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Minecraft Mod Reviews! | Advanced Genetics - Cool Abilities! Part 1/2
Open Our Website: http://yngmain20.wix.com/yngnetwork Today #39;s mod is called Advanced Genetics by Team Gene, it #39;s a REALLY cool mod that allows you to extra...

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Newswise WASHINGTON (Feb. 20, 2014) After a heart attack, there is often permanent damage to a portion of the heart. This happens, in part, because cardiac muscle cells are terminally differentiated and cannot proliferate after blood flow is blocked off to the heart. This partial healing can be attributed to heart disease being one of the leading causes of death. What if the cells could be stimulated to divide and the heart could be induced to repair itself? This was the question posed by George Washington University (GW) researcher Scott Shapiro, M.D., Ph.D., and his co-authors, who found that cardiac regeneration may be a possibility with gene therapy.

The research, published yesterday in Science Translational Medicine, found that gene therapy can elicit a regenerative response in pig hearts. Shapiro and his research team first looked to small animals such as the zebrafish, which are able to regenerate heart tissue after a heart attack. This animal has a key protein at play, Cyclin A2 (Ccna2).

After seeing the effects of CCna2 in small animals, we began looking at the effects of the gene in larger animals, such as pigs, said Shapiro, assistant professor of medicine at the GW School of Medicine and Health Sciences. We delivered Ccna2 directly into the heart and found that pigs not only had improved cardiac function, but also found evidence of cellular regeneration.

Ccna2 is a prenatal gene normally turned off in humans after birth. Shapiro believes using gene therapy as a tool for cardiac regeneration, optimized for humans, could lead to a viable treatment option for patients who suffer from myocardial infarction, or heart attack.

The study, titled Cyclin A2 Induces Cardiac Regeneration After Myocardial Infarction Through Cytokinesis of Adult Cardiomyocytes, is available at http://stm.sciencemag.org/content/6/224/224ra27.short.

Additional authors of the study include researchers from the Cardiovascular Institute at the Mount Sinai School of Medicine, the Centro Nacional de Investigaciones Cardiovasculares at the Hospital Universitario La Paz, and the Division of Cardiology at the Albert Einstein College of Medicine.

Media: To interview Dr. Shapiro about this study, please contact Lisa Anderson at lisama2@gwu.edu or 202-994-3121.

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Researcher Finds Gene Therapy a Promising Tool for Cardiac Regeneration

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20-Feb-2014

Contact: Lisa Anderson lisama2@gwu.edu 202-994-3121 George Washington University

WASHINGTON (Feb. 20, 2014) After a heart attack, there is often permanent damage to a portion of the heart. This happens, in part, because cardiac muscle cells are terminally differentiated and cannot proliferate after blood flow is blocked off to the heart. This partial healing can be attributed to heart disease being one of the leading causes of death. What if the cells could be stimulated to divide and the heart could be induced to repair itself? This was the question posed by George Washington University (GW) researcher Scott Shapiro, M.D., Ph.D., and his co-authors, who found that cardiac regeneration may be a possibility with gene therapy.

The research, published yesterday in Science Translational Medicine, found that gene therapy can elicit a regenerative response in pig hearts. Shapiro and his research team first looked to small animals such as the zebrafish, which are able to regenerate heart tissue after a heart attack. This animal has a key protein at play, Cyclin A2 (Ccna2).

"After seeing the effects of CCna2 in small animals, we began looking at the effects of the gene in larger animals, such as pigs," said Shapiro, assistant professor of medicine at the GW School of Medicine and Health Sciences. "We delivered Ccna2 directly into the heart and found that pigs not only had improved cardiac function, but also found evidence of cellular regeneration."

Ccna2 is a prenatal gene normally turned off in humans after birth. Shapiro believes using gene therapy as a tool for cardiac regeneration, optimized for humans, could lead to a viable treatment option for patients who suffer from myocardial infarction, or heart attack.

###

The study, titled "Cyclin A2 Induces Cardiac Regeneration After Myocardial Infarction Through Cytokinesis of Adult Cardiomyocytes," is available at http://stm.sciencemag.org/content/6/224/224ra27.short.

Additional authors of the study include researchers from the Cardiovascular Institute at the Mount Sinai School of Medicine, the Centro Nacional de Investigaciones Cardiovasculares at the Hospital Universitario La Paz, and the Division of Cardiology at the Albert Einstein College of Medicine.

