Archive for the ‘Gene Therapy Research’ Category

Public release date: 5-Sep-2013 [ | E-mail | Share ]

Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY -- Among a group of women with symptoms of angina who were tested for a suspected coronary blockage, nearly 3 times as many black women as white women died of heart disease. The study determined whether differences in the women's angina symptoms could affect the risk of death in these two groups, and the researchers report their findings in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

Jo-Ann Eastwood, PhD and a team of researchers from medical institutions across the U.S. found that for white women, the severity or type of anginal symptoms -- whether typical chest pain or more atypical symptoms such as stomach pain -- did not affect outcomes. However black women tended to have more atypical symptoms, a worse prognosis when diagnosed with heart disease, and a higher risk of related death.

In the article "Anginal Symptoms, Coronary Artery Disease, and Adverse Outcomes in Black and White Women: The NHLBI-Sponsored Women's Ischemia Syndrome Evaluation (WISE) Study," the authors conclude that these racial differences in symptom presentation for coronary artery disease may be a barrier to correct and timely diagnosis and an important contributor to poorer outcomes for black women.

"These results indicate that we need to raise awareness among women and their healthcare providers of racial differences in anginal symptom presentation in order to improve both diagnosis and outcomes," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

###

About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

Read this article:
Why do black women have a higher risk of death from heart disease than white women?

When it comes to carving out a future, figure skater Victoria Reynolds is keeping an open mind.

The 18-year-old Aspengrove graduate is heading to Vancouver Island University this fall, with plans to explore genetic engineering.

But dont expect this student to lock herself into any career path yet.

If there is one thing this athlete has learned in the rink, its the importance of being open to possibilities.

Reynolds discovered figure skating three years ago through a Nanaimo parks and recreation program.

She was the oldest person in the group and had more fear and reservations about hitting the ice than any of the other aspiring skaters. If that wasnt enough, most skaters her age outside the recreation program were much faster and skilled than she was, Reynolds said.

Its difficult starting out when you are older and watching a lot of the people your age being miles ahead of where you are, she said.

But with an open mind, discipline and determination, Reynolds opted to persevere in the sport. Any time she sees someone her age in the rink, it pushes her to be at a higher level, she said.

Reynolds plans to apply the same outlook on possibilities and hard work in her post-secondary school studies.

At the moment I am interested in genetics, but who knows if I will find something else I will enjoy? she asked, adding she hopes to get her bachelor of science. At the moment I am keeping everything open.

Visit link:
Best & Brightest: Victoria Reynolds, Aspengrove

Public release date: 5-Sep-2013 [ | E-mail | Share ]

Contact: Bill Schappert bschappert@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, September 4, 2013Despite tens of thousands of studies in the literature on the thyroid gland, thyroid hormone, and thyroid disease, lack of standardization in study design makes it difficult to compare the results and apply them to the development of improved diagnostic and treatment approaches. A new report from the American Thyroid Association's Taskforce on Approaches and Strategies to Investigate Thyroid Hormone Economy includes 70 specific recommendations and accompanying commentaries on a range of topics. The report is available free online on the Thyroid website. Thyroid, the peer-reviewed journal from Mary Ann Liebert, Inc., publishers, is the official journal of the American Thyroid Association (ATA).

Understanding the physiology of the thyroid gland and the activity of thyroid hormone in healthy individuals and in patients with disorders such as hypothyroidism, hyperthyroidism, and thyroid cancer is essential for developing new, more effective clinical practice and therapeutic strategies. Much knowledge is gained from studying thyroid tissue and thyroid hormone in animal and cell models.

Antonio C. Bianco, University of Miami Miller School of Medicine, and Chair of the ATA Taskforce, led a team of specialists in basic thyroid research in a review of the literature to identify which experimental practices would benefit from standardization. The panel of experts then defined consensus recommendations for how best to standardize study design and experimental approaches to achieve more reproducible results, in the "American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models."

"This is an outstanding and comprehensive guide for translational and basic research scientists that has filled an important gap in our thyroid research field," says Bryan R. Haugen, MD, President of the ATA and Professor of Medicine and Pathology, Head, Division of Endocrinology, Metabolism & Diabetes, Mary Rossick Kern and Jerome H. Kern Chair in Endocrine Neoplasms Research, University of Colorado School of Medicine. "Dr. Bianco and the entire Taskforce are to be commended for developing this authoritative and extremely useful reference."

"This is a unique compilation of detailed recommendations for performing experiments focusing on the pathophysiology of the thyroid using cell and animal models. It will guide numerous researchers how to best conduct these experiments and will lead to more standardized approaches in many laboratories worldwide," says Peter A. Kopp, MD, Editor-in-Chief of Thyroid and Associate Professor of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, and Interim Director of the Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago.

###

About the Society

The American Thyroid Association (ATA) is the leading organization devoted to thyroid biology and to the prevention and treatment of thyroid disease through excellence in research, clinical care, education, and public health. ATA is an international membership medical society with over 1,600 members from 43 countries around the world. Celebrating its 90th anniversary, ATA delivers its mission through several key endeavors: the publication of highly regarded monthly journalsThyroid, Clinical Thyroidology, and Clinical Thyroidology for Patients; annual scientific meetings; biennial clinical and research symposia; research grant programs for young investigators, support of online professional, public and patient educational programs; and the development of guidelines for clinical management of thyroid disease and thyroid cancer. The ATA has extensive online information on their website on thyroid disease and thyroid cancer for patients in both English and Spanish. The ATA website serves as the authoritative clinical resource for patients and the public who look for reliable information and physician referral on the Internet.

See the original post here:
New recommendations for standardizing studies of thyroid hormone and disease from ATA taskforce

Newswise PHILADELPHIA - Falling asleep in your bed at night and being put to sleep under general anesthesia as well as waking up in the morning or coming out of anesthesia arent quite the same thing, yet they share some important similarities. Max Kelz, MD, PhD, assistant professor of Anesthesiology and Critical Care at the Perelman School of Medicine at the University of Pennsylvania, along with colleagues from Penn, UCSD, Howard Hughes Medical Institute, and Thomas Jefferson University, explored the distinctions between anesthetic unconsciousness and sleep by manipulating the genetic pathways known to be involved in natural sleep and studying the resulting effects on anesthetic states. Their work will be published in PLOS Genetics.

