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Researchers at Yale School of Medicine have, for the first time, described the genetic basis of endometriosis, a condition affecting millions of women that is marked by chronic pelvic pain and infertility. The researchers' discovery of a new gene mutation provides hope for new screening methods.

Published in the Feb. 3 early online issue of EMBO Molecular Medicine, the study explored an inherited mutation located in part of the KRAS gene, which leads to abnormal endometrial growth and endometrial risk. In endometriosis, uterine tissue grows in other parts of the body, such as the abdominal cavity, ovaries, vagina, and cervix. The condition is often hereditary and is found in 5%-15% of women of reproductive age, affecting over 70 million women worldwide.

Although the disorder has been studied for many years, its exact cause and how it develops remained unclear. It was previously shown that activating the KRAS gene caused mice to develop endometriosis. However, no mutations in this gene have been identified in women with endometriosis.

Led by senior author Hugh S. Taylor, M.D., professor and chief of the Division of Reproductive Endocrinology and Infertility in the Department of Obstetrics, Gynecology & Reproductive Sciences, the authors studied 132 women with endometriosis and evaluated them for a newly identified mutation in the region of the KRAS gene responsible for regulation. This mutation was previously linked to an increased risk of lung and ovarian cancer by study co-author Joanne Weidhaas, M.D., assistant professor of therapeutic radiology.

“We found that 31% of the women with endometriosis in the study carried this mutation, compared to only 5.8% of the general population,” said Taylor. “The presence of this mutation was also linked to higher KRAS protein levels and associated with an increased capacity for these cells to spread. It also may explain the higher risk of ovarian cancer in women who have had endometriosis.”

The Yale team is the first to identify a cause of this common and previously little understood disease. “This mutation potentially represents a new therapeutic target for endometriosis as well as a basis of potential screening methods to determine who is at risk for developing endometriosis,” said Taylor.

Source: Yale University

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Researchers describe genetic basis of endometriosis

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Life Technologies this week named Alan Sachs as head of global research and development and Ronnie Andrews as president of medical sciences.

Sachs was previously the vice president of exploratory and translational sciences for Merck Research Laboratories, where he spent 10 years in various leadership roles, Life Tech said. Prior to that Sachs served an associate professor of biochemistry and molecular biology at the University of California, Berkeley, and as a Whitehead fellow at the Whitehead Institute for Biomedical Research.

Andrews joins Life Tech from GE Molecular Diagnostics, where he served as a segment leader following GE's 2010 acquisition of Clarient, where Andrews was CEO. Andrews has also held executive positions with Abbott Diagnostics, Roche Diagnostics, and Immucor.

Stephen O'Brien has left the National Cancer Institute's Laboratory of Genomic Diversity after 25 years to help launch a genome bioinformatics program at St. Petersburg University in Russia. O'Brien received a $5 million grant from the Russian Ministry of Education and Science last year under a program that aims to lure big-name researchers to Russia. Over the coming three years, O'Brien will spend at least four months per year in Russia working at the center, which is scheduled to open in May.

Saladax Biomedical said today that President and CEO Edward Erickson has resigned due to personal and family reasons, and that he will be replaced by Kevin Harter on an interim basis. Erickson will remain a member of the company's board of directors. Harter is a co-founder and senior VP of the Life Sciences Greenhouse, and he has served as executive chairman at Saladax.

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'ROCK' off: Study establishes molecular link between genetic defect and heart malformation

By Claire Bates

Last updated at 9:19 AM on 6th February 2012

A single genetic mutation can double your risk of stroke, according to a new study.

Researchers found the gene variant increased the risk of large artery ischemic strokes, which account for over a third of all cases.

The discovery may lead to screening tests to identify those at risk along with earlier treatments and could potentially save thousands of lives.

Impact: Around 110,000 people in England have a stroke every year, while 300,000 people are living with resulting disabilities

Stroke is the second leading cause of death worldwide and a major cause of chronic disability in developed countries. The condition costs the NHS ?2.8billion a year.

One of the most common types is when blood flow is impaired because of a blockage to one or more of the large arteries supplying blood to the brain, known as large artery ischemic stroke.

Researchers from St George's, University of London and Oxford University compared the genetic make-up of 10,000 people who had suffered from a stroke with 40,000 healthy individuals. The study was funded by the Wellcome Trust.

They found that an alteration in a gene called HDAC9 occurs on about 10 per cent of human chromosomes. Those people who carry two copies of the variant (one inherited from each parent) have nearly twice the risk for this type of stroke compared to those with no copies of the variant. 