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GW researcher finds gene therapy a promising tool for cardiac regeneration

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19-Feb-2014

Contact: Andrea Baird bairda@mskcc.org 212-639-3573 Memorial Sloan-Kettering Cancer Center

NEW YORK, February 19, 2014 Investigators from Memorial Sloan Kettering Cancer Center have reported more encouraging news about one of the most exciting methods of cancer treatment today. The largest clinical study ever conducted to date of patients with advanced leukemia found that 88 percent achieved complete remissions after being treated with genetically modified versions of their own immune cells. The results were published today in Science Translational Medicine.

"These extraordinary results demonstrate that cell therapy is a powerful treatment for patients who have exhausted all conventional therapies," said Michel Sadelain, MD, PhD, Director of the Center for Cell Engineering at Memorial Sloan Kettering and one of the study's senior authors. "Our initial findings have held up in a larger cohort of patients, and we are already looking at new clinical studies to advance this novel therapeutic approach in fighting cancer."

Adult B cell acute lymphoblastic leukemia (B-ALL), a type of blood cancer that develops in B cells, is difficult to treat because the majority of patients relapse. Patients with relapsed B-ALL have few treatment options; only 30 percent respond to salvage chemotherapy. Without a successful bone marrow transplant, few have any hope of long-term survival.

In the current study, 16 patients with relapsed B-ALL were given an infusion of their own genetically modified immune cells, called T cells. The cells were "reeducated" to recognize and destroy cancer cells that contain the protein CD19. While the overall complete response rate for all patients was 88 percent, even those with detectable disease prior to treatment had a complete response rate of 78 percent, far exceeding the complete response rate of salvage chemotherapy alone.

Dennis J. Billy, C.Ss.R, of Wynnewood, Pennsylvania, was one of the first patients to receive this treatment more than two years ago. He was able to successfully undergo a bone marrow transplant and has been cancer-free and back at work teaching theology since 2011. Paolo Cavalli, a restaurant owner from Oxford, Connecticut, remains in complete remission eight months after receiving his personalized T cell treatment.

A History of Scientific Achievements for Cell-Based Therapies

Cell-based, targeted immunotherapy is a new approach to treating cancer that harnesses the body's own immune system to attack and kill cancerous cells. Unlike with a common virus such as the flu, our immune system does not recognize cancer cells as foreign and is therefore at a disadvantage in eradicating the disease. For more than a decade, researchers at Memorial Sloan Kettering have been exploring ways to reengineer the body's own T cells to recognize and attack cancer. In 2003, they were the first to report that T cells engineered to recognize the protein CD19, which is found on B cells, could be used to treat B cell cancers in mice.

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New findings on cell therapy to treat leukemia bring more encouraging news of the promise that this experimental area of cancer treatment holds for patients for whom conventional approaches do not work.

In the journal Science Translational Medicine, researchers from Memorial Sloan Kettering Cancer Center, New York, NY, report the results of the largest clinical study yet conducted in patients with advanced leukemia.

These show that 14 of the 16 patients - that is 88% - treated with genetically modified versions of their own immune cells, achieved complete remission - at least in the short term; the long-term effects of the therapy are yet to be tested.

Co-senior author Dr. Michel Sadelain, director of the Center for Cell Engineering at Memorial Sloan Kettering, describes the results as "extraordinary," saying they show how cell therapy might offer hope where other treatments have failed.

"Our initial findings have held up in a larger cohort of patients," he notes, "and we are already looking at new clinical studies to advance this novel therapeutic approach in fighting cancer."

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Cell therapy to treat leukemia shows more promise

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19-Feb-2014

Contact: Raymond MacDougall macdougallr@mail.nih.gov 301-443-3523 NIH/National Human Genome Research Institute

National Institutes of Health researchers have identified gene variants that cause a rare syndrome of sporadic fevers, skin rashes and recurring strokes, beginning early in childhood. The team's discovery coincides with findings by an Israeli research group that identified an overlapping set of variants of the same gene in patients with a similar type of blood vessel inflammation.

