Public release date: 28-Nov-2012 [ | E-mail | Share ]

Contact: Rob Dawson 01-793-413-204 Biotechnology and Biological Sciences Research Council

Scientists have unlocked key components of the genetic code of one of the world's most important crops. The first analysis of the complex and exceptionally large bread wheat genome, published today in Nature, is a major breakthrough in breeding wheat varieties that are more productive and better able to cope with disease, drought and other stresses that cause crop losses.

The identification of around 96,000 wheat genes, and insights into the links between them, lays strong foundations for accelerating wheat improvement through advanced molecular breeding and genetic engineering. The research contributes to directly improving food security by facilitating new approaches to wheat crop improvement that will accelerate the production of new wheat varieties and stimulate new research. The analysis comes just two years after UK researchers finished generating the sequence.

The project was led by Neil Hall, Mike Bevan, Keith Edwards, Klaus Mayer, from the University of Liverpool, the John Innes Centre, the University of Bristol, and the Institute of Bioinformatics and Systems Biology, Helmholtz-Zentrum, Munich, respectively, and Anthony Hall at the University of Liverpool. W. Richard McCombie at Cold Spring Harbor Laboratory, and Jan Dvorak at the Univerisity of California, Davis, led the US contribution to the project.

The team sifted through vast amounts of DNA sequence data, translating the sequence into something that scientists and plant breeders can use effectively. All of their data and analyses were freely available to users world-wide.

Professor Neil Hall said: "The raw data of the wheat genome is like having tens of billions of scrabble letters; you know which letters are present, and their quantities, but they need to be assembled on the board in the right sequence before you can spell out their order into genes."

"We've identified about 96,000 genes and placed them in an approximate order. This has made a strong foundation for both further refinement of the genome and for identifying useful genetic variation in genes that scientists and breeders can use for crop improvement."

Minister for Universities and Science David Willetts said: "This groundbreaking research is testament to the excellence of Britain's science base and demonstrates the capability we want to build on through the agri-tech strategy currently being developed.

"The findings will help us feed a growing global population by speeding up the development of new varieties of wheat able to cope with the challenges faced by farmers worldwide."

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Major breakthrough in deciphering bread wheat's genetic code

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There are nearly 70 different varieties of wheat recommended for farming and suitable for bread, biscuits or for distilling. By improving wheat varieties, scientists hope to increase crops yields by engineering them to be more tolerant to disease, climate change, pests and other factors which currently affect harvests.

Co-author of the paper published in the journal Nature, Professor Neil Hall of University of Liverpool, said: "The raw data of the wheat genome is like having tens of billions of scrabble letters. You know which letters are present, and their quantities, but they need to be assembled on the board in the right sequence before you can spell out their order into genes.

"We've identified about 96,000 genes and placed them in an approximate order. This has made a strong foundation for both further refinement of the genome and for identifying useful genetic variation in genes that scientists and breeders can use for crop improvement."

The researchers created "genetic markers" from wheat varieties and compared them to ancestral grasses like rice and barley to see if desired traits were present. New varieties were then created through artificial selection for "precision breeding".

By altering the genetic code sequence of bread, wheat scientists will be able to modify the new varieties for specific characteristics, making them more resilient to guarantee good crop yields.

The raw data of the wheat genome is like having tens of billions of scrabble letters. Prof Neil Hall, Liverpool University

According to the British Society of Plant Breeders (BSPB), breeding aims to improve the quality, diversity and performance of agricultural and horticultural crops. It says none of the major food crops grown in Britain are native to this country.

Cereals, potatoes, root crops and oilseeds which make up our farmland have their origins in many different parts of the world which have been adapted through plant breeding, to thrive under UK growing conditions.

More than 680 million tonnes of wheat is processed globally each year. Scientists believe that as the world's population continues to grow, the demand for more wheat harvests will also rapidly rise and the need for sustainable farming will be greater than ever.

Professor Denis Murphy, head of the Life Sciences Research Unit at the University of Glamorgan, who was not involved in this research, said: "This is a landmark paper that outlines the genetic blueprint of one of the major global crops. Bread wheat provides a vital staple food to billions of people across the world and is found in products ranging from chapattis and pita breads to biscuits and western-style leavened (raised) bread.