Previous research by Kelzs team pointed to a neurological barrier, called neural inertia, that separates awareness from anesthetic unconsciousness and resists the transition from one state to the other. They also found that the processes by which the brain enters anesthesia and then later reemerges into consciousness are actually quite different -- one isnt simply the reverse of the other. With this knowledge in hand, Kelz and his colleagues used a Drosophila model system to focus on the genetic pathways controlling neural inertia. In this new study we sought to understand whether anesthetics were working on some of the natural systems that regulate normal sleep and wakefulness, says Kelz.

They found that four genes involved in natural sleep, Sh (Shaker), sss (sleepless), na, and unc79, also control neural inertia and thus the effects of induction and emergence of anesthetic unconsciousness. Various mutations in these four genes profoundly affect neural inertia and can even collapse it completely. For example, says Kelz, Mutations in the sleepless gene can cause some resistance to entering an anesthetic state, and an even larger impact on the exit from the anesthetic state. Flies with the sleepless mutation pop out of the anesthetic state at doses at which their normal siblings are still entering. When we moved sleepless around to different parts of the fly brain to figure out the circuits in which the gene works to alter wakefulness or the propensity to enter an anesthetic state, we found that we could completely dissociate the forward process of entering an anesthetic state from the reverse process of exiting.

This latest work confirms the existence of neural inertia as a state that naturally resists a change in the brains consciousness, similar to a phenomenon studied by sleep scientists. Sleep inertia is a phenomenon in which it can take minutes to hours before full cognitive power returns to us when we are abruptly awakened from natural sleep, Kelz explains. We modeled the idea [neural inertia] off the natural process of sleep inertia. Not much is known mechanistically about sleep inertia or why that happens, but here we see the anesthetics as a model potentially for helping to understand sleep inertia.

Aside from distinct differences between induction of and emergence from anesthesia, the work shows that the neural pathways involved can vary with different anesthetic drugs. The present study was largely conducted using isofluorane, a common general anesthetic, but there seem to be many neurological roads to anesthetically-induced unconsciousness, not all of which involve the same genes. The experimenters found that with a different drug, halothane, their Drosophila subjects reacted quite differently.

While Id like to say that theres one general set of neurons upon which anesthetic drugs work, its very clear that its not that simple, Kelz says. Individual anesthetic agents probably have distinct molecular targets and have differential effects on some of the underlying circuits that help maintain wakefulness. When we looked at halothane, we found is that the story of these four genes [Sh, sss, na, and unc79] doesnt explain halothanes action. So were really just scratching the surface in understanding a single anesthetic, isofluorane. Theres undoubtedly much more going on before we can start to speak about any anesthetic or a generic anesthetic.

Trying to identify just how well the analogy of sleep as a metaphor for anesthesia holds is important not just from a scientific standpoint, but also from a therapeutic one. There are some downsides to using existing anesthetic drugs, Kelz points out. If we understood the good features of the anesthetics, the ways in which they cause a loss of consciousness, and if we could replicate the desirable effects by specifically tuning the brains natural systems that regulate arousal, we might be able to avoid some of the undesirable actions of the anesthetic.

Such understanding could also benefit coma patients and those suffering from sleep disorders. We might be able to come up with strategies for helping to extract patients from vegetative states, or come up with some novel therapies or ideas to treat many of the issues that plague sleep medicine, Kelz says.

Other Penn authors include Eliot B. Friedman, MD, Hsiao-Tung Hung, Mallory Sowcik, and Amita Sehgal, PhD.

The study was funded by grants from the National Institutes of Health (R01 GM088156, R01 NS072431), the Howard Hughes Medical Institute, the University of Pennsylvania's Institute for Translational Medicine and Therapeutics, the Whitehall Foundation, the Harold Amos Medical Faculty Development Program from the R.W. Johnson Foundation, and the Perelman School of Medicine Department of Anesthesiology and Critical Care.

See original here:
Penn Medicine Researchers Pin Down the Genetics of Going Under

Public release date: 5-Sep-2013 [ | E-mail | Share ]

Contact: Dan Meyers dan.meyers@ucdenver.edu 303-724-7904 University of Colorado Denver

An international team of scientists, including University of Colorado School of Medicine and Children's Hospital Colorado researchers, has discovered a new disease related to an inability to process Vitamin B12.

The disorder is rare but can be devastating.

"Some people with rare inherited conditions cannot process vitamin B 12 properly," says CU researcher Tamim Shaikh, PhD, a geneticist and senior author of a paper about the new disease. "These individuals can end up having serious health problems, including developmental delay, epilepsy, anemia, stroke, psychosis and dementia."

The discovery is important because it could help doctors diagnose the disease and, eventually, could lead to prevention or treatment. But there is more to the story than that.

A 9-year-old Colorado boy named Max Watson, who because of his metabolic disease uses a computer to communicate, was the first patient in whom this discovery was made.

His older sister Abbey, 15, volunteered in the CU lab that helped achieve this medical breakthrough.

His parents cooperated with the study knowing that the results likely would not help their son but might help future patients.

The discovery, published today in The American Journal of Human Genetics, illustrates the complex and relatively new realm of medical discovery where researchers peer into the genetic make-up of patients to discern what went wrong to cause a disease.

Read the original:
Peering into genetic defects, CU scientists discover a new metabolic disease

Neurologist Prof Sam Berkovic and molecular geneticist Prof David Goldstein describe their work uncovering chance mutations that cause childhood epilepsy.