The NIH group first encountered a patient with the syndrome approximately 10 years ago. The patient, then 3 years old, experienced fevers, skin rash and strokes that left her severely disabled. Because there was no history of a similar illness in the family, the NIH group did not at first suspect a genetic cause, and treated the patient with immunosuppressive medication. However, when the NIH team evaluated a second patient with similar symptoms two years agoa child who had experienced recurrent fevers and six strokes by her sixth birthdaythey began to suspect a common genetic cause and embarked on a medical odyssey that has led not only to a diagnosis, but to fundamental new insights into blood vessel disease.

In their study, which appears in the Feb. 19, 2014, advance online edition of the New England Journal of Medicine, the researchers describe how next-generation genome sequencing, only recently available, facilitated a molecular diagnosis for patients in their study. The researchers found that harmful variants in the CECR1 gene impede production of a protein vital to the integrity of healthy blood vessel walls.

"This discovery is another example of genome sequencing playing a central role in revealing the genomic basis for an important rare disease," said Eric D. Green, M.D., Ph.D., director of the National Human Genome Research Institute (NHGRI), where the lead members of the research team are based. "Such studies illustrate how genomics is paving the way to improved human health."

The researchers showed that faulty variants in their patients' DNA that encode the CECR1 gene cause a loss of function of the gene's ability to produce of an enzyme called adenosine deaminase 2 (ADA2). Without it, abnormalities and inflammation in blood vessel walls result. The researchers call the new syndrome, deficiency of ADA2, or DADA2. The enzyme ADA2 is chemically similar to the enzyme ADA1, whose deficiency results in severe combined immunodeficiency disease.

NHGRI Scientific Director Daniel Kastner, M.D., Ph.D., led the team of collaborators from NIH and beyond in mounting the study of nine patients. "It has been incredibly fantastic to see this kind of progress being made within the last decade," he said. "Our study raises the possibility that the ADA2 pathway may contribute to susceptibility to stroke in the more general population."

For children, as with adults, stroke can affect physical, cognitive and emotional functioning. Some outcomes, such as blindness and deafness, can be lasting; others, such as the ability to walk, can be relearned.

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NIH team discovers genetic disorder causing strokes and vascular inflammation in children

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Babies who develop leukemia during the first year of life appear to inherit an unfortunate combination of genetic variations that can make the infants highly susceptible to the disease, according to a new study at Washington University School of Medicine in St. Louis and the University of Minnesota.

The research is available online in the journal Leukemia.

Doctors have long puzzled over why it is that babies just a few months old sometimes develop cancer. As infants, they have not lived long enough to accumulate a critical number of cancer-causing mutations.

Parents always ask why their child has developed leukemia, and unfortunately we have had few answers, said senior author Todd Druley, MD, PhD, a Washington University pediatric oncologist who treats patients at St. Louis Childrens Hospital. Our study suggests that babies with leukemia inherit a strong genetic predisposition to the disease.

The babies appear to have inherited rare genetic variants from both parents that by themselves would not cause problems, but in combination put the infants at high risk of leukemia. These variants most often occurred in genes known to be linked to leukemia in children, said Druley, an assistant professor of pediatrics.

Leukemia occurs rarely in infants, with only about 160 cases diagnosed annually in the United States. But unlike leukemia in children, which most often can be cured, about half of infants who develop leukemia die of the disease.

The researchers sequenced all the genes in the DNA of healthy cells from 23 infants with leukemia and their mothers. Looking at genes in the healthy cells helped the researchers understand which genetic variations were passed from a mother to her child, and by process of elimination, the scientists could determine the fathers contribution to a babys DNA.

Among the families studied, there was no history of pediatric cancers. The scientists also sequenced the DNA of 25 healthy children as a comparison.

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Infants with Leukemia Inherit Susceptibility

Genetic testing can help doctors choose the most effective and economical drugs to prevent blood clots in the half a million patients in the U.S. who receive coronary stents each year, according to a new study led by a UC San Francisco researcher.

The work, reported in the February 18, 2014 Annals of Internal Medicine, demonstrates that genetically guided personalized medicine, often perceived as pricier than traditional approaches, can both lower costs and increase the quality of health care.

Dhruv Kazi, MD, MSc, MS

Our results counter the general perception that personalized medicine is expensive, said Dhruv Kazi, MD, MSc, MS, assistant professor of medicine at UCSF and first author of the new study. What we have shown is that individualizing care based on genotype may in fact be very cost-effective in some settings, because it allows us to target the use of newer, more expensive drugs to the patients who are most likely to benefit from them.

