Newswise Bethesda, MDJune 14, 2012 Listed below are the selected highlights for the June 2012 issue of the Genetics Society of Americas journal, GENETICS. The June issue is available online at http://www.genetics.org/content/current. Please credit GENETICS, Vol. 191, JUNE 2012, Copyright 2012.

Please feel free to forward to colleagues who may be interested in these articles.

ISSUE HIGHLIGHTS

APL-1, the Alzheimers amyloid precursor protein in Caenorhabditis elegans, modulates multiple metabolic pathways throughout development, pp. 493507 Collin Y. Ewald, Daniel A. Raps, and Chris Li A hallmark of Alzheimers disease is the deposition of senile plaques, whose major component is the beta-amyloid peptide, which is a cleavage product of the amyloid precursor protein (APP). The function of APP and its cleavage products is still unclear. This article reports that the Caenorhabditis elegans APP-related protein APL-1 has multiple functions during development, including modulating the insulin pathway.

Population genetics models of local ancestry, pp. 607619 Simon Gravel Genomes are mosaics of chromosomal tracts that originate from a finite number of ancestors. These mosaics, which are shaped by historical migration patterns, are key to understanding genomic diversity in complex populations. This article presents gene flow models for inferring migration history using such patterns. When applied to HapMap African-American (ASW) data, a two-epoch migration model agrees with the data better than the commonly used single-migration model.

Synaptic polarity depends on phosphatidylinositol signaling regulated by myo-inositol monophosphatase in Caenorhabditis elegans, pp. 509521 Tsubasa Kimata, Yoshinori Tanizawa, Yoko Can, Shingo Ikeda,Atsushi Kuhara, and Ikue Mori Lithium relieves bipolar disorder by inhibiting the evolutionarily conserved enzyme myo-inositol monophosphatase (IMPase), which is essential for polarized localization of synaptic molecules. These authors show that mutations in two enzymes that degrade membrane phosphatidylinositol 4,5-bisphosphate (PIP2) suppress the synaptic defects of IMPase mutants and confer resistance to lithium treatment. These results provide the first in vivo evidence that lithium impairs neuronal PIP2 synthesis through inhibition of IMPase.

Analysis of Cryptococcus neoformans sexual development reveals rewiring of the pheromone-response network by a change in transcription factor identity, pp. 435449 Emilia K. Kruzel, Steven S. Giles, and Christina M. Hull Gene regulatory networks evolve, sometimes radically. This article describes the pheromone response network of the human pathogen Cryptococcus neoformans. The authors map transcriptional regulatory changes that occur during sexual development leading to the discovery of a key cis-regulatory element and its binding protein. The resulting regulatory architecture could not have been predicted based on comparative sequence analyses.

A non-Mendelian MAPK-generated hereditary unit controlled by a second MAPK pathway in Podospora anserina, pp. 419433 Herv Lalucque, Fabienne Malagnac, Sylvain Brun, Sbastien Kicka,and Philippe Silar There are many ways to produce a prion, and this article describes yet another one. The Podospora anserina PaMpk1 MAP kinase signaling pathway can generate C, a hereditary unit resembling prions. These authors show that another MAP kinase pathway, PaMpk2, controls the generation of C by activating PaMpk1, revealing unexpectedly complex regulation of a prion-like trait.

Allopolyploidization lays the foundation for evolution of distinct populations: Evidence from analysis of synthetic Arabidopsis allohexaploids, pp. 535547 Starr C. Matsushita, Anand P. Tyagi, Gerad M. Thornton, J. Chris Pires, and Andreas Madlung Allopolyploidycarrying complete chromosome sets of at least two different specieshas been seen as a mechanism for instant speciation. This article shows that different somatic cells of the same neoallopolyploid individual can exhibit different karyotypes, and that somatic mosaics can persist in subsequent generations. The authors characterize and quantify aneuploidy over seven generations in several sibling lines of a synthetic allopolyploid. Their results suggest that this phenomenon has the potential to lead not only to instant speciation but also to instant radiation.