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Genetic breakthrough could guarantee wheat supplies

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ScienceDaily (Nov. 28, 2012) Nearly three-quarters of mutations in genes that code for proteins -- the workhorses of the cell -- occurred within the past 5,000 to 10,000 years, fairly recently in evolutionary terms, said a national consortium of genomic and genetic experts, including those at Baylor College of Medicine.

"One of the most interesting points is that Europeans have more new deleterious (potentially disease-causing) mutations than Africans," said Dr. Suzanne Leal, professor of molecular and human genetics at BCM and an author of the report. She is also director of the BCM Center for Statistical Genetics. "Having so many of these new variants can be partially explained by the population explosion in the European population. However, variation that occur in genes that are involved in Mendelian traits and in those that affect genes essential to the proper functioning of the cell tend to be much older." (A Mendelian trait is controlled by a single gene. Mutations in that gene can have devastating effects.)

How events affected genome

The amount variation or mutation identified in protein-coding genes (the exome) in this study is very different from what would have been seen 5,000 years ago, said Leal and her colleagues in the report that appears online in the journal Nature. The report shows that "recent" events have a potent effect on the human genome.

Eighty-six percent of the genetic variation or mutations that are expected to be harmful arose in European-Americans in the last five thousand years, said the researchers.

The researchers used established bioinformatics techniques to calculate the age of more than a million changes in single base pairs (the A-T, C-G of the genetic code) that are part of the exome or protein-coding portion of the genomes (human genetic blueprint) of 6,515 people of both European-American and African-American decent. The research was an offshoot of the National Heart, Lung and Blood Institute Exome Sequencing Project.

Human population increase

"The recent dramatic increase in human population size, resulting in a deluge of rare functionally important variation, has important implications for understanding and predicting current and future patterns of human disease and evolution," wrote the authors in their report.

Others institutions that took part in this research include the University of Washington, Seattle; University of Michigan, Ann Arbor; the Broad Institute of MIT and Harvard.

Funding for the research came from the GO (Grand Opportunity) Exome Sequencing Project (NHLBI grants RC2 HL-103010 (Heart GO), RC2 HL-102923 (Lung GO) and RC2 HL-102924 (WHISP). The exome sequencing was supported by NHLBI grants RC2HL-102925 (Broad GO) and RC2 HL-102926 (Seattle GO).

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Public release date: 28-Nov-2012 [ | E-mail | Share ]

Contact: Jeffrey Bright jeffrey.bright@joslin.harvard.edu 617-309-1957 Joslin Diabetes Center

BOSTON November 28, 2012 As part of their ongoing research on the role of genes in the development of type 1 diabetes, Joslin Diabetes Center scientists, in collaboration with scientists at the University of Wrzburg, have demonstrated how a genetic variant associated with type 1 diabetes and other autoimmune diseases influences susceptibility to autoimmunity. The findings appear in the upcoming issue of Diabetes.

Recent studies of the human genome have identified genetic regions associated with autoimmune diseases such as type 1 diabetes. Joslin scientists in the Section of Immunobiology seek to understand how genes that are most widely associated with various autoimmune diseases contribute to disease risk.

One of these genes is PTPN22, which plays a role in lymphocyte (immune cell) function. A PTPN22 variant (or mutation) has been implicated as a risk factor for type 1 diabetes and several other autoimmune disorders. PTPN22 is involved in the formation of a key protein known as lymphoid tyrosine phosphatase (LYP), which helps control the activity of T and B cells in the immune system. The PTPN22 mutation generates a variation of LYP with a different molecular structure.

Most studies of the PTPN22 disease variant have suggested that this variant is a gain-of-function genetic mutation that enhances LYP activity and lessens the activity of T and B cells, which increases susceptibility to autoimmunity. "When immune cells are less reactive during the maturation phase of their development, the cells can evade mechanisms that help protect against autoimmunity," says study lead author Stephan Kissler, PhD, of the Section of Immunobiology. However, one study which analyzed data from humans and genetically modified mice suggested that the LYP variant associated with type 1 diabetes is a loss-of-function mutation that reduces LYP activity.