According to the American Heart Association, about 500,000 patients per year in the U.S. receive stents to open up coronary arteries after experiencing unstable angina or a heart attack. These patients routinely begin a one-year regimen of aspirin taken daily in combination with a prescription antiplatelet medication, a dual therapy that can significantly reduce the risk of stent-clogging clots by preventing blood cells known as platelets from sticking together.

Historically, most patients have taken aspirin in combination with clopidogrel (trade name Plavix), but the effectiveness of that drug in preventing clotting and recurrent cardiovascular problems varies considerably among patients. One cause of this variability is that clopidogrel is a pro-drug: to work it must first be activated by a liver enzyme known as CYP2C19, and it is therefore less effective in patients who carry genetic variations that reduce the activity of the CYP2C19 gene. Approximately 28 percent of the population carries these genetic variations, which are known as loss-of-function alleles.

Two newer drugs, prasugrel (Effient) and ticagrelor (Brilinta), prevent clotting more reliably than clopidogrel in most patients, but they are considerably more expensive, and they can have troublesome side effects. Prasugrel can cause fatal bleeding in some patients, and ticagrelor can cause uncomfortable shortness of breath.

Juggling these variables of effectiveness, expense, side effects, and genetic factors has made it challenging for doctors to choose the right drug for their patients, particularly since neither the benefit of genetic testing for CYP2C19 variants nor the relative advantages of prasugrel versus ticagrelor have been tested in randomized clinical trials.

In the new research, Kazi and colleagues built a computer simulation based on 100,000 hypothetical 65-year-old patients receiving stents for heart problems. The model incorporated more than 100 quantitative parameters that might affect the choice of anti-platelet therapy, including clinical data from the medical literature and Medicare claims, procedure and hospitalization costs from national datasets, as well as actuarial information from published life tables.

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Personalized Medicine a Cost-Effective Way to Tailor Drug Therapy After Stents

PHILADELPHIA A newly developed, more specific approach to classifying tumors by molecular type can help cancer researchers to determine tumor characteristics and guide treatment strategies. A team of researchers from the Perelman School of Medicine at the University of Pennsylvania and the Wistar Institute have created the first isoform-level assay for stratifying tumors at a molecular level, in patients with glioblastoma, the most common and most aggressive type of malignant primary brain tumor. This new classifier is more efficient and replicable in a laboratory setting than existing diagnostic tools, and can provide more accurate predictions for survival and how glioblastoma patients may respond to different treatments.

"Current tests can help classify tumor types to a lesser degree. This new classifying system improves both the diagnostic accuracy and the efficiency of the testing process," said Donald O'Rourke, MD, associate professor of Neurosurgery with Penn's Abramson Cancer Center and director of the Penn Brain Tumor Tissue Bank. "The more detailed information we have about the tumor, at a molecular level, the better we can target new immunotherapies and other treatments for our patients with glioblastoma."

Penn Medicine's Center for Personalized Diagnostics (CPD) currently analyzes all brain tumors to determine the best treatment approach for a given tumor type. This new approach would be complementary to the work of the CPD on brain tumor specimens and enhance the overall effort of molecular sub typing of GBM tumors.

This new isoform-based classifier, which looks at variations within cellular RNA, improves prediction accuracy and requires half the variables for the analysis than the genetic-based analysis. The isoform classifier glioblastoma tumor noted the correct subtype with 92 percent accuracy, according to the study, published in Nucleic Acids Research.

The study was completed in collaboration with Ramana Davuluri, PhD, formerly at The Wistar Institute and now at Northwestern University and colleagues. For more details on the study, please see the Wistar Institute press release.

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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 theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania(founded in 1765 as the nation's first medical school) and theUniversity of Pennsylvania Health System, which together form a $4.3 billion enterprise.

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

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 byU.S. News & World Report; Penn Presbyterian Medical Center; Chester County Hospital; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Chestnut Hill Hospital and Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.

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$827million to benefit our community.

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Penn Medicine and Wistar Scientists Create Precise Tumor Classifier for Glioblastoma

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NEW YORK(CBSNewYork) It has been called the cancer breakthrough of the year by a major scientific journal.