The nearly neutral and selection theories of molecular evolution under the Fisher geometrical framework: Substitution rate, population size, and complexity, pp. 523534 Pablo Razeto-Barry, Javier Daz, and Rodrigo A. Vsquez This article puts forth that nearly neutral evolution cannot explain the high rate of fixations driven by positive selection found in DNA sequences. The authors use Fishers geometrical model (FGM) to simulate evolution from biologically interpretable distributions of mutations. They find that nearly neutral and selection scenarios predict molecular patterns different from previous models. In a selective scenario in the FGM, evolutionary rate depends not on population size, but rather on the complexity of organisms and mutation size.

Excerpt from:

Genetics Society of America's GENETICS Journal Highlights

By John Lauerman - 2012-06-14T16:00:01Z

Screening the genomes of healthy people may give important clues about their cancer risk, according to a study that suggests advanced DNA technology might be employed early in a patients health assessment.

Among 572 people who underwent a broad analysis, 12 were found to have genes that put them or their children at elevated risk of dangerous tumors, according to the report from researchers at the U.S. National Human Genome Research Institute in Bethesda, Maryland. Eight of the participants had no family history of cancer that doctors normally look to for signals of heightened susceptibility to malignancies, the study said.

The research, released today by the American Journal of Human Genetics, highlights the role that sequencing machines made by Illumina Inc. (ILMN) and Life Technologies Corp. (LIFE) may play in alerting healthy individuals to their risk of disease. The machines can decipher swaths of human DNA in hours, giving massive amounts of information about inherited traits.

The current medical approach for finding susceptibility to disease requires that you or your family members have the condition or have died of it, said Leslie Biesecker, chief of the genetics disease research branch at the Human Genome Research Institute, in a telephone interview. This suggests that it doesnt have to be that way, that we can find susceptibility before all that suffering.

Bieseckers study, called ClinSeq, sequences all the genes in participants DNA to find clues to health and disease. About 1 percent of the human genome, the reproductive code found in each cell, is composed of genes, which are the blueprints for making proteins.

The researchers screened 37 genes in participants DNA for changes that have been linked to cancers. The screen yielded 334 variants of potential clinical importance, most of which were associated with unknown cancer risk.

Eight participants were found to have gene mutations that significantly elevated their risk. Seven had changes in the BRCA1 and BRCA2 genes that sometimes appear in families affected with high rates of breast and ovarian cancer, the study said.

Another participant had a mutation in a gene called SDHC, which has been linked to head and neck tumors that sometimes cause severe nerve damage. This person, along with three of those with BRCA1 and BRCA2 mutations, had no family history of the cancers related to these genes.

This demonstrates that theres fairly high frequency of useful information that one can gain from the whole exome or whole genome, said Robert Nussbaum, chief of the division of medical genetics at the University of California, San Francisco.

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Genome-Wide Search May Provide Early-Warning System

Public release date: 14-Jun-2012 [ | E-mail | Share ]

Contact: Mary Rice mary.rice@riceconseil.eu European Society of Human Genetics

The use of genetic testing to establish racial origins for political purposes is not only scientifically foolish, but also unethical and should be condemned, the European Society of Human Genetics (ESHG) said today (Thursday June 14). The society, which promotes research in basic and applied human and medical genetics and ensures high standards in clinical genetic practice, said that the use by a member of parliament from the Hungarian far-right Jobbik party of a genetic test to attempt to prove his 'ethnic purity' was ethically unacceptable.

The company Nagy Gn scanned 18 positions in the MP's genome for variants that it said were characteristic of Roma and Jewish ethnic groups and concluded that Roma and Jewish ancestry could be ruled out.

Professor Joerg Schmidtke, President of ESHG, said on behalf of the Executive Board: "This is a gross distortion of the values of genetic testing, which is intended to be used to diagnose disease rather than to claim racial purity. In addition, the test proves nothing; it is impossible to deduce someone's origins from testing so few places in the genome. I am sure that clinical geneticists worldwide will join me in condemning this scandalous abuse of a technology that was developed to help the sick, rather than to promote hatred."