To help resolve the conflicting data, Joslin scientists conducted studies with a unique mouse model developed by Dr. Kissler's graduate student and co-author, Peilin Zheng. Using a technology that combines RNA interference, a method to silence gene expresson, with lentiviral transgenesis, a method to genetically modify animals, the scientists can manipulate gene activity in the most widely used mouse model for type 1 diabetes, the nonobese diabetic mouse (NOD). In this study, the researchers were able to easily turn off and on the PTPN22 gene in the NOD mouse. "We are the first to use this approach in the NOD mouse model," says Dr. Kissler. "It provides a very powerful way to study the contribution of PTPN22 to disease."

When PTPN22 was turned off in mice, mimicking a loss-of-function mutation, the researchers observed an increase in regulatory T cells and a decreased risk of autoimmune diabetes. "This is the first study conducted on the diabetic mouse model that supports the LYP gain-of-function hypothesis," says Dr. Kissler. "Our work should help to resolve the controversy."

By providing additional data that suggests the potential therapeutic value of PTPN22 manipulation, the study may further the development of new therapeutic options that inhibit LYP to reduce or prevent autoimmunity. "Our goal is to treat autoimmunity. Inhibiting LYP in patients may increase regulatory immune cells and could confer protection against autoimmunity, but it remains to be tested if our promising findings in this mouse model are reflected in humans," says Dr. Kissler.

The Joslin scientists are following up on this study to deepen understanding of how inhibiting PTPN22 affects T and B cells.

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Joslin researchers increase understanding of genetic risk factor for type 1 diabetes

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

The vast majority (80 percent) of parents with at least one child with Autism Spectrum Disorder (ASD) would pursue genetic testing if a test were available that could identify risk in a younger sibling, citing the desire for earlier identification of children at risk, earlier evaluation and intervention, closer monitoring and lessened anxiety. The findings were reported in Parental Interest in a Genetic Risk Assessment Test for Autism Spectrum Disorders, a survey published online today in the journal Clinical Pediatrics.

The survey of 162 parents of children with ASD also reported an almost three-year lag from the time ASD was initially suspected until a child received a diagnosis--even in families with a previously diagnosed child. Link to publication.

The internet-based survey was sponsored by IntegraGen, Inc. and conducted during February and March 2012. Earlier this year, the CDC announced that ASD prevalence in the United States has increased to one in 88 children, and even with increased awareness, the average age of ASD diagnosis is greater than four years.

The majority of parents surveyed said they would be interested in having their child tested if a genetic test was available that could identify ASD risk--even if it could not confirm a diagnosisin order to facilitate an earlier diagnosis and access to therapies known to make a positive impact on their childs development, stated the studys primary investigator Elizabeth Couchon, M.S., L.G.C., a licensed genetic counselor and medical sciences liaison for IntegraGen, Inc., which recently launched the ARISk Autism Risk Assessment Test. This multi-SNP (Single Nucleotide Polymorphism), gender-specific genetic screening test looks at 65 genetic markers associated with ASD to assess the risk of autism in children under the age of 36 months who have an older sibling with ASD, paving the way for early diagnosis, early intervention and better outcomes Our goal was to better understand parents experiences with the ASD diagnostic process, assess their anxiety levels about the risk of ASD recurring in their family, and gauge attitudes regarding the use of a genetic risk assessment test to evaluate risk for ASD in younger siblings, she added. The survey found that families experienced a significant delay in the time it took to get an ASD diagnosis when they realized something was wrong, even when they had an older child with ASD.

Parents who have one child with ASD are often anxious about younger siblings since we know there is a genetic component and that ASD runs in families, says national autism expert Antonio Hardan, M.D., a member of IntegraGen's advisory board and one of the studys co-authors. These parents often know the signs and symptoms of ASD, and typically recognize issues with their younger childrens development. Many also know earlier diagnosis and intervention leads to better outcomes, so the availability of an early screening tool that could aid with early diagnosis would relieve some of their anxiety.

The average recurrence risk for siblings of children affected with ASD has been reported as 18.7%, a 20-fold increase compared to the prevalence of ASD in the general population, suggesting a strong genetic component to the cause of ASD. However, despite the increased risk to siblings, the earlier identification and diagnosis of those siblings at highest risk remains a challenge. The survey was limited to parents living in the United States with at least one child diagnosed with ASD. The survey also focused on parents who had both an older child with ASD and undiagnosed siblings under the age of 48 months.