Therapy that eradicates cancer using a patients own cells has already saved a number of terminal leukemia patients, CBS 2s Dr. Max Gomez reported.

It has been the Holy Grail of cancer therapy and it harnesses the patients own immune system to attack cancer.

Now, a major new study has shown how to do that when treating leukemia. It involves using gene therapy to convert a patients white blood cells into killers.

Ive had several doctors tell me there is nothing else that can be done, leukemia patient Paolo Cavalli said, It is difficult with a new family to think about those things.

After six years of chemotherapy, stem cell transplants, and multiple relapses Cavalli was out of options for his leukemia.

I dont think I had many days left, he said.

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Dr. Max Gomez: Gene Therapy Could Be Lifesaver For Cancer Patients

Injections of a normally silent gene sparked recovery in pigs induced to have heart attacks

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When a heart attack brings blood flow to a screeching halt, thats only the first assault on our fist-size organ. Among survivors, the recovery itself fuels more permanent damage to the heart. Scar tissue can harden once-flexible heart muscle, making it less elastic. And as tentacles of this tissue creep over the aorta the heart muscle can no longer fully contract. This long-term damage can minimize the amount of oxygen-rich blood sent throughout the body, which can send patients spiraling into heart failure. Heart transplants are one way to circumvent these scar tissue issues, but donor hearts are always in short supply. Devising other truly effective solutions has long eluded researchers. A form of gene therapy, however, is now showing promise in pigs. It turns out that a normally silent gene called Cyclin A2, or CCNA2, can be coaxed into action to combat the formation of scar tissue in pigs that suffer a heart attack. This treatment sparked regeneration of heart muscle cells in pigs as well as improvements in the volume of blood pushed out with every beat. The finding is published in the February 19 issue of Science Translational Medicine. Gene therapy, the authors hope, may one day join stem cell treatments as a contender for transforming the way doctors treat heart failure. Stem cellbased therapies have already resulted in more healthy tissue and decreased scar mass in human clinical trials as well as small improvements in how much blood the heart can pump from one chamber to another. But as Scientific American reported in April 2013, many questions remain about which stem cells to use and how to prepare them. For this study, researchers randomly assigned 18 pigs recovering from heart attacks to either receive injections of the gene expressed under a promoter (which would force it to be expressed) or the same solution without the gene. Pigs treated with the gene had greater success pushing out blood with each heartbeat, but also produced a greater number of heart muscle cells. These findings echo the teams earlier heart regeneration successes in mice and rats. The researchers replicated their findings in a petri dish and watched adult porcine heart muscle cells treated with the same regimen of gene therapy undergo complete cell division in the dishdemonstrating under a microscope how the heart cells were dividing and thriving with the gene therapy. This new approach mimics the kind of regeneration we see in the newt and zebra fish, says lead author Hina Chaudhry, the director of cardiovascular regenerative medicine at The Mount Sinai Hospital in New York City. If the technique proves successful in humans, it could boost patient recovery rates by helping strengthen heart muscles and improving blood flow, all while giving a needed lift to gene therapy research, which has been slow to gain momentum in the U.S. In 1999 Jesse Gelsinger, 18, died after a gene therapy experiment cost him his life. The virus used to deliver a gene that would potentially control his rare digestive disorder fueled a massive and fatal immune reaction. That highly publicized case, along with other gene therapy missteps, put a pall on the field. Chaudhry says that her team is proceeding with caution and plans to be careful when administering this treatment to patient populations. For patients who have a large heart attack who are at risk of heart failure, I think the therapy is going to be very beneficial, she says. If you have a small heart attack, it probably wont make as much of a difference in overall survival because of advances with todays medicines. As more researchers look to gene therapy for previously intractable human conditions, a success with heart attack treatments could send ripples throughout the field.

2014 Scientific American, a Division of Nature America, Inc.

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Gene Therapy Shows Promise for Treating Heart Attack Victims

Stem Cell Treatment at "EmCell"
http://www.emcell.com/ Stem cell therapy is the rapidly developing area of modern medicine. Unique properties of fetal stem cells, the core of EmCell treatme...

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B.C.-based genome research published this week is expected to help doctors target treatment of lymphoma tumours.

We found novel mutations in a gene that have not been described before in any cancer, said Dr. Christian Steidl, a scientist at the BC Cancer Agency and a professor in the University of British Columbias Department of Pathology who led the study team. Its a first description with a state-of-the-art technology.