Professor Bla Melegh, President of the Hungarian Society of Human Genetics added: "We were shocked to hear that a laboratory authorised to carry out genetic analysis for diagnostic purposes carried out such a test. Not only does it not serve a diagnostic purpose, but it has been used to create tension between people of different ethnic origins. We are asking the Hungarian government to prosecute the company concerned under the 2008 law on genetics, and to take action to ensure that similar abuse of genetic testing cannot take place in our country in future."

The 2012 European Genetics Conferences in Nuremberg, Germany (June 23-26) will provide a further opportunity for the ESHG to denounce such an unethical perversion of genetic science, and insist, at the same time, on the importance of genetic testing in the medical or scientific context of good practice.

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European geneticists condemn use of testing to establish 'racial purity'

13-06-2012 13:10 Why do humans get sick? Why are diabetes and obesity on the rise? Why have cancer and cardiovascular diseases become so prevalent? Is there a mismatch between the environments in which we evolved and environments in which we now live? Why did cholera, measles, mumps, whooping cough, and malaria become epidemic diseases? Why has evolution failed to make us immune to disease? Based in cutting-edge genetic and evolutionary biology research conducted at Rutgers, "Genetics, Evolution, and Human Health" explores what science can tell us about what it means to be human and why humans get sick. How can genetics be used and misused? What social, political, environmental, and medical changes would be required to improve human health in the 21st century? This course is particularly recommended for students who intend to pursue majors or minors in anthropology, criminal justice, ecology, geography, history, philosophy, political science, psychology, public health, public policy, and sociology and it is of interest to students in the biological sciences and chemistry. For more information visit:

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Spotlight on Terry McGuire - Genetics, Evolution, and Human Health - Video

The Bonobo Genome and Rewinding the Tape of Life

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The Bonobo Genome and Rewinding the Tape of Life

Public release date: 13-Jun-2012 [ | E-mail | Share ]

Contact: Jennifer Kelly jkelly@forsyth.org 617-892-8602 Forsyth Institute

Forsyth scientists have made a significant contribution to the Human Microbiome Project (HMP), an initiative which has defined the normal bacterial makeup of the human body for the first time in history. As leading experts in oral and craniofacial microbiology, the Forsyth team provided three of the four body site experts for the mouth and oralpharyngeal surfaces.

The Forsyth Scientists from the Department of Molecular Genetics are Floyd Dewhirst, DDS., Ph.D., Senior Member of Staff; Katherine P. Lemon, M.D., Ph.D., Assistant Member of Staff; and Jacques Izard, Ph.D., Assistant Member of Staff. They provided key advice on the biology of the oral cavity, expert analysis of the complex microbiome, and advice on the methodology.

In a series of coordinated scientific reports to be published on June 14, 2012, in Nature and several journals in the Public Library of Science (PLoS), some 200 members of the Human Microbiome Project (HMP) Consortium from nearly 80 multidisciplinary research institutions report on five years of research. The HMP, launched in 2007, received $153 million from the NIH Common Fund, a trans-NIH initiative that finances high-impact, large-scale research. Over 240 adults were carefully screened and phenotyped before sampling one to three times at 15 (male) or 18 (female) body sites using a common sampling protocol.

Microbes inhabit just about everywhere in the human body, inside the mouth, living on the skin, in the gut, up the nose, etc. Most microorganisms live in harmony with their human hosts and are essential for humans to thrive, although a few sometimes cause illness. Studying human-bacteria interactions could lead to new ways to monitor human health status and to new methods for preventing or treating oral and systemic human diseases. The Forsyth efforts are supported by the National Institute of Dental and Craniofacial Research, NIH.

"Like 15th century explorers describing the outline of a new continent, HMP researchers employed a new technological strategy to comprehensively define, for the first time, the normal microbial makeup of the human body," said NIH Director Francis S. Collins, M.D., Ph.D. "HMP created a remarkable reference database by using genome sequencing techniques to directly detect microbes in healthy volunteers. This lays the foundation for accelerating infectious disease research previously impossible without this community resource."

HMP researchers also reported that this plethora of microbes contribute more genes responsible for human survival than humans themselves. Where the human genome contains some 22,000 protein-coding genes that carry out metabolic activities, researchers estimate that the microbiome contributes some 8 million unique protein-coding genes or 360-times more bacterial genes than human genes.