DYANI LEWIS I'm Dyani Lewis, thanks for joining us. The Human Genome Project, which published a completed sequence of our entire genetic code in 2003, introduced the world to large scale genomic sequencing efforts. Since then genome sequencing has become both faster and far more affordable. The result is that researchers and geneticists are now employing powerful sequencing strategies to investigate a great number of conditions, many for which a genetic cause has long been a mystery.

Epilepsy is one such condition and today on Up Close I am joined by two researchers who are using genomic sequencing technologies to identify the needle, or in this case the needles, in the haystack. They are looking for which genes out of the 20,500-odd genes in our genome are the faulty ones that cause epilepsy. My first guest today on Up Close is neurologist and epileptologist Professor Sam Berkovic. Sam is director of the Epilepsy Research Centre in Melbourne and Laureate Professor in the Department of Medicine at the University of Melbourne. Welcome to Up Close, Sam.

SAM BERKOVIC Thank you, Dyani.

DYANI LEWIS I'm also joined by Professor David Goldstein, Professor of Molecular Genetics and Microbiology, Professor of Biology and Director of the Centre for Human Genome Variation at Duke University. Welcome to Up Close, David.

DAVID GOLDSTEIN Thank you, it's good to be here.

DYANI LEWIS Sam, we refer to epilepsy as a single condition, but it's actually more correct to say epilepsies, isn't it?

SAM BERKOVIC That's absolutely right. The epilepsies signify a group of diseases where the sufferers have epileptic seizures and we've learned that far from being a single condition it's very heterogeneous, both from what we see as clinicians and even more so now that we're digging into their molecular bases.

DYANI LEWIS When you make a diagnosis of epilepsy, is it just on the basis of these seizures then?

SAM BERKOVIC The diagnosis is based on what the patient suffers, which are the epileptic seizures, but together we traditionally put together investigations, such as the electro-encephalogram, the recording of brainwaves, and also and very importantly brain imaging, where we get a picture of the structure of the brain, which sometimes gives us the answer to what caused the epilepsy. But more often than not it does not and that's particularly where genetics comes in.

Go here to read the rest:
Sequencing seizures: Discovering new genetic mutations behind epilepsy

Washington, Sept. 05 (ANI): A genetic factor that blocks the blood vessel inflammation that can lead to heart attacks, strokes and other potentially life-threatening events has been identified by a Indian origin researcher.

The breakthrough involving Kruppel-like factor (KLF) 15 is the latest in a string of discoveries from the laboratory of professor of medicine Mukesh K. Jain, MD, FAHA, that involves a remarkable genetic family.

School of Medicine instructor Yuan Lu, MD, a member of Jain's team and colleagues observed that KLF-15 blocks the function of a molecule called NF-kB, a dominant factor responsible for triggering inflammation.

"It had been suspected that smooth muscle cells were related to inflammation, but it hadn't been pinpointed and specifically linked to disease," Jain, Ellery Sedgwick Jr. Chair and director, Case Cardiovascular Research Institute at Case Western Reserve School of Medicine said.

He said that this work provides cogent evidence that smooth muscle cells can initiate inflammation and thereby promote the development of vascular disease.

Smooth muscle cells are only one of two major cell types within blood vessels walls. The other cell type, endothelium, has traditionally taken the blame for inflammation, but Jain's study suggests that both cells are critically important in the development of vascular disease.

The researchers learned that expression of this factor appeared mainly in smooth muscle cells and that levels were markedly reduced in atherosclerotic human blood vessels. To establish causality, the team generated genetically-modified mice where they deleted KLF-15 gene in smooth muscle cells.

The study is published in the Journal of Clinical Investigation. (ANI)

Read more:
Genetic factor responsible for triggering heart attacks identified

Genetics problems 1 (introduction)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

By: Suman Bhattacharjee

Originally posted here:
Genetics problems 1 (introduction) - Video

Genetics problems 6 (Codominance)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

By: Suman Bhattacharjee

Read more:
Genetics problems 6 (Codominance) - Video

Genetics problems 4 (incomplete dominance)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

By: Suman Bhattacharjee

Go here to see the original:
Genetics problems 4 (incomplete dominance) - Video

Genetics problems 7 (lethal gene)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

By: Suman Bhattacharjee

See more here:
Genetics problems 7 (lethal gene) - Video

(Courtesy photo) The myRisk Hereditary Cancer test is a multi-gene panel that analyzes 25 genes associated with eight major cancers, including gastric, pancreatic, prostate, colorectal (for colon and rectal cancers), endometrial, melanoma, ovarian and breast. It was developed by Myriad Genetics Inc. in Salt Lake City.

Health Analysis of 25 genes is more extensive than older tests but costs same.

Myriad Genetics Inc., has launched Thursday an all-in-one cancer test that is more extensive but costs the same as older tests.

The myRisk Hereditary Cancer test analyzes 25 genes associated with eight major cancers, including breast, gastric, pancreatic, prostate, colorectal (for colon and rectal cancers), endometrial, melanoma and ovarian. Before, Myriad had five cancer tests that analyzed a total of 11 genes.

"The tests have gone through extensive validation to assure there is a 100 percent accuracy of the test result," said Mark Capone, president of Myriad Genetics, which is headquartered at the University of Utahs Research Park in Salt Lake City. "If you get a positive test result and there is a mutation. . .there is a very high risk you could end up with one of these eight cancers."

Capone said that if a patient tests positive for a mutant form of one of the 25 genes, it could mean the person has a 20 to 87 percent increased chance of getting the cancer associated with that gene.

"Any one of these genes would significantly increase your risk for at least one of the eight cancers," he said. "So you would definitely want to immediately take some additional medical management as a result of that."

The myRisk Hereditary Cancer test will replace Myriads five older cancer panels or tests. One of those older tests was the BracAnalysis, a Myriad panel that analyzed a patient for a mutant form of the BRCA1 and BRCA2 genes, the same test that actress Angelina Jolie took to find out if she was at high risk for breast cancer. When the results were positive for the mutant gene, Jolie underwent a double mastectomy as a preventative measure.