The protein produced by HDAC9 is already known to play a role in the formation of muscle tissue and heart development. However, the exact mechanism by which the genetic variant increases the risk of stroke is not yet known.

Professor Hugh Markus, from St George's, University of London, who co-led the study says: 'This discovery identifies a completely new mechanism for causing stroke. The next step is to determine in more detail the relationship between HDAC9 and stroke and see whether we can develop new treatments that reduce the risk of stroke.

'Interestingly, there are already drugs available which inhibit the HDAC9 protein. However, it is important that we understand the mechanism involved before trialling the effects of these drugs on stroke.'

The researchers went on to show that the new variant does not have the same effect on the risk of other types of stroke which include bleeding in the brain.

Professor Peter Donnelly, Director of the Wellcome Trust Centre for Human Genetics in the University of Oxford, who co-led the study, says: 'This is really fascinating, and if it holds up more generally, will move us closer to personalised medicine, where treatments and preventions can be tailored more precisely to individual patients.'

The study was published online in Nature Genetics today.

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Single genetic mutation can double your risk of stroke – but scientists hope it could lead to tailored treatments

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Genetic variant increases risk of common type stroke

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London, Feb 6 (ANI): Scientists have now identified a genetic variant that increases the risk of a common type of stroke.

This is one of the few genetic variants to date to be associated with risk of stroke and the discovery opens up new possibilities for treatment.

Several different mechanisms underlie strokes. One of the most common types is when blood flow is impaired because of a blockage to one or more of the large arteries supplying blood to the brain – large artery ischemic stroke. This accounts for over a third of all strokes.

Researchers from St George's, University of London and Oxford University, working with scientists from Europe, America and Australia, in one of the largest genetic studies of stroke to date, compared the genetic make-up of 10,000 people who had suffered from a stroke with 40,000 healthy individuals.

The researchers discovered an alteration in a gene called HDAC9, which affects a person's risk of large artery ischemic stroke. This variant occurs on about 10 per cent of human chromosomes.

Those people who carry two copies of the variant (one inherited from each parent) have nearly twice the risk for this type of stroke compared to those with no copies of the variant.

The protein produced by HDAC9 is already known to play a role in the formation of muscle tissue and heart development. However, the exact mechanism by which the genetic variant increases the risk of stroke is not yet known.

A better understanding of the mechanism could lead to new drugs to treat or prevent stroke; however, the researchers stress that this is still some way off.

“This discovery identifies a completely new mechanism for causing stroke,” Professor Hugh Markus, from St George's, University of London, who co-led the study, said.

“The next step is to determine in more detail the relationship between HDAC9 and stroke and see whether we can develop new treatments that reduce the risk of stroke.

“Interestingly, there are already drugs available which inhibit the HDAC9 protein. However, it is important that we understand the mechanism involved before trialling the effects of these drugs on stroke.”

The researchers went on to show that the new variant does not have the same effect on the risk of other types of stroke, which include bleeding in the brain (haemorrhagic stroke).

“Our study shows that the different subtypes of stroke could involve quite different genetic mechanisms,” Professor Peter Donnelly, Director of the Wellcome Trust Centre for Human Genetics in the University of Oxford, who co-led the study, said.

“This is really fascinating, and if it holds up more generally, will move us closer to personalised medicine, where treatments and preventions can be tailored more precisely to individual patients.”

According to Dr Peter Coleman, Deputy Director of Research at The Stroke Association, who funded collection of some of the samples used in this study, over a third of strokes are caused due to a blockage in one of the large blood vessels supplying blood to the brain (large artery stroke).

“Findings from this ground breaking study appear to show a genetic link which may affect a person's risk of large vessel stroke,” Dr Coleman said.

“Further study is needed, but this research could potentially lead to new methods of screening and prevention for large vessel stroke, and ultimately, new methods of treatment,” Dr Coleman added.

The study has been recently published online in Nature Genetics. (ANI)

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SAN DIEGO, Feb. 2, 2012 /PRNewswire/ — Sequenom, Inc. (NASDAQ: SQNM – News), a life sciences company providing innovative genetic analysis solutions, today announced that a new publication of an independent multi-center study on Sequenom Center for Molecular Medicine's MaterniT21™ laboratory-developed test (LDT) appears today in the online issue of Genetics in Medicine. The study demonstrated the LDT can detect fetal trisomy 21, 18 and 13 with high accuracy from a maternal blood sample and will be published in the March issue. The full results of the study can be found online at http://journals.lww.com/geneticsinmedicine/.