After NIH launched HMP in December 2007, the International Human Microbiome Consortium (IHMC) formed in 2008 to represent funding organizations (including NIH) and scientists from around the world interested in studying the human microbiome. The consortium has coordinated research to avoid duplication of effort and insure rapid release of molecular and clinical data sets. It also has developed common data quality standards and tools to share research results.

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Forsyth Team collaborates with Human Microbiome Project

Public release date: 13-Jun-2012 [ | E-mail | Share ]

Contact: jlaloup@plos.org jlaloup@plos.org 415-624-1220 Public Library of Science

The healthy adult body hosts ten times as many microbial cells as human cells, including bacteria, archaea, viruses, and eukaryotic microbes resident on nearly every body surface. The metagenome carried collectively by these microbial communities dwarfs the human genome in size. For the first time, a consortium of researchers has mapped the full community of microbes that inhabit various parts of the healthy body.

The new PLoS Human Microbiome Project Collection encompasses genome sequencing research that shows reference data for microbes living with healthy adults. The studies were conducted by individual groups that make up the Human Microbiome Consortium and include publications from PLoS ONE, PLoS Computational Biology and PLoS Genetics.

The manuscripts within the Collection provide a comprehensive baseline of the microbial diversity at 18 different human body sites. This includes reference genomes of thousands of host-associated microbial isolates, 3.5 terabases of metagenomic sequences, assemblies, and metabolic reconstructions, and a catalogue of over 5 million microbial genes.

A number of studies also look at the relationships between the microbiome and the host, and how these interactions relate to health. They describe the shifts in the composition of various microbial communities as they relate to a number of specific conditions: the gut microbiome and Crohn's disease, ulcerative colitis and esophageal adenocarcinoma; the skin microbiome and psoriasis, and atopic dermatitis and immunodeficiency; urogenital microbiome and reproductive and sexual history and circumcision and a number of childhood disorders, including pediatric abdominal pain and intestinal inflammation, and neonatal necrotizing enterocolitis.

Accompanying this Collection are two articles published in the journal Nature by the Human Microbiome Project Consortium. The results of these two papers provide the foundation for the research published in the Human Microbiome Project Collection.

"Recently developed genome sequencing methods now provide a powerful lens for looking at the human microbiome," said Eric D. Green, M.D., Ph.D., director of the National Human Genome Research Institute, which managed HMP for NIH. "The astonishing drop in the cost of sequencing DNA has made possible the kind of large survey performed by the Human Microbiome Project."

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Collection Citation: PLoS Collections: The Human Microbiome Project Collection (2012) http://www.ploscollections.org/hmp

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Announcing the Human Microbiome Project Collection

U.S. researchers say they've created genetically modified mosquitoes incapable of transmitting the deadly disease malaria to humans.

IRVINE, Calif., June 12 (UPI) -- U.S. researchers say they've created genetically modified mosquitoes incapable of transmitting the deadly disease malaria to humans.

Scientists at the University of California, Irvine, say the genetic option of breeding mosquitoes unable to infect people with the malaria parasite could help curb one of the world's most pressing public health issues.

Researchers at the Irvine campus, along with colleagues from the Pasteur Institute in Paris, have produced a model of the Anopheles stephensi mosquito -- a major source of malaria in India and the Middle East -- that impairs the development of the malaria parasite so it cannot transmit the disease through their bites.

"Our group has made significant advances with the creation of transgenic mosquitoes," UCI microbiology Professor Anthony James said in a university release Tuesday.

"But this is the first model of a malaria vector with a genetic modification that can potentially exist in wild populations and be transferred through generations without affecting their fitness."

The genetic modification can be applied to the dozens of different mosquito types that harbor and transmit the Plasmodium falciparum parasite, researchers said.

In the genetically modified mosquitoes antibodies are released that render the parasite harmless to others, they said.

"We see a complete deletion of the infectious version of the malaria parasite," James said. "This blocking process within the insect that carries malaria can help significantly reduce human sickness and death."