The listed price for the myRisk Hereditary Cancer test is about $4,000, the same cost of one of the older tests. "The price for the 25-gene panel is the same as the price for the two-gene BracAnalysis product, so we have kept the price the same but significantly increased the amount of information," Capone said.

He added, however, that most out-of-pocket expenses for the test through insurance would be less than $100. More than 97 percent of insurance companies cover the test, he said.

Read the original:
Myriad Genetics launches improved test for breast, other cancers

Public release date: 5-Sep-2013 [ | E-mail | Share ]

Contact: John Fleischman jfleischman@ascb.org 513-706-0212 American Society for Cell Biology

BETHESDA, MD, SEPTEMBER 4, 2013--Behind the acronyms GSA + ASCB = LSE stands a new editorial partnership between the Genetics Society of America (GSA) and the American Society for Cell Biology (ASCB) to support the online journal, CBELife Sciences Education (LSE). Today, the two societies announced the joint editorial partnership in the latest issue of LSE. The journal was started by ASCB in 2002 as Cell Biology Education but changed its name to CBELife Sciences Education in 2006 to reflect the breadth of its coverage, which spans topics in education across all life science disciplines. GSA will become a full editorial partner, promoting the journal, soliciting manuscripts, and helping to defray, in part, the costs of operation while ASCB will remain the only publisher. The journal will have a joint editorial board drawn from scientists in both societies as well as from other disciplines. The current editor, Erin Dolan, PhD from the University of Georgia, will continue as LSE Editor-In-Chief.

In a joint editorial published yesterday in the new Fall 2013 issue of LSE, the executive directors of the two societies, Stefano Bertuzzi, PhD, for ASCB, and Adam P. Fagen, PhD, for GSA, say that the journal, which has become known for its data-driven analysis and evidence-based approach to improved teaching of the life sciences at all levels, has never been more important than in today's crisis atmosphere of plummeting budgets, workforce uncertainty, and lagging public knowledge about science. "From K-12 to secondary and higher education and lifelong learning, science education is in desperate need of data-driven reform, reinvestment, and reinvigoration," they write.

Fagen and Bertuzzi continue, "ASCB and GSA believe that there is neither time nor room for flag planting and parochialism. Rather than remaining only in our own silos, we will be more effective together, so we must join forces now."

Additionally, GSA will extend its science education outreach activities through a new peer-reviewed educational resource database ("GSA PREP") and a new educational feature series called "Primers" in its flagship journal GENETICS, aimed at bringing cutting-edge research into the classroom by making the latest "hot" scientific papers accessible to undergraduates and their instructors. The ASCB will still handle the production of LSE along with its flagship journal, Molecular Biology of the Cell. The ASCB's Education Committee and Minorities Affairs Committee run a variety of educational programs at the ASCB Annual Meeting and year round for science teachers and science students.

###

ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes GENETICS, a leading journal in the field since 1916, and G3: Genes|Genomes|Genetics, an open-access journal launched in 2011. For more information about GSA, please visit http://www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.

ABOUT ASCB: The American Society for Cell Biology (ASCB) is a professional society of basic biomedical researchers and represents about 9,000 scientists in the United States and over 60 countries around the world. The ASCB Annual Meeting, attended by about 8,000 scientists, is the world's largest scientific meeting in the field of cell biology. For more information about ASCB, please visit http://www.ascb.org. Also follow ASCB on Facebook at facebook.com/AmerSocCellBio and on Twitter @ASCBiology.

Link:
Genetics society and cell biologists partner for life sciences education journal

Public release date: 5-Sep-2013 [ | E-mail | Share ]

Contact: Elizabeth Ruedi eruedi@genetics-gsa.org 301-634-7371 Genetics Society of America

BETHESDA, MDToday, the Genetics Society of America (GSA) and the American Society for Cell Biology (ASCB) announced a joint editorial partnership for the journal CBELife Sciences Education (LSE). This partnership adds to GSA's continually expanding efforts to offer a wide array of educational resources and research to its members and the public. LSE is the premier journal for education research in the life sciences and is renowned for its data-driven analysis and evidence-based approach to pedagogical research. By combining forces, the two societies hope to give the journal even more exposure. Writing in a joint editorial published this week in LSE, the executive directors of the two societies, Stefano Bertuzzi, PhD (ASCB), and Adam Fagen, PhD (GSA), say that "ASCB and GSA believe that there is neither time nor room for flag planting and parochialism. Rather than remaining only in our own silos, we will be more effective together, so we must join forces now." Many members of GSA and ASCB are already actively involved with LSE, but with this official partnership the two societies hope that their "collective expertise and energy can have a significant impact on science education across campuses and national boundaries.

In 2002, ASCB began the journal as Cell Biology Education but changed its name to CBELife Sciences Education in 2006 to reflect the breadth of its coverage, which spans topics in education across all life science disciplines. GSA will become a full editorial partner, promoting the journal, soliciting manuscripts, and helping to defray, in part, the costs of operation while ASCB will remain the only publisher. The journal will have a joint editorial board drawn from scientists in both societies as well as from other disciplines. The current editor, Erin Dolan, PhD from the University of Georgia, will continue as LSE Editor-In-Chief.

Although the partnership is new, the two societies have a long-standing commitment to education. This partnership expands GSA's science education outreach activities, which include a new and growing Peer-Reviewed Educational resource Database "GSA PREP" and an educational feature series called "Primers" in its flagship journal GENETICS, which brings cutting-edge research into the classroom by making original scientific papers accessible to undergraduates and their instructors. GSA also provides a variety of educational programming at each of its scientific conferences, ranging from pedagogy workshops to an outreach program introducing local community college students to the process of scientific research and exchange. In addition to producing LSE, the ASCB's Education Committee and Minorities Affairs Committee run a variety of educational programs at the ASCB Annual Meeting and year round for science teachers and science students. ASCB is also strengthening its world-renowned iBiology video program, offers enhanced educational webinars year-round, and added a new professional development thread at its annual meeting.