Published in the scientific journal Nature Genetics Sunday, the work is part of a worldwide effort to identify gene mutations in all kinds of cancer tumours so treatment can be tailored to an individuals specific illness.

Thats what we mean by personalized medicine, that we dont just use a drug off the shelf and hope it works. Thats what we currently do. We use a drug combination that is very unspecific. It works in a proportion of patients, but we dont really know why.

Projecting five to 10 years in the future, this type of research will be the foundation of the shift that will happen in personalized medicine, said Steidl.

The study took samples from healthy cells and cancer tumours in about 100 patients, which were then analyzed using advanced gene sequencing techniques that have become available in only the last few years. Lead researcher Jay Gunawardana, a PhD student in pathology at UBC, found about 20 per cent of patients with Hodgkins lymphoma and a subtype of non-Hodgkin lymphoma (primary mediastinal B cell lymphoma) carry the same genetic mutation. While there is currently no therapy that can fix the damage caused by this mutation in the gene called PTPN1, experts say it opens the door for other scientists to find a treatment now that the target is known.

The term lymphoma covers about 50 different types of cancer that affect the glands of the lymphatic system that control the bodys immune response. It is divided into two groups, Hodgkin and non-Hodgkin lymphoma, and is the fifth most common cancer type in Canada. Its cause is unknown and it is rising among young adults, according to Lymphoma Canada. Each year, about 8,800 Canadians are diagnosed with lymphoma and more than 3,000 die from the disease.

Dr. Andrew Zelenetz, a lymphoma specialist at Memorial Sloan Kettering Cancer Center in New York who has no connection to the study, said in a telephone interview the discovery is incremental in adding one more piece to the advancement of cancer treatments. But it is a significant contribution to the understanding of lymphoma as diverse rather than a single ailment.

We often mistakenly think of cancer as one thing, that there will be a single magical cure, he said. What genomics has taught us is that we can walk up to three people with the same lymphoma, but if we look inside we see its three different diseases that should be treated in different ways. Today we dont have all the treatment tools that we need, but we would like to get away from having to use poisons as chemotherapy. Wed like to get away from drugs that work non-specifically.

The scale of interest in this area of research can be seen in the International Cancer Genome Consortium which aims to create a catalogue of gene abnormalities found in tumours from 50 different types of cancer. In the U.S., the Cancer Genome Atlas project is focused on specific cancers of the brain, lung and ovary. So far, the missteps in gene coding that cause tumour growth are known in only a tiny fraction of the myriad types of cancer

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New B.C. research lays the groundwork for personalized cancer treatment

Scientists at The Wistar Institute have developed a mathematical method for classifying forms of glioblastoma, an aggressive and deadly type of brain cancer, through variations in the way these tumor cells "read" genes. Their system was capable of predicting the subclasses of glioblastoma tumors with 92 percent accuracy. With further testing, this system could enable physicians to accurately predict which forms of therapy would benefit their patients the most.

Their research was performed in collaboration with Donald M. O'Rourke, M.D., a neurosurgeon at the University of Pennsylvania Brain Tumor Center, who provided the glioblastoma samples necessary to validate the Wistar computer model. Their findings were published online in the journal Nucleic Acids Research.

"It has become increasingly obvious that understanding the molecular makeup of each patient tumor is the key to personalizing cancer treatments for individual patients," said Ramana Davuluri, Ph.D., Wistar's Tobin Kestenbaum Family Professor and associate director of Wistar's Center for Systems and Computational Biology. "We have developed a computational model that will allow us to predict a patient's exact variety of glioblastoma based on the transcript variants a given tumor produces."

"A gene can produce multiple variants, in the form of transcript variants and protein-isoforms. We found that when you use the gene expression information at variant/isoform-level, the statistical analyses recaptured the four known molecular subgroups but with a significant survival difference among the refined subgroups." said Davuluri. "Using patient data, we found that certain subgroups when combined with patient age, for example, could predict better outcomes using a given course of therapy."

"As more targeted therapies come into use, this is exactly the sort of information clinicians will need to provide the best hope of survival for their patients," Davuluri said. "In time, we think this could form the basis of a clinical test that will help oncologists decide a patient's course of treatment."