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Genetics used as weapon against malaria

Newswise BETHESDA, MD June 12, 2012 -- Its hard to imagine that a zebrafish, a small tropical freshwater fish that is often found in home aquariums, could help scientists solve complicated problems about melanoma, a type of human skin cancer. But zebrafish and other small organismssuch as fruit flies, roundworms, yeast and mice are helping research scientists uncover how human cancersskin, colon, breast and othersbegin, invade, spread and can be treated. Many of the top scientists in the model organism and human cancer fields will be meeting to discuss their research at the Genetics Society of Americas (GSAs) Model Organisms to Human Biology (MOHB): Cancer Genetics Meeting on June 17-20, 2012 at the Omni Shoreham Hotel in Washington, D.C.

Nature reuses the same building blocks to construct organisms as different as yeasts, worms, flies, fish, mice, and humans. Key aspects of most human disorders, including cancer, can be modeled in these organisms, said Phil Hieter, PhD, (University of British Columbia), president of the GSA. This MOHB meeting is occurring at a very exciting time when the genetic mutations that cause cancer are being discovered at an unprecedented pace. This meeting will showcase the power of the multi-organismal approach to understanding gene function relevant to disease and will stimulate cross-talk and collaboration between cancer researchers and basic scientists, Dr. Hieter added.

Model organisms are used to study complex diseases like cancer because of their short life cycles and well-understood biology, which enable researchers to dissect the disease, conduct experiments, and even try out treatments in ways that wouldnt be possible in people.

We study model organisms to improve the health of people, said Judith Greenberg, PhD, Acting Director of the National Institute of General Medical Sciences at the National Institutes of Health. They enable us to identify the root causes of disease, track disease progression, and test out potential therapies. These days, as scientists sort through the ever increasing wealth of genomic data, model organisms are more important than ever to help us understand the molecular underpinnings of cancer and other complex diseases. Several model organisms are featured in talks at the GSA MOHB: Cancer Genetics Meeting, suggesting the broad application of different experimental systems to explore human disease. In addition to the zebrafish mentioned above, other model organisms featured include: The tiny worm, Caenorhabditis elegans, which exhibits single cell movements that mimic the migration of a tumor cell in humans. Fruit flies with the same set of sequential mutations that causes cancer in human colons. Mice with isolated tumor cells in which chromosomes are lost and gained, and cancer-regulating genes turned on and off in addition to epigenetic or outside the genome influences that start and propel a cancer. Yeast with telomereschromosome tipsthat fail to whittle down in cancer cells and consequently enable the cells to ignore the clocks that normally regulate cell division.

Collectively, model organisms provide a unique window to the mechanistic heart of cancer: the loss of normal cell division controls, failed response to DNA damage, telomeres which are too long, and profound genomic instability. Some model organisms have their own version of human cancer cell mutations naturally, while others are modified to bear human genes. In addition, by using model organisms to study cancer, researchers are able to deftly separate genetic causes from environmental ones within a short timeframe since the life cycle of these organisms is considerably shorter than those of humans.

In addition to the informative talks like the ones mentioned above, GSAs MOHB: Cancer Genetics Meeting features keynote addresses from Bert Vogelstein, MD (Johns Hopkins University) on cancer genomes and their implications for basic and applied research; Eric S. Lander, PhD (Broad Institute of MIT and Harvard and co-chair of the Presidents Council of Advisors on Science & Technology) on the secrets of the human genome, and Angelika Amon, PhD (MIT) , on the consequences of aneuploidy, which is a different number of chromosomes than the normal set.

The meeting, which runs from Sunday, June 17 to Wednesday, June 20, 2012, is intended to bring together basic scientists conducting research using model organisms with those engaged in human cancer research more directly. Registration is available online until June 12 and onsite during the meeting. For more information, see the website at http://www.mohb.org/2012/. Media interested in covering the meeting should contact Phyllis Edelman, pedelman@genetics-gsa.org. ABOUT THE MODEL ORGANISM TO HUMAN BIOLOGY MEETING: The GSA MOHB Meeting has been held every other year since 2006. The GSA Board of Directors developed this meeting to enable basic research scientists studying genetic diseases in model organisms and scientists studying these diseases in humans to have a forum for discussion of their findings and to forge collaborative investigations.

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 and an online, open-access j, G3: Genes|Genomes|Genetics. 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.