Among the key findings:

About IntegraGen:

IntegraGen SA (ALINT.PA) is a biotechnology company dedicated to molecular biomarker discovery. The company is headquartered in Evry, France-based and has a wholly-owned US subsidiary is located in Cambridge, Massachusetts. The Companys goal is the development of molecular diagnostic products and services that provide clinicians with new tools to personalize diagnosis, treatment and therapy for complex debilitating diseases. Its Genetic Services Business provides state-of-the-art genotyping services to the research community. Focusing its efforts on the early identification of children at risk for autism spectrum disorder (ASD), IntegraGen has made inroads in identifying a number of common genetic variants associated with ASD. The Company has recently launched the ARISk Test in the United States providing a genetic screening tool for the early identification of children at risk for ASD.

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Journal Clinical Pediatrics Reports 80% of Parents Surveyed Would be Interested in Genetic Risk Assessment Testing for ...

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Public release date: 28-Nov-2012 [ | E-mail | Share ]

Contact: Glenna Picton picton@bcm.edu 713-798-4710 Baylor College of Medicine

HOUSTON -- (Nov. 29, 2012) Nearly three-quarters of mutations in genes that code for proteins the workhorses of the cell occurred within the past 5,000 to 10,000 years, fairly recently in evolutionary terms, said a national consortium of genomic and genetic experts, including those at Baylor College of Medicine.

"One of the most interesting points is that Europeans have more new deleterious (potentially disease-causing) mutations than Africans," said Dr. Suzanne Leal, professor of molecular and human genetics at BCM and an author of the report. She is also director of the BCM Center for Statistical Genetics. "Having so many of these new variants can be partially explained by the population explosion in the European population. However, variation that occur in genes that are involved in Mendelian traits and in those that affect genes essential to the proper functioning of the cell tend to be much older." (A Mendelian trait is controlled by a single gene. Mutations in that gene can have devastating effects.)

The amount variation or mutation identified in protein-coding genes (the exome) in this study is very different from what would have been seen 5,000 years ago, said Leal and her colleagues in the report that appears online in the journal Nature. The report shows that "recent" events have a potent effect on the human genome.

Eighty-six percent of the genetic variation or mutations that are expected to be harmful arose in European-Americans in the last five thousand years, said the researchers.

The researchers used established bioinformatics techniques to calculate the age of more than a million changes in single base pairs (the A-T, C-G of the genetic code) that are part of the exome or protein-coding portion of the genomes (human genetic blueprint) of 6,515 people of both European-American and African-American decent. The research was an offshoot of the National Heart, Lung and Blood Institute Exome Sequencing Project.

"The recent dramatic increase in human population size, resulting in a deluge of rare functionally important variation, has important implications for understanding and predicting current and future patterns of human disease and evolution," wrote the authors in their report.

###

Others institutions that took part in this research include the University of Washington, Seattle; University of Michigan, Ann Arbor; the Broad Institute of MIT and Harvard. Other BCM researchers who took part include Dr. Christie M. Ballantyne, Mengyuan Kan, Fremiet Lara-Garduno, Dajiang J. Liu, Gao Wang and Dr. Haleh Sangi-Haghpeykar.

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The Wonderful World of Planaria - Genetics 3452
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Experts at the prestigious University of Cambridge will conduct research into the "extinction-level risks" posed to humanity by artificially intelligent robots. The Cambridge Project for Existential Risk is dedicated to "ensuring that our own species has a long-term future" by studying the risks posed by AI, nanotechnology and biotechnology. "The scientists said that to dismiss concerns of a potential robot uprising would be "dangerous," reports the BBC. The project was co-founded by Huw Price, Bertrand Russell Professor of Philosophy at Cambridge, Martin Rees, Emeritus Professor of Cosmology Astrophysics at Cambridge, and Jaan Tallinn, the co-founder of Skype. It also counts amongst its advisers Max Tegmark, Professor of Physics, MIT and George M Church, Professor of Genetics at Harvard Medical School. An article written by Tallinn and Price warns that artificially intelligent computers or robots could take over "the speed and direction of technological progress itself," and shape the environment of planet earth to their own ends while displaying about as much concern for humanity as we do for a bug on the windscreen. Far from being resigned to works as science fiction such as in the Terminator films, the threat posed by a potential future "rise of the robots" has never been closer to reality. The study echoes the predictions of respected author, inventor and futurist Ray Kurzweil, renowned for his deadly accurate technological forecasts. http://www.infowars.com ORDER THIS ...From:InfowarsHeadlineHDViews:0 0ratingsTime:08:55More inNonprofits Activism