"While several GSA members have served as editors of LSE," added Fagen, "our society is enthusiastic about the opportunity to join with ASCB and more formally engage the entire GSA community in the publication of a leading venue for the dissemination of original research that is improving teaching and learning in the life sciences."

###

ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes GENETICS, a leading journal in the field since 1916, and G3: Genes|Genomes|Genetics, an open-access journal launched in 2011. For more information about GSA, please visit http://www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.

ABOUT ASCB: The American Society for Cell Biology (ASCB) is a professional society of basic biomedical researchers and represents about 9,000 scientists in the United States and over 60 countries around the world. The ASCB Annual Meeting, attended by about 8,000 scientists, is the world's largest scientific meeting in the field of cell biology. For more information about ASCB, please visit http://www.ascb.org/. Also follow ASCB on Facebook at facebook.com/AmerSocCellBio and on Twitter @ASCBiology.

Read more:
Genetics Society of America joins editorial partnership for CBE-Life Sciences Education

RUTHERFORD, N.J., Sept. 5, 2013 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGIX), an emerging leader in DNA-based cancer diagnostics that personalizes the diagnosis and prediction of treatment outcomes for difficult to diagnose cancers, today announced a partial exercise of the over-allotment option granted to the underwriters to purchase an additional 105,000 shares of common stock at a price of $10.00 per share, bringing the total gross proceeds from the offering to $16,050,000, before underwriting discounts and commissions and other offering expenses payable by Cancer Genetics.

Aegis Capital Corp. acted as sole book-running manager for the offering.

Feltl and Company, Inc. acted as co-lead manager for the offering.

This offering was made only by means of a prospectus.

A copy of the prospectus relating to this offering may be obtained by contacting: Aegis Capital Corp., Prospectus Department, 810 Seventh Avenue, 18th Floor, New York, NY 10019, telephone: 212-813-1010, e-mail: prospectus@aegiscap.com.

A registration statement relating to these securities was declared effective by the Securities and Exchange Commission on August 13, 2013. This press release shall not constitute an offer to sell or a solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction.

About Cancer Genetics:

Cancer Genetics, Inc. is an emerging leader in DNA-based cancer diagnostics that personalizes the diagnosis and prediction of treatment outcomes for difficult to diagnose cancers. These cancers include hematological, urogenital and HPV-associated cancers. The Company's comprehensive range of oncology-focused tests and laboratory services provide critical genomic information to healthcare professionals, cancer centers, and biopharma companies. Through its CLIA certified and CAP accredited state-of-the-art reference lab, Cancer Genetics services some of the most prestigious medical institutions in the world and has strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please see http://www.cancergenetics.com.

Forward-Looking Statements:

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, future growth in research, technology, clinical development and potential opportunities for Cancer Genetics, Inc. products and services, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements. In addition, the offering is subject to market and other conditions and there can be no assurance as to the estimated proceeds from the offering and the anticipated use of proceeds from the offering. Any statements that are not historical fact (including, but not limited to, statements that contain words such as "will," "believes," "plans," "anticipates," "expects," "estimates") should also be considered to be forward-looking statements. Forward-looking statements involve risks and uncertainties, including, without limitation, risks inherent in the development and/or commercialization of potential products, uncertainty in the results of clinical trials or regulatory approvals, need and ability to obtain future capital, and maintenance of intellectual property rights and other risks discussed in the Company's Form 10-Q for the quarter ended June 30, 2013 and other filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. Cancer Genetics disclaims any obligation to update these forward-looking statements.

Here is the original post:
Cancer Genetics Announces Exercise of Underwriters' Over-Allotment Option

SALT LAKE CITY, Sept. 5, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that it has launched myRisk Hereditary Cancer, a new multi-gene diagnostic test that will provide increased sensitivity by analyzing 25 genes associated with eight major cancers including: breast, colorectal, ovarian, endometrial, pancreatic, prostate, gastric and melanoma.

"We are excited to launch myRisk Hereditary Cancer, which is a significant scientific advancement in hereditary cancer testing for a range of clinically-actionable cancers," said Mark Capone, president of Myriad Genetics Laboratories. "myRisk Hereditary Cancer will improve the quality of patient care by empowering healthcare providers with knowledge about their patients' risk of hereditary cancer and the appropriate medical management options available based on that risk."

myRisk Hereditary Cancer is being launched in a phased approach beginning with an early-access, clinical-experience program to a limited number of medical and scientific thought leaders followed by an expanded access program later in the year. The Company will present extensive clinical validity data for myRisk Hereditary Cancer at The Collaborative Group of the Americas on Inherited Colorectal Cancer (CGA) annual meeting in October and the San Antonio Breast Cancer Symposium in December.

The new myRisk Hereditary Cancer test represents the next generation of hereditary cancer testing and will provide healthcare providers with clear and actionable information to improve patient care, regardless of whether the patient receives a positive or negative test result. Each test report will include a genetic test result, a clinical risk and healthcare management tool based on professional society guidelines.

"Myriad is taking a stepwise, careful approach to responsibly gather clinical experience with the myRisk Hereditary Cancer test before fully launching this potentially revolutionary new diagnostic test for hereditary cancer," said Lee S. Schwartzberg, M.D., chief, Division of Hematology and Oncology at the University of Tennessee Health Science Center. "Myriad's unparalleled experience bolstered by extensive clinical research provides the reassurance healthcare providers require to utilize new methods of hereditary cancer testing. Also, the breadth of Myriad's new test report should empower medical professionals with the right information to facilitate better education and counselling for their patients."