“Together with the previously published results on the test's ability to detect trisomy 21 with high accuracy, this publication provides further evidence that this valuable non-invasive technology can identify nearly all cases of T18 and T13, as well as T21, at a low false positive rate,” said Harry F. Hixson, Jr., Ph.D., Chairman and CEO, Sequenom, Inc. “This research continues to validate the use of our MaterniT21 LDT as a valuable tool in the care of pregnant women who are at high risk for fetal aneuploidy.”  

The published results represent a large international, multi-center study conducted at 27 prenatal diagnostic centers. Participating sites collected and processed maternal plasma samples from 4,664 pregnant women at high risk for fetal aneuploidy undergoing diagnostic testing in the late first and early second trimester. The results of a blinded testing of 212 pregnancies with trisomy 21 and their 1,484 matched controls were previously published in Genetics in Medicine. During that same testing period, blinded samples from pregnancies with trisomy 18 and trisomy 13 and their controls were also tested. Inclusion criteria were the same as for the earlier study of trisomy 21. 

A total of sixty-two trisomy 18 and twelve trisomy 13 pregnancies along with their matched controls (including the trisomy 21 cases and matched controls) were tested using the MaterniT21 LDT. When unblinded, the detection rate for trisomy 18 was 100 percent and for trisomy 13, was 91.7 percent, with false positive rates of 0.28 and 0.97 percent, respectively. 

The research was led by Jacob Canick, PhD, and Glenn Palomaki, PhD, of the Division of Medical Screening and Special Testing in the Department of Pathology and Laboratory Medicine at Women & Infants Hospital and The Warren Alpert Medical School of Brown University, and included scientists at Sequenom Center for Molecular Medicine, San Diego, CA, and an independent academic laboratory at the University of California at Los Angeles. The MaterniT21 test is available exclusively through Sequenom CMM as a testing service to physicians.

An estimated 1,330 cases of trisomy 18 and 600 cases of trisomy 13 are expected at term among the estimated 4.25 million pregnancies in the United States each year.

About Sequenom

Sequenom, Inc. (NASDAQ: SQNM – News) is a life sciences company committed to improving healthcare through revolutionary genetic analysis solutions. Sequenom develops innovative technology, products and diagnostic tests that target and serve discovery and clinical research, and molecular diagnostics markets. The company was founded in 1994 and is headquartered in San Diego, California. Sequenom maintains a Web site at http://www.sequenom.com to which Sequenom regularly posts copies of its press releases as well as additional information about Sequenom. Interested persons can subscribe on the Sequenom Web site to email alerts or RSS feeds that are sent automatically when Sequenom issues press releases, files its reports with the Securities and Exchange Commission or posts certain other information to the Web site.

About Sequenom CMM

Sequenom Center for Molecular Medicine® (Sequenom CMM), a CAP accredited and CLIA-certified molecular diagnostics laboratory, is developing a broad range of diagnostics with a focus on prenatal diseases and conditions. These laboratory-developed tests provide beneficial patient management options for obstetricians, geneticists and maternal fetal medicine specialists. Sequenom CMM is changing the landscape in genetic disorder diagnostics using proprietary cutting edge technologies.

Forward-Looking Statement

Except for the historical information contained herein, the matters set forth in this press release, including statements regarding the use of the MaterniT21 test as a valuable tool in the care of pregnant women, expectations regarding the future performance, utility, and impact of the test, the Company's commitment to improving healthcare through revolutionary genetic analysis solutions, and Sequenom CMM changing the landscape in genetic disorder diagnostics, are forward-looking statements within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially, including the risks and uncertainties associated with market demand for and acceptance and use by customers of new tests such as the MaterniT21 LDT, reliance upon the collaborative efforts of other parties, the Company's financial position, its ability to position itself for product launches and growth and develop and commercialize new technologies and products, particularly new technologies such as noninvasive prenatal diagnostics, laboratory developed tests, and genetic analysis platforms, the Company's ability to manage its existing cash resources or raise additional cash resources, competition, intellectual property protection and intellectual property rights of others, government regulation particularly with respect to diagnostic products and laboratory developed tests, obtaining or maintaining regulatory approvals, litigation involving the Company, and other risks detailed from time to time in the Company's most recently filed Quarterly Report on Form 10-Q and Annual Report on Form 10-K for the year ended December 31, 2010, and other documents subsequently filed with or furnished to the Securities and Exchange Commission. These forward-looking statements are based on current information that may change and you are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. All forward-looking statements are qualified in their entirety by this cautionary statement, and the Company undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

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