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Model Organisms Help Researchers Learn About Human Cancers

Models will facilitate a better understanding of the disease and aid in therapeutic development.Sioux Center, Iowa (PRWEB) June 11, 2012 CHDI Foundation, Inc. and Exemplar Genetics today announced a collaborative research agreement to create multiple miniature swine models of Huntington’s disease (HD), a devastating disorder for which there are currently no effective treatments. Models that ...

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Exemplar Genetics and CHDI Foundation to Create Large Animal Models of Huntington’s Disease

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/3lsg2r/forwardtime_popul) has announced the addition of John Wiley and Sons Ltd's new book "Forward-Time Population Genetics Simulations: Methods, Implementation, and Applications" to their offering.

The only book available in the area of forward-time population genetics simulationsapplicable to both biomedical and evolutionary studies

The rapid increase of the power of personal computers has led to the use of serious forward-time simulation programs in genetic studies. Forward-Time Population Genetics Simulations presents both new and commonly used methods, and introduces simuPOP, a powerful and flexible new program that can be used to simulate arbitrary evolutionary processes with unique features like customized chromosome types, arbitrary nonrandom mating schemes, virtual subpopulations, information fields, and Python operators.

The book begins with an overview of important concepts and models, then goes on to show how simuPOP can simulate a number of standard population genetics modelswith the goal of demonstrating the impact of genetic factors such as mutation, selection, and recombination on standard Wright-Fisher models. The rest of the book is devoted to applications of forward-time simulations in various research topics.

Key Topics Covered:

1. Basic concepts and models

2. Simulation of population genetics models

3. Ascertainment bias in population genetics

4. Observing properties of evolving populations

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Research and Markets: Forward-Time Population Genetics Simulations: Methods, Implementation, and Applications

June 5, 2012

Brett Smith for redOrbit.com

Despite inhabiting the same waters, two populations of Great White sharks living in the coastal waters of Australia are genetically distinct, according to a new study published in the journal Marine Ecology Progress Series.

The two groups of Great Whites, or white sharks, are separated by the Bass Strait, a stretch of water between the Australian mainland and Tasmania to the south. The research team, led by Dean Blower from the University of Queensland, used genetic tests from 97 shark tissue samples dating back to 1989 confirmed this geographical divide.

The genetic makeup of white sharks west of Bass Strait was different from those on the eastern seaboard of Australia despite the lack of any physical barrier between these regions, said Professor John Pandolfi, a Chief Investigator at the University of Queensland.

Our tagging and tracking showed that white sharks travel thousands of kilometers, said Barry Bruce, a lead study researcher from the Commonwealth Scientific and Industrial Research Organization (CSIRO).

But sharks tagged and tracked off eastern Australia did not go west of Bass Strait, and sharks tagged off Western and South Australia rarely went east. When they did they often returned, so we started to wonder whether there was more than one breeding population.

Now we know that while white sharks across Australia can mix, the intriguing thing is that they seem to return to either east or western regions to breed, Bruce said.

While previous work by other international research teams have identified separate genetic populations of white sharks across ocean basins, this is the first time such segregation has been found at the regional level.

The Bass Strait, which is named after George Bass who sailed around Tasmania in the late 18th century, measures 240 km across and averages about 50 meters deep. The shallow waters have been known to be notoriously rough and have taken down many sailing vessels. The strait has even been linked to a Bermuda Triangle-type mysticism at times.

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Australian Great White Shark Populations Separated By Genetics

Public release date: 6-Jun-2012 [ | E-mail | Share ]

Contact: Fran Yates fyates@faseb.org 301-634-7109 Federation of American Societies for Experimental Biology

Bethesda, MD FASEB MARC (Maximizing Access to Research Careers) Program has announced the travel award recipient for the 2012 Genetics Society of America (GSA) Model Organisms to Human Biology-Cancer Genetics Meeting in Washington, DC from June 17-20, 2012. These awards are meant to promote the entry of underrepresented minority students, postdoctorates and scientists into the mainstream of the basic science community and to encourage the participation of young scientists at the 2012 GSA Model Organisms to Human Biology-Cancer Genetics Meeting.