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo and BRACAnalysis, myRisk, myRisk Hereditary Cancer, and Myriad Practice Advisor are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G

Safe Harbor Statement

This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the timing, scope and success of the initial and follow-on expanded access launch of myRisk Hereditary Cancer, the Company's new multi-gene diagnostic test to provide increased sensitivity by analyzing 25 genes associated with eight major cancers; the ability of myRisk Hereditary Cancer to improve the quality of patient care by empowering healthcare providers with knowledge about their patients' risk of hereditary cancer and the appropriate medical management options available based on that risk; the presentation of extensive clinical validity data for myRisk Hereditary Cancer at The Collaborative Group of the Americas on Inherited Colorectal Cancer (CGA) annual meeting in October and the San Antonio Breast Cancer Symposium in December; the actionable information resulting from myRisk Hereditary Cancer to improve patient care, regardless of whether the patient receives a positive or negative test result; the information provided in each test report, including a genetic test result, a personalized cancer risk, and healthcare management tool based on professional society guidelines; and the Company's strategic directives under the caption "About Myriad Genetics". These "forward-looking statements" are management's present expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those described in the forward-looking statements. These risks include, but are not limited to: the risk that sales and profit margins of our existing molecular diagnostic tests and companion diagnostic services may decline or will not continue to increase at historical rates; risks related to changes in the governmental or private insurers reimbursement levels for our tests; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and companion diagnostic services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and companion diagnostic services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and companion diagnostic services tests and any future tests are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities; risks related to public concern over our genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to increased competition and the development of new competing tests and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents; risks related to changes in intellectual property laws covering our molecular diagnostic tests and companion diagnostic services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decision in the lawsuit brought against us by the Association for Molecular Pathology et al; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

Read the original:
Myriad Genetics Launches myRisk(TM) Hereditary Cancer Panel

PHILADELPHIA A $1.5 million gift to the University of Pennsylvania has established the Barbara and Edward Netter Associate Professorship in Cancer Gene Therapy at the Abramson Cancer Center.Bruce Levine, PhD, a faculty member in the department of Pathology and Laboratory Medicine in the Perelman School of Medicine and the director of the Clinical Cell and Vaccine Production Facility, has been appointed to this new associate professorship.

Barbara Netter and her late husband, Penn alumnus Edward Netter (C53), have supported Penn since the early 1980s. Their contributions created the Netter Center for Community Partnerships on campus, and they have been longtime champions for research to advance gene therapy, having founded the Alliance for Cancer Gene Therapy in 2001 following the loss of their daughter-in-law to breast cancer. The foundation has provided funding to numerous Penn Medicine scientists, including the team Levine is part of, led by Carl June, MD, that has conducted trials demonstrating the first successful and sustained demonstration of the use of gene transfer therapy to turn the bodys own immune cells into weapons aimed at cancerous tumors. This new personal gift from Mrs. Netter will further this breakthrough research.

Dr. Levine is an alumnus of the University of Pennsylvania (C84), where he earned a bachelors degree in biology. He began his scientific career at the Wistar Institute during summers in high school and as an undergraduate at Penn, and in the division of Infectious Diseases at the Children's Hospital of Philadelphia examining immune responses following Varicella vaccination. Dr. Levine received his PhD in Immunology and Infectious Diseases from the Johns Hopkins University in 1992, and served as a post-doctoral fellow with Dr. Carl June at the Naval Medical Research Institute in Bethesda, MD, and later as an Investigator at NMRI and a Research Assistant Professor of Medicine at the Uniformed Services University for the Health Sciences. He joined returned to Philadelphia to join the Penn Medicine faculty in 1999. The Clinical Cell and Vaccine Production Facility at the Hospital of the University of Pennsylvania, which Dr. Levine directs, is charged with developing, manufacturing, and testing novel cell, gene, and biologic therapies being investigated in clinical trials at Penn, the Childrens Hospital of Philadelphia, and collaborating institutions.

This appointment and professorship establishment will be celebrated by Penn Medicine in January 2014.

###

Penn Medicine is 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 the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University 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 to U.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.

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.

Follow this link:
$1.5 Million Gift To Penn Medicine Establishes Associate Professorship In Cancer Gene Therapy

5 September 2013 Last updated at 13:15 ET

Please turn on JavaScript. Media requires JavaScript to play.

Carol Gedda: 'It could improve the heart muscle. I'm really pleased to be part of it.'

It is 18 months since Carol Gedda suffered a massive heart attack. It left her with just 20% of her heart functioning.

"I have a lot of trouble with stairs, and sometimes I can even run out of breath in a conversation", says Mrs Gedda, who is 65.

She is one of at least 750,000 people in the UK with heart failure. It occurs when the heart is damaged and becomes unable to pump blood adequately.

There are treatments for the condition but nothing so far that can reverse the damage.

Mrs Gedda, from Essex, is among 200 patients being enrolled on a gene therapy trial to test whether introducing genetic material into damaged heart cells can improve their function.

Researchers at Imperial College London found that levels of the protein SERCA2a are lower in patients with heart failure.

Royal Brompton Hospital in London, where Mrs Gedda is being treated, is one of only two British centres taking part in the international study, The Golden Jubilee National Hospital in Glasgow is also involved.

See more here:
Heart gene therapy trial begins

In 1980, though, he opened up the journal Science and suddenly understood how doctors might someday cure Lesch-Nyhan, along with thousands of other genetic disorders that had once seemed incurable. Two Stanford biologists, Richard Mulligan and Paul Berg, had figured out a way to transplant genes into cells, effectively rewriting their DNA. The phrase gene therapy had been floating around medical circles for decades, but Wilson realized that its time had come. As soon as he finished his degrees, he and his wife moved to Boston so he could learn about gene transplantation from Mulligan, now at MIT. After nearly three years under Mulligans tutelage, he headed back to Michigan to set up his own lab.

The first disease that Wilson targeted was called familial hypercholesterolemia, in which the patient lacks the gene that produces receptors for grabbing bad cholesterol, or LDL, from the blood, which the liver normally filters out. Vessels become so badly clogged that many sufferers have heart attacks in their forties and fifties, and sometimes even before age 30.

Wilson figured out how to make a vector to attack the conditiona virus with a working version of the gene loaded on it. He first tested it on a type of rabbit genetically prone to high levels of LDL, and the gene therapy lowered those levels considerably. For a human trial in 1992, he and his colleagues chose a 28-year-old woman from Canada. Surgeons removed part of her liver, and then Wilson and his colleagues infected its cells with the virus, which delivered a working version of the defective gene. Finally, Wilson and his colleagues injected those cells back into the womans liver, where they took hold and grew. The womans LDL levels dropped by 23 percent.