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Rural TV NZ in association with New Zealand #39;s leading agriculture company, PGG Wrightson, present the PGG Wrightson Stud Tour 2012. MOTU-NUI ROMNEYS - Masterton - Taihape - Wyndham This week we catch up with the many families that now make up the Motu-Nui brand of sheep genetics spanning from Taihape to Southland with the hub of the operation based at ICA station the home of Jason LeGrove. Tony Glynn, of RuralTV.co.nz, meets with the satelite studs of Bruce and Carolyn Robertson at Motu-Nui South near Wyndham and Donald Sandra Fannin of Motu-Nui Hiwi near Taihape, who were both well established Romney studs in their own right before coming under the Motu-Nui umbrella. We also catch up with Davey Wendy Moore who look after the Terminal rams at Holmwood and Mike Kate Tosswill who look after the composite rams at Pakaraka both near Masterton According to Castlepoint Station manager, Stu Neale, the Motu-Nui rams are no-nonsense sheep bred on steep hill country. Jason LeGrove - Phone : 06 372 3841 MAKE SURE YOU SUBSCRIBE TO OUR YOU-TUBE CHANNEL TO WATCH THE NEXT EPISODE OF THE PGG WRIGHTSON STUD TOUR! JOIN RURAL TV NZ on FACEBOOK : http://www.facebook.com FOLLOW Us on TWITTER : twitter.comFrom:RURALTVNZViews:0 0ratingsTime:26:59More inEntertainment

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See more at: http://www.empowernetwork.com Most people don #39;t know about this secret.. By watching this video, you #39;re going to learn a secret, most people don #39;t know. HOW TO MASTER ANY SKILL * Everything #39;s a skill. If someone has done it - you can do it to. Luck and genetics have very little do do with it. The proof is insurmountable. #1- UNCONSCIOUS INCOMPETENCE We are all unconsciously incompetent at something. We don #39;t know what we don #39;t know. We don #39;t know the little intricacies about what make the possible stuff possible. #2- CONSCIOUS INCOMPETENCE * You know what you don #39;t know. It #39;s like when you were learning how to tie your shoe and you were learning the process, but you were incompetent at it. Just like, you were incompetent in the beginning at driving. #3- CONSCIOUS COMPETENCE * You know now how to do it and you have to think about it as you do it. #4- UNCONSCIOUS COMPETENCE * You don #39;t have to think about doing the thing and you just automatically do it. This is the stage you must strive to aim for - by taking massive action and powerful focus at the stage of "conscious competence" - by constantly doing it, by constantly practicing the "practice". ...and then... there will come a time where it just happens... automatically. THE HIERARCHY OF LEARNING *low - receiving by lecture or reading *better - discussing *one of the best - by teaching SECRET WAY OF LEARNING FAST: Modeling * Find a mentor - find someone who #39;s really good at that skill. Modeling their actions, their ...From:RJ BulaongViews:6 0ratingsTime:18:10More inPeople Blogs

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BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) announced today that ADCETRIS (brentuximab vedotin) has been granted orphan drug designation by the U.S. Food and Drug Administration (FDA) for the treatment of mycosis fungoides (MF). MF is the most common type of cutaneous T-cell lymphoma (CTCL). Seattle Genetics and its ADCETRIS collaborator, Millennium: The Takeda Oncology Company, are conducting the ALCANZA trial, a phase III clinical trial of ADCETRIS for patients with CD30-positive relapsed CTCL, including MF. ADCETRIS is not approved for the treatment of CTCL.

This orphan drug designation is a part of our ADCETRIS regulatory strategy, designed to complement the Special Protocol Assessment for the ongoing ALCANZA study, said Clay B. Siegall, President and Chief Executive Officer of Seattle Genetics. The encouraging data from investigator-sponsored trials of ADCETRIS in CTCL, which will be presented at ASH, provide further support for our activities in this patient population.

FDA orphan drug designation is intended to encourage companies to develop therapies for the treatment of diseases that affect fewer than 200,000 individuals in the United States. This designation provides Seattle Genetics with the opportunity for seven years of marketing exclusivity, grant funding to defray costs of clinical trial expenses, tax credits for clinical research expenses and potential waiver of the FDA's application user fee.