Glioblastomamultiforme is the most lethal of the malignant adult brain tumors, and accounts for over 50 percent of all cases of brain cancer. Even with aggressive combination therapies, the prognosis remains bleak, with median patient survival of 15 months after diagnosis. The disease is also molecularly heterogeneous, that is, composed of subtypes that are not genetically alike or produce the same array of proteins. Genetic data from the Cancer Genome Atlas (TCGA) consortium has led to the identification of four subtypes of glioblastoma, but Davuluri and his researchers sought to find a way to quickly identify which patient was which subtype.

In previous studies, Davuluri and his Wistar colleagues have established how changes in the way a cell reads its own DNA can create multiple variations of a single protein. These variant proteins are called isoforms, and they are produced as cells alter how they transcribe a given gene into RNA. Slight changes in how the cellular machine reads a gene can result in protein isoforms with subtle differences in enzymatic activity or longevity.

For example, their earlier research determined how human brains produce different isoforms of specific proteins throughout their lives. Developing fetal brains produce different isoforms of certain genes than adult brains. They also found that changes that trigger the production of the wrong isoform at the wrong time could lead to cancer.

In the Nucleic Acids Research study, the researchers combined assays of these protein isoforms with a computer model they call PIGExClass, or the Platform-independent Isoform-level Gene-EXpression based Classification-system. To categorize glioblastomas with PIGExClass, Davuluri and his colleagues first began with Cancer Genome Atlas data to develop a set of 121 isoform variants whose combination of differences could denote a specific subtype of the brain cancer. PIGExClass is, essentially, a software that ranks gene isoform data into sets based on a set of pre-determined values. The researchers found that, by using this classification system, they could predict the subtype of glioblastoma in the database with 92 percent accuracy.

"When we knew what combination of isoforms could create a specific signature for each type of glioblastoma, we could then create a simple laboratory assay that would look for these differences in patient samples," Davuluri said. "In this case the test would measure variations in the RNA abundance associated with these 121 isoforms that make up the signature."

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Gene test developed to accurately classify brain tumors

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19-Feb-2014

Contact: John Paul Gutierrez jpgutierrez@icahdq.org International Communication Association

Washington, DC (February 19 2014) The lifelong debate of nature versus nurture continuesthis time in what your children watch. A recent paper published in the Journal of Communication found that a specific variation of the serotonin-transporter gene was linked to children who engaged in increased viewing of violent TV and playing of violent video games.

Sanne Nikkelen, Helen Vossen, and Patti Valkenburg of the University of Amsterdam's School of Communication Research, in collaboration with researchers at the Erasmus University Medical Centre in Rotterdam, analyzed survey data of 1,612 parents of Dutch children ages 5-9. The parents noted how much violent TV programming their children viewed, as well as how often they played violent video games. DNA samples collected at the children's birth were then analyzed to determine a certain gene variant. The researchers found that children that had the specific variant of the serotonin-transporter gene on average consumed more violent media and displayed more ADHD-related behaviors. However, these links are subtle and more factors can influence these behaviors in children.

Earlier studies have shown that overall amount of media use is partly heritable. These studies, however, did not examine the use of specific media content and did not examine specific gene variants, but only looked at heritability. This study is the first to specifically examine violent media content and to examine a specific gene variant. There have been earlier studies looking at whether violent media use is related to ADHD-related behaviors, but these have found mixed results.

"Our results indicate that children's violent media use is partly influenced by genetic factors. This could mean that children with this gene variant are more likely to seek out stimulating activities, such as violent television viewing and video game playing," said Nikkelen. "It is important to study the relationship between media use and ADHD-related behaviors because children who show increased ADHD-related behaviors often face peer and academic difficulties and are at increased risk for substance abuse. Examining factors that may contribute to the development of these behaviors is essential."

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"Media Violence and Children's ADHD-Related Behaviors: A Genetic Susceptibility Perspective'" by Sanne Nikkelen, Helen Vossen, Patti Valkenburg, Fleur Velders, Dafna Windhorst, Vincent Jaddoe, Albert Hofman, Frank Verhulst, & Henning Tiemeier, Journal of Communication, Volume 64 No. 1, pgs. 42-60, 2014 doi:10.1111/jcom.12073

Contact: To schedule an interview with the author or a copy of the research, please contact John Paul Gutierrez, jpgutierrez@icahdq.org.