Awards are given to poster/platform presenters and faculty mentors paired with the students/trainees they mentor. This year MARC conferred 1 award totaling $1,650.

The FASEB MARC Program is funded by a grant from the National Institute of General Medical Sciences, National Institutes of Health. A primary goal of the MARC Program is to increase the number and competitiveness of underrepresented minorities engaged in biomedical and behavioral research.

The following has been selected to receive a FASEB MARC Travel Award for her poster/platform presentation:

Shanelle Joseph, Southern University and A&M College [EMS member]

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FASEB is composed of 26 societies with more than 100,000 members, making it the largest coalition of biomedical research associations in the United States. Celebrating 100 Years of Advancing the Life Sciences in 2012, FASEB is rededicating its efforts to advance health and well-being by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

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MARC travel award announced for the 2012 GSA Model Organisms to Human Biology-Cancer Genetics Meeting

WEDNESDAY, June 6 (HealthDay News) -- Researchers report they have decoded the entire genome of a fetus using only a blood sample from the mother and a saliva sample from the father.

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Entire Genome of Human Fetus Deciphered

SALT LAKE CITY, June 6, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics announced today that the Company is the honorable recipient of the 2012 Charles R. Smart Visionary Award from the American Cancer Society's Salt Lake City office, a part of the Great West Division. This award is presented annually at the Society's Legacy & Leadership event to recognize organizations that have made extraordinary efforts in the fight against cancer.

Myriad and its employees are dedicated to saving lives and improving the quality of life of patients with cancer. In addition to its life-saving molecular diagnostic tests, Myriad is a local community leader with the American Cancer Society in the fight against cancer. The Company and its employees have played an important role in events to benefit the American Cancer Society including the Hope Gala, Making Strides Against Breast Cancer and Relay for Life.

"We are deeply honored to receive the Charles R. Smart Visionary award," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics. "Myriad and the American Cancer Society share the goal of improving the quality of life for patients with cancer. Everyday our activities are guided by this mission and therefore we have been pleased to offer our financial support, leadership involvement and volunteer participation to this cause."

The late Dr. Charles R. Smart, a lifelong resident of Utah, was a pioneer in the study of cancer. Dr. Smart spent more than 35 years focused on establishing computerized cancer research and was the founder of the Utah Cancer Registry, a population based registry that has been doing systematic cancer surveillance in the state since 1966.

About Myriad Genetics

Myriad Genetics, Inc., an internationally recognized leader in molecular diagnostics, is dedicated to making a difference in patient's 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, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. 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 Company's strategic directives under the caption "About Myriad Genetics". These "forward-looking statements" are based on management's current 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 set forth in or implied by forward-looking statements. These risks and uncertainties 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; the risk that we may be unable to expand into new markets outside of the United States; 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 and any future products are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with manufacturing our products or operating our laboratory testing facilities; risks related to public concern over 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 healthcare payment systems; risks related to our ability to obtain new corporate collaborations 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 acquire; the development of competing tests and services; the risk that we or our licensors may be unable to protect the proprietary technologies underlying our tests; the risk of patent-infringement and invalidity claims or challenges of our patents; 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 in 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.

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Myriad Genetics Receives the Charles R. Smart Visionary Award From the American Cancer Society(R)

ScienceDaily (June 4, 2012) In the first comprehensive census of human cells' export workers, scientists at EMBL Heidelberg, found an unexpected variety of genes involved in transporting molecules to the cell membrane and beyond.

Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have conducted the first comprehensive census of human cells' export workers. In a study published online June 3 in Nature Cell Biology, they found an unexpected variety of genes involved in transporting molecules to the cell membrane and beyond.

Using a combination of genetics and sophisticated microscopy, Rainer Pepperkok and colleagues systematically silenced each of our 22 000 genes, and observed to what extent this affected the cell's ability to transport a protein. They found that 15% of human genes somehow influence this transport network -- known as the secretory pathway -- including genes that provide a link to other events in and around the cell. Their findings suggest, for instance, that our cells evolved a complex strategy for adapting to changes in their environment. When a cell senses a growth factor called EGF in its surroundings, a protein on the cell membrane aptly named the EGF receptor is taken from the membrane into the cell, starting a chain reaction that ultimately leads the cell to divide, and during which the EGF receptor is degraded. The EMBL scientists have now found that the process also triggers an increase in activity at the early steps of the secretory pathway to transport newly synthesised EGF receptor back to the membrane, where it will be needed again.