The result, published in 1994, was a milestone in the young field. Gene Experiment to Reverse Inherited Disease is Working, The New York Times reported, noting that Wilsons paper was the first to report any therapeutic benefits of human gene therapy. Thanks to this study and others, the FDA gave the green light to more clinical trials every year, jumping from zero in 1989 to 91 in 1999. Universities set up gene therapy programs to stake a claim in the new field.

One of those was the Institute for Human Gene Therapy at the University of Pennsylvania. At age 38, Wilson became the institutes head, overseeing a staff that soon grew to more than 200. They launched new clinical trials, including a sequel to Wilsons study on familial hypercholesterolemia and on another genetic disorder in the liver: OTCD. Wilson now wanted to take the surgery out of gene therapy, so he and his colleagues searched the scientific literature for a virus that could seek out liver cells in the body.

They settled on a virus known as an adenovirus. Adenoviruses are best known for causing the common cold, but other scientists had found that they were very good at delivering genes into cells. Everything seemed to be moving forward nicelyuntil Jesse Gelsinger checked into Childrens Hospital of Philadelphia.

More here:
A Man and His Virus: Gene Therapy Emerges From Disgrace to Be the Next Big Thing, Again

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/l9rw32/gene_therapy_in) has announced the addition of the "Gene Therapy in Oncology Drug Pipeline Update 2013" report to their offering.

There are today 120 companies plus partners developing 108 gene therapy drugs in 263 developmental projects in cancer. In addition, there are 4 suspended drugs and the accumulated number of ceased drugs over the last years amount to another 96 drugs. Gene Therapy In Oncology Drug Pipeline Update lists all drugs and gives you a progress analysis on each one of them. Identified drugs are linked to 102 different targets. All included targets have been cross-referenced for the presence of mutations associated with human cancer. To date 92 out of the 92 studied drug targets so far have been recorded with somatic mutations. The software application lets you narrow in on these mutations and links out to the mutational analysis for each of the drug targets for detailed information. All drugs targets are further categorized on in the software application by 44 classifications of molecular function and with pathway referrals to BioCarta, KEGG, NCI-Nature and NetPath.

Reasons To Buy

- Show investors/board/management that you are right on top of drug development progress in your therapeutic area.

- Find competitors, collaborations partners, M&A candidates etc.

- Jump start competitive drug intelligence operations

- Excellent starting point for world wide benchmarking

- Compare portfolio and therapy focus with your peers

- Speed up pro-active in-/out licensing strategy work

Originally posted here:
Research and Markets: Gene Therapy in Oncology Drug Pipeline Update 2013

MOUNTAIN VIEW, Calif., Sept. 4, 2013 /PRNewswire/ -- SanBio Inc. today announced the successful completion of enrollment of patients in its Phase 1/2 clinical trial testing the safety and efficacy of a novel allogeneic cell therapy product, SB623, in patients suffering from chronic deficits resulting from previous stroke injuries. A total of 18 patients have been successfully administered SB623. The trial is being conducted at Stanford University and the University of Pittsburgh. No safety concerns have been attributed to the cell therapy product. For details regarding this clinical trial, please refer to http://www.clinicaltrials.gov/ct2/show/NCT01287936.

SB623 is derived from bone marrow and has shown safety and efficacy in rodent models of chronic stroke. "Complete enrollment of this clinical trial is a major step in the development of SB623 for stroke patients. Planning for the next phase of testing is already underway." said Keita Mori, SanBio CEO.

SB623 is being delivered to the damaged region of the brains of patients who have suffered an ischemic stroke. Product safety is the primary focus of the study but various measurements of efficacy are also being tested.

"Stroke is the major cause of disability in the United States. Regenerative medicine offers hope to those with otherwise permanent functional limitations. This trial represents an important advance in bringing restorative therapeutics for neurologic disorders into the clinical arena. Three measures of efficacy (NIHSS, ESS, Fugl-Meyer) all show a trend toward improvement. We are looking forward to the next clinical trial," said Dr. Gary K. Steinberg, M.D., Ph.D., Bernard and Ronni Lacroute-William Randolph Hearst Professor of Neurosurgery and the Neurosciences, Director, Stanford Institute for Neuro-Innovation and Translational Neurosciences, Chairman, Department of Neurosurgery, Stanford University School of Medicine.

Dr. Steinberg will be presenting preliminary results from this clinical trial at the International Stroke Conference February 12-14 in San Diego, California.

"Completion of this study is an important milestone in development of cell therapy treatment for chronic stroke. The demonstration of safety and feasibility is encouraging and we look forward to further trials using these cells," said Dr. Lawrence R. Wechsler, M.D., Henry B. Higman Professor and Chair, Department of Neurology, University of Pittsburgh Medical School

"The SanBio trial was completed smoothly and will help to guide important research into stroke repair and regenerative medicine strategies. It is hoped that the next study can begin soon and advance patient care," said Dr. Douglas Kondziolka, MD, MSc ,FRCSC, FACS,Professor of Neurosurgery, Vice-Chair, Clinical Research (Neurosurgery), Professor of Radiation Oncology, Director, Center for Advanced Radiosurgery, NYU Langone Medical Center.

About SB623: SB623 is a proprietary allogeneic cell therapy product consisting of cells derived from bone marrow. SB623 is administered adjacent to the area damaged by stroke and functions by producing proteins that aid the regenerative process.

About SanBio: SanBio is a privately held San Francisco Bay Area biotechnology company focused on the discovery and development of new regenerative cell therapy products.

For more information: http://www.san-bio.com

Go here to read the rest:
SanBio Announces The Completion Of Enrollment Of Its Clinical Trial Of Cell Therapy For Chronic Stroke Deficits

A genetic mutation that can lead to haemorrhagic stroke has been identified by scientists along with a drug to potentially treat it.

