worldwide research foundations. The study also benefited from resources gathered by the Breast Cancer Family Registry, the Kathleen Cuningham Foundation Consortium for Research into Familial Breast Cancer, and several other breast cancer research efforts taking place around the world.

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New breast cancer susceptibility gene

The expression of a gene, when an organism's DNA is transcribed into a useable product, requires activation via a promoter or an external trigger. Plant research to be published in Science helps to show that later stages of transcription are just as important. This is likely to apply to other organisms, including humans.

Termination is the final stage of transcription. Successful termination is dependent on DNA being transcribed into RNA with the correct sections, including a certain length tail.

Scientists at the John Innes Centre on Norwich Research Park have found that where effective termination through the normal mechanisms has not occurred, DICER-LIKE 4 (DCL4) steps in to tidy up. Without termination, transcription continues down the chromosome unchecked.

In this way, DCL4 plays a crucial and previously unknown role in transcription termination. It helps formation of the gene product. DCL4 is more commonly known to play a part in the opposite effect, gene silencing.

"DCL4 is a back-up to termination processes, helping a gene to be successfully expressed," said lead author Professor Caroline Dean from JIC, which is strategically funded by the BBSRC.

The findings may help explain why gene silencing happens so often with transgenes. It was not known that so much attention should be given to the tail end of a gene.

"Our research shows that for successful expression the end of a gene is just as important as its beginning," said Dean.

When termination fails a lot of aberrant RNA is made this is degraded as part of a cell's quality control mechanism. This can have consequences for other sequences in the genome that match the aberrant RNA.

"If a gene ends badly, aberrant RNA will trigger silencing pathways," said Dean.

DCL4's ability to step in to rescue poor termination makes it important for both successful gene expression, a previously unknown role for it, and gene silencing.

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Plant research reveals new role for gene silencing DICER protein

ScienceDaily (Mar. 29, 2012) A DICER protein, known to produce tiny RNAs in cells, also helps complete an important step in gene expression, according to research on Arabidopsis thaliana. The expression of a gene, when an organism's DNA is transcribed into a useable product, requires activation via a promoter or an external trigger. Plant research to be published in Science helps to show that later stages of transcription are just as important. This is likely to apply to other organisms, including humans.

Termination is the final stage of transcription. Successful termination is dependent on DNA being transcribed into RNA with the correct sections, including a certain length tail.

Scientists at the John Innes Centre on Norwich Research Park have found that where effective termination through the normal mechanisms has not occurred, DICER-LIKE 4 (DCL4) steps in to tidy up. Without termination, transcription continues down the chromosome unchecked.

In this way, DCL4 plays a crucial and previously unknown role in transcription termination. It helps formation of the gene product. DCL4 is more commonly known to play a part in the opposite effect, gene silencing.

"DCL4 is a back-up to termination processes, helping a gene to be successfully expressed," said lead author Professor Caroline Dean from JIC, which is strategically funded by BBSRC.

The findings may help explain why gene silencing happens so often with transgenes. It was not known that so much attention should be given to the tail end of a gene.

"Our research shows that for successful expression the end of a gene is just as important as its beginning," said Dean.

When termination fails a lot of aberrant RNA is made -- this is degraded as part of a cell's quality control mechanism. This can have consequences for other sequences in the genome that match the aberrant RNA.

"If a gene ends badly, aberrant RNA will trigger silencing pathways," said Dean.

DCL4's ability to step in to rescue poor termination makes it important for both successful gene expression, a previously unknown role for it, and gene silencing.

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Plant research reveals new role for gene silencing protein

A plan by Lawrence Berkeley Laboratory to merge its energy labs into a major new research facility in Richmond where scientists would work to develop biofuels through genetic engineering came under fire Wednesday by activists who fear that dangerous new microbes would be created there.

And even if the venture succeeds in transforming plants into biofuels by altering the genes of microbes, the activists argued, the Richmond lab could become an unregulated front for corporate interests and turn millions of acres of croplands used to grow food in underdeveloped countries into huge plantations for energy production.

Their protests reflect deep concerns about the dramatic new science called "synthetic biology," an unfamiliar term that in part involves engineering the genes of microbes to transform worthless plants like switchgrass into potentially unlimited sources of energy. The controversy also recalls an epic time in science nearly 40 years ago when manipulating genes was in its infancy and the public was deeply fearful that some genetically altered "Andromeda Strain" microbe might escape and imperil the world with unknown diseases.

That fear was largely ended when, after a 1975 conference at Asilomar near Monterey, biologists, lawyers and physicians agreed on enforceable guidelines for proceeding with genetic engineering projects.

It marked the first time that scientists agreed to be regulated and led to the public start of recombinant DNA research and what would become the huge international biotech industry.

Concerns about engineering "synthetic biology" are arising anew among activists.

On Wednesday, they gathered at the Center for Genetics and Society in Berkeley to express their concerns that the new research lab would be a poorly regulated entity with ties to unknown energy companies, that the work there would expose employees to dangerous microbes and, if successful, ultimately rob undeveloped nations of their croplands.