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Genetics linked to children viewing high amounts of violent media

PUBLIC RELEASE DATE:

19-Feb-2014

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, February 19, 2014Joseph C. Glorioso, III, PhD (University of Pittsburgh School of Medicine, PA) devoted much of his research career to developing herpes viruses as efficient vectors for delivering therapeutic genes into cells. In recognition of his leadership and accomplishments, he has received a Pioneer Award from Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. Human Gene Therapy is commemorating its 25th anniversary by bestowing this honor on the leading 12 Pioneers in the field of cell and gene therapy selected by a blue ribbon panel* and publishing a Pioneer Perspective by each of the award recipients. The Perspective by Dr. Glorioso is available on the Human Gene Therapy website.

As he recounts in his essay "Herpes Simplex Viral Vectors: Late Bloomers with Big Potential," it took 30 years to create broadly applicable HSV vector designs and a useful gene delivery platform. Since herpes simplex virus has a natural affinity for the nervous system, Dr. Glorioso believes that "gene delivery to the brain represents the most important frontier for HSV-mediated gene therapy and provides a unique opportunity to study complex processes such as learning and memory and to treat complex genetic and acquired diseases, including brain degeneration, epilepsy, and cancer."

In addition, says Dr. Glorioso, some herpes viral delivery systems are proving useful for gene transfer in the emerging field of cellular reprogramming to produce stem cells for tissue regeneration.

"Joe began his work in gene therapy early in the development of the field focusing on the very challenging objective of targeting the central nervous system. His work with HSV vectors represents an incredibly elegant blending of basic virology and translational science," says James M. Wilson, MD, PhD, Editor-in-Chief of Human Gene Therapy, and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

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*The blue ribbon panel of leaders in cell and gene therapy, led by Chair Mary Collins, PhD, MRC Centre for Medical Molecular Virology, University College London selected the Pioneer Award recipients. The Award Selection Committee selected scientists that had devoted much of their careers to cell and gene therapy research and had made a seminal contribution to the field--defined as a basic science or clinical advance that greatly influenced progress in translational research.

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Joseph Glorioso, Ph.D., receives Pioneer Award

February 19, 2014

Image Credit: Christof Angst, Biberfachstelle

Brett Smith for redOrbit.com Your Universe Online

Long-prized for their thick fur, the cuddly Eurasian beaver has been hunted by humans for thousands of years and a new genetic study from a large group of international researchers has found that predation by humans has significantly cut down the genetic diversity of these animals.

While beaver populations have been growing rapidly since the late 19th century when conservation efforts began, genetic diversity within modern beaver populations remains considerably reduced to what was present prior to the period of human hunting and habitat reduction, said study author Michi Hofreiter, a biology professor from the University of York in the United Kingdom.

In the study, which was published in the journal Molecular Ecology, the research team found that the Eurasian beaver can be divided into three different groups. The two predominant ones are in western and Eastern Europe and a now extinct, and previously unknown, third group inhabiting the Danube river basin. This population was around at least 6,000 years ago but vanished during the transition to modern society.

The rapid loss of diversity prior to conservation efforts appears to have established a very strong pattern for the geographic distribution of genetic diversity among present-day beaver populations, Hofreiter said.

After centuries of being hunted by humans, the Eurasian beaver had faded from the majority of its original range at the end of the 1800s, with approximately 1,200 beavers remaining. The researchers said they wanted to see if the lack of genetic diversity and strong distribution of genetic diversity seen today are caused by hunting or had already existed before the beavers range was diminished.

To reach their conclusion, the team analyzed DNA from 48 ancient beaver samples, ranging in age from a few hundred to about 11,000 years old, and over 150 modern beavers. The analytical work was performed at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.

We found that overall there was more genetic diversity in the past, said study author Susanne Horn, from the institute. Apparently, already in ancient times an ancient contact zone existed between the eastern and western populations of beavers in the Oder River area. This is close to a present-day contact zone in Germany and Poland.

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Genetic Diversity Of The European Beaver In Peril Due To Human Predation

Mendelian Genetics Law of Segregation tutorial
Genetics with Professor Matthew Schmidt and Dimitra Hasiotis For more information and to view the full video go to streamingtutors.com.

By: Streaming Tutors

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Mendelian Genetics Law of Segregation tutorial - Video