Research published in the journal Human Molecular Genetics highlights a mutation in the gene COL4a2 that causes bleeding in the brain.

COL4a2 is a protein that is expressed by the gene of the same name, which forms a structure outside the cell called a basement membrane. This membrane is present in many tissues including blood vessels. Mutations in this protein have been expected to cause disease due to structural defects in those membranes.

However, scientists have now identified for the first time that accumulation of the mutant protein inside the cell can influence the development of haemorrhagic stroke.

Importantly, however, the scientists were able to treat the disease in cells grown in a culture dish by using a drug which has been approved for human patients. These results highlight its potential future therapeutic use for stroke.

Dr Tom Van Agtmel of the Institute of Cardiovascular and Medical Sciences at the University of Glasgow who led the study, said: Haemorrhagic stroke accounts for half of all stroke cases in children and currently there is no treatment.

Although it is expected that only a small number of patients will have defects in this membrane, this research gives us a better understanding of how this type of stroke develops. Importantly, it has identified how we might treat it in some cases. However, this is just one genetic mutation weve identified and analysed so there is still a long way to go, but its a start.

The researchers obtained their results by analysing skin biopsies from a father a son with a family history of porencephaly a cavity in the brain caused by perinatal haemorrhagic bleeding which can result in seizures and paralysis.

Both father and son carried the genetic mutation but only the son displayed the accumulation of the mutant protein inside the cell.

Dr Van Agtmael added: The next stage will be to see if the drug treatment works in an animal model. If it does then this is a first step towards investigating its potential in human patients with this type of stroke using the pre-existing, approved drug.

Original post:
Stroke-causing mutant gene identified by scientists

Scientists have discovered a gene in mice that could help protect against ovarian cancer.

The gene, known as Helq, repairs damage to DNA, which occurs when it is copied as cells multiply. If the gene is missing or faulty, it could increase the chance of developing the disease, according to research published in Nature.

Mice without either of the two copies of the Helq gene were twice has likely to develop ovarian tumours, the team from Cancer Research UKs London Research Institute found.

Our findings show that if there are problems with the Helq gene in mice it increases the chance of them developing ovarian and other tumours, Dr Simon Boulton, the studys senior author said.

This is an exciting finding because this might also be true for women with errors in Helq, and the next step will be to see if this is the case.

If it plays a similar role in humans, this may open up the possibility that, in the future, women could be screened for errors in the Helq gene that might increase their risk of ovarian cancer.

In the UK around 7,000 women are diagnosed with ovarian cancer each year and around 4,300 die from the disease.

See the original post:
Scientists discover gene that could help protect against ovarian cancer

Sep. 4, 2013 Obesity gene testing does not put people off weight loss and may help to reduce self-blame, according to a new study by researchers from the Health Behaviour Research Centre at UCL (University College London).

Previous studies have shown that genes play a role in a person's risk of becoming overweight. One gene, called FTO, has been found to have the biggest influence so far.

FTO has two variants, one associated with greater risk of weight gain (A) and one associated with lower risk (T). One in two people carries at least one copy of the A variant. People who inherit two A variants (one from their mother and one from their father) are 70% more likely to become obese than those with two T variants. Even those who inherit one have a higher weight than those with two T variants.

Researchers can now use a gene test for FTO (although this is not yet commercially available). However, it was not known how people would react to finding out the results of the genetic test.

Some clinicians thought it would help people to become motivated to manage their weight. Others thought that the 'genes as destiny' perspective might mean people felt there was nothing they could do about their weight. If people responded fatalistically it could be harmful because diet and exercise are still very important for health and weight control, perhaps even more so if a person is 'battling against their biology'.

UCL's Professor Jane Wardle and Susanne Meisel decided to test a small number of volunteers (18) for their FTO status and interview them about their experience. The sample of volunteers included men and women, who spanned the weight range from underweight to obese.

They found that the volunteers were very enthusiastic about receiving their genetic test result. Those who struggled with their weight said that the genetic test result was helpful because it removed some of the emotional stress attached to weight control and relieved some of the stigma and self-blame

No one reported a negative reaction to the genetic test result, or said it made them feel there was nothing they could do to about their weight.

Susanne Meisel, who led the study said: "These results are encouraging. Regardless of gene status or weight, all the volunteers recognised that both genes and behaviour are important for weight control. The results indicate that people are unlikely to believe that genes are destiny and stop engaging with weight control once they know their FTO status. Although they knew that FTO's effect is only small, they found it motivating and informative. We are now doing a larger study to confirm whether more people react in the same way."

Dr Laura McGowan, Executive Director of the charity Weight Concern added: "The causes of obesity are multiple and complex, and this research is encouraging for those who struggle with their weight. Although we know genetics play a part in weight, people can learn strategies to deal with this increased risk for weight gain, so finding out you carry the high-risk version of the gene shouldn't mean you surrender to fate."

Continued here:
Psychological effects of genetic testing for risk of weight gain

4 September 2013 Last updated at 14:19 ET

UK scientists have found a gene in mice that, if faulty, may increase the risk of ovarian cancer.

Mice lacking the gene were twice as likely to develop ovarian tumours, as well as showing signs of infertility, according to a new study.

If the gene has a similar role in humans, it could lead to new screening tests, say scientists at the London Research Institute, Cancer Research UK.

The research is published in the journal Nature.

The study looked at a gene known as Helq, which is involved in repairing damaged DNA.

Mice lacking the gene were twice as likely to develop ovarian tumours compared with those with a normal copy.

Ovarian cancer can be hard to diagnose early and treat successfully so the more we know about the causes of the disease, the better equipped we will be to detect and treat it

Dr Simon Boulton, senior author from Cancer Research UK's London Research Institute, said: "Our findings show that if there are problems with the Helq gene in mice it increases the chance of them developing ovarian and other tumours.

"This is an exciting finding because this might also be true for women with errors in Helq, and the next step will be to see if this is the case.

Read more here:
New gene clue to ovarian cancer