"This is a wild, wild, dangerous world," said Becky McClain, a onetime molecular biologist at a Pfizer lab in Connecticut who claimed that she had been sickened by a genetically engineered virus and was fired for speaking out about it.

"We can't afford to leave it to the corporations to self-regulate," said McClain, who won a $1.37 million lawsuit against Pfizer as a whistle-blower.

Gopal Dayaneni, an Oakland organizer, argued that the entire project - with so many engineered microbes - should never be built where earthquake hazards are high.

Originally posted here:
Plan to merge labs for biofuel research criticized

ScienceDaily (Mar. 29, 2012) Developed in Canada and conducted by researchers from the University of Ottawa Heart Institute (UOHI), in partnership with Spartan Bioscience, the world's first bedside genetic test has received acknowledgment by The Lancet.

The article "Point-of-care genetic testing for personalisation of antiplatelet treatment (RAPID GENE): a prospective, randomised, proof-of-concept trial," reports on the use of a simple cheek swab test, the Spartan RX CYP2C19, performed by nurses at the patient's bedside. This revolutionary technology allows doctors to rapidly identify patients with a genetic variant known as CYP2C19*2. Cardiac stent patients with this variant are at risk of reacting poorly to standard anti-platelet therapy with Plavix (clopidogrel).

The study demonstrated that tailored drug treatment therapy made possible by the genetic testing successfully protected all of the patients with the at-risk genetic variant from subsequent adverse events, while 30 per cent of patients treated with standard therapy did not receive adequate protection.

"For the first time in medicine, nurses were able to perform DNA testing at the patient's bedside. This is a significant step towards the vision of personalized medicine," said Dr. Derek So, Interventional Cardiologist at the University of Ottawa Heart Institute (UOHI), and principal investigator of the RAPID GENE study.

Study Details

The RAPID GENE study enrolled 200 patients who were being treated with cardiac stenting for an acute coronary syndrome or stable angina. Patients were randomized to a treatment strategy of rapid point-of-care genotyping and Effient (prasugrel) for CYP2C19*2 carriers, or to standard therapy with Plavix (clopidogrel). The Spartan RX CYP2C19 bedside DNA test was performed by nurses who received a 30-minute training session, but had no prior laboratory training. The test had a sensitivity of 100% and a specificity of 99.4% compared with DNA sequencing. For CYP2C19*2 carriers, treatment with prasugrel completely eliminated High on-treatment Platelet Reactivity (HPR). HPR is a marker for patients at risk of complications after stenting. In contrast, 30.4% of carriers receiving clopidogrel had HPR at 1 week.

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The above story is reprinted from materials provided by University of Ottawa Heart Institute.

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World's first bedside genetic test

Public release date: 29-Mar-2012 [ | E-mail | Share ]

Contact: Elizabeth Lynch elynch@marchofdimes.com 914-997-4286 March of Dimes Foundation

CHARLOTTE, NC -- A long-time clinician and researcher on Marfan syndrome who helped identify the syndrome's genetic cause and a potential treatment will be honored by the March of Dimes.

Harry (Hal) Dietz, MD, the Victor A. McKusick Professor of Institute of Genetic Medicine and Professor of Pediatrics, at Johns Hopkins University School of Medicine and Howard Hughes Medical Institute Investigator, will receive the March of Dimes/Colonel Harland Sanders Award for Lifetime Achievement in the field of genetic sciences. Dr. Joe Leigh Simpson, senior vice president for Research and Global Programs of the March of Dimes, will present the award to Dr. Dietz today during the annual Clinical Genetics Meeting of the American College of Medical Genetics at Charlotte Convention Center.

Marfan syndrome is an inherited connective tissue disorder that affects about 1 in 5,000 people. The syndrome is caused by a genetic defect which causes overgrowth of the body's long bones and affects the tissue that strengthens the body's structures, including the skeletal system, cardiovascular system, eyes, and skin.

Those who have the syndrome tend to be tall with arms and legs much longer than expected for their height. Also, in those with Marfan syndrome, the aorta, the main blood vessel that takes blood from the heart to the body, may stretch or become weak, leading to an aneurysm.

In 1991, Dr. Dietz was a member of the team that identified the gene for Marfan syndrome. In 2006, his team's research showed that an FDA-approved high blood pressure medication, losartan, prevented and reversed aortic enlargement in mice with Marfan syndrome.

Dr. Dietz received his medical degree from the State University of New York Upstate Medical Center in 1984. He joined Johns Hopkins University Hospital in 1984 as a pediatric resident, became a Fellow in Cardiology there 1988, went on to pursue his post doctorate work at John Hopkins as wells and continues his research there today.

He was named the Richard Starr Ross Research Scholar, he received the Richard D. Rowe Award for outstanding research in Pediatric Cardiology, the Young Investigator Award, Society for Pediatric Research, and the Antoine Marfan Award, from the National Marfan Foundation. Dr. Dietz also is a member of the Board of Governors, National Human Genome Research Institute, a member of the American Society for Pediatric Research and the American Society for Clinical Investigation.

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Researcher who identifed genetic cause and possible treatment for Marfan syndrome honored

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AKESOgen and London Genetics International Alliance to Enhance Drug Development Through Pharmacogenetics and Related ...