The ALCANZA trial is a randomized phase III clinical trial of ADCETRIS for relapsed CD30-positive CTCL patients. The trial is assessing ADCETRIS versus investigators choice of methotrexate or bexarotene in patients with CD30-positive CTCL, including those with primary cutaneous anaplastic large cell lymphoma (pcALCL) or MF. The primary endpoint of the study is overall response rate lasting at least 4 months. Approximately 124 patients will be enrolled in the pivotal trial. The ALCANZA trial is being conducted under a Special Protocol Assessment agreement from the FDA. The study also received European Medicines Agency scientific advice. For more information about the ALCANZA trial, visit http://www.clinicaltrials.gov.

At the 54th American Society of Hematology (ASH) Annual Meeting and Exposition being held December 8-11, 2012 in Atlanta, GA, data from two investigator-sponsored trials of ADCETRIS in CTCL will be reported:

Brentuximab vedotin demonstrates significant clinical activity in relapsed or refractory mycosis fungoides with variable CD30 expression (Abstract #797)

Results of a phase II trial of brentuximab vedotin (SGN-35) for CD30-positive cutaneous T-cell lymphomas and lymphoproliferative disorders (Abstract #3688)

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

Continued here:
Seattle Genetics Receives FDA Orphan Drug Designation for ADCETRIS® (Brentuximab Vedotin) in Mycosis Fungoides

Recommendation and review posted by Bethany Smith

SALT LAKE CITY, Nov. 28, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that a presentation entitled "CCP Score Significantly Predicts PSA Failure After EBRT," was presented on Wednesday, November 28th, 2012 at the Annual Meeting of the Society of Urological Oncology in Bethesda, Maryland. The study demonstrates that the Prolaris(R) test, which measures cell cycle progression (CCP) genes, significantly predicts PSA biochemical recurrence in patients after treatment with external beam radiation therapy (EBRT).

Researchers at Durham VA Medical Center, Duke University School of Medicine, and Myriad Genetics analyzed biopsy specimens from 152 patients with prostate cancer. In this prospectively collected cohort, the Prolaris test was a significant predictor of biochemical recurrence in patients that had undergone radiation treatment (p=0.0017). After adjustment for Gleason score, PSA percent positive cores, and concurrent anti-hormone therapy, the Prolaris test accurately predicted those patients who would benefit from radiation therapy (p=0.034).

"Current approaches to the management of patients with prostate cancer lead to significant under and overtreatment of patients," said Dr. Stephen Freedland, Durham VA Medical Center and Duke University School of Medicine. "Measurement of the CCP score identifies prostate cancer patients at high risk of progression despite conventional radiation therapy who might be considered for more aggressive treatment regimens."

Approximately 25% of men who undergo primary radiation therapy will suffer potentially life threatening disease recurrence and progression. The Prolaris test could be used to identify these at-risk patients prior to their initial treatment. These patients may be appropriate candidates for more aggressive combination therapies such as radiation with anti-androgen therapy or chemotherapy.

The clinically important information that Prolaris provides cannot be obtained from currently available clinical parameters. In addition, this is the first Prolaris study that contained a significant number of African American men, a population known to be at especially high risk for aggressive prostate cancer.

About Prolaris

Prolaris is a genomic risk stratification test developed to aid physicians in predicting prostate cancer aggressiveness in conjunction with clinical parameters such as Gleason score and PSA. Prolaris is a direct molecular measure of prostate cancer tumor biology. By measuring the expression levels of genes involved with cancer replication, Prolaris is able to more accurately predict disease progression and enable physicians to better define a treatment/monitoring strategy for their patients. Prolaris is significantly more prognostic than currently used clinicopathologic variables and provides unique additional information that can be combined with other clinical factors to make the most accurate prediction of a patient's cancer aggressiveness and therefore disease progression.

Prolaris has been proven to predict clinical progression in 4 different clinical cohorts, in both pre and post-treatment scenarios.

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.

The rest is here:
Myriad Genetics' Prolaris Test Predicts Biochemical Recurrence in Prostate Cancer Patients Following Radiation Therapy

Recommendation and review posted by Bethany Smith