Next, the scientists would like to tease out how mechanisms like sensing the environment, controlling genes and transmitting signals are connected to transporting molecules to the membrane, in an effort to better understand how cells work as whole.

The study's data is freely available to the scientific community at http://www.mitocheck.org, alongside results of previous screens focused on essential cellular functions like cell division. Pepperkok is working with Jan Ellenberg at EMBL in Heidelberg and Alvis Brazma at EMBL's European Bioinformatics Institute (EMBL-EBI) in Hinxton, UK, to develop a public repository for such image-based screens, which others will be able to turn to when studying the function of human genes.

The work was carried out by Jeremy Simpson, who is now at University College Dublin, Ireland.

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The above story is reprinted from materials provided by European Molecular Biology Laboratory (EMBL), via AlphaGalileo.

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Export extravaganza in human cells

AMES, Iowa, June 4, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (Nasdaq:NLNK - News) announces that its HyperAcute(R) Pancreas (algenpantucel-L) Immunotherapy will be featured today in a poster presentation (abstract number 4049) at the American Society of Clinical Oncology (ASCO) 2012 Annual Meeting being held in Chicago, IL. The abstract entitled "Addition of algenpantucel-L immunotherapy to standard of care (SOC) adjuvant therapy for pancreatic cancer" will be shown in S Hall A2 from 8:00AM to 12:00PM . The study results show 37%, 59% and 121% improvement in 1-, 2- and 3-year survival, respectively, as compared to standard-of-care.

Dr. Jeffrey M. Hardacre, the study's Principal Investigator, from the University Hospitals Seidman Cancer Center and Case Western Reserve University, Cleveland, OH stated, "As a surgeon who regularly treats patients suffering from pancreatic cancer, and being accustomed to the dismal prognosis for these patients, I am highly encouraged with the exceptional overall survival data from this study."

"Given that the primary endpoint in our pivotal Phase 3 study targeting similar patients is overall survival, this data supports our cautious optimism," said Dr. Nicholas Vahanian, President and Chief Medical Officer of NewLink Genetics.

Key data from the 69 patient Phase 2 algenpantucel-L trial demonstrated:

The primary endpoint of the study, 12-month disease free survival (DFS), was 62%. The median DFS was 14.1 months. Subgroup analysis showed that patients receiving 300 million cells/dose had a 12-month DFS of 81%, while those receiving 100 million cells/dose had a 12-month DFS of 51% (p=0.02, Fisher's Exact). Prognostic criteria did not significantly differ between the two groups.

Overall 12-month survival was 86%. The predicted 12 month overall survival in our study was 63%. Subgroup analysis showed that patients receiving 300 million cells/dose had an overall 12-month survival of 96%, while those receiving 100 million cells/dose had an overall 12-month survival of 79% (p=0.053, Fisher's Exact). Two-year overall survival in our study was 51% with a predicted survival of 32% and 3-year overall survival was 42% with a predicted survival of 19%. Predicted survivals were computed using prognostic factors gathered for each patient and calculated using a nomogram published by Brennan et al from Memorial Sloan Kettering Cancer Center. Over the 33 month median follow up period of the study, the percentage improvement in overall survival rate compared to nomogram analysis increased over time. These data are consistent with recent studies of active immunotherapies (Sipuleucel-T and Ipilimumab) in that immune benefits appear greater in some patients over time.

Prominent eosinophil responses have been observed with the majority of patients demonstrating measurable increases in peripheral blood eosinophilia. In addition to eosinophilic infiltrates at the injection site in all tested patients, 70% developed eosinophilia, with 30% showing persistent eosinophilia for up to 2 years.

The HyperAcute(R) Pancreas immunotherapy product candidate, also referred to as algenpantucel-L, demonstrated good tolerability and a favorable safety profile with no grade four adverse events considered attributable to the immunotherapy. The predominant adverse events related to the immunotherapy were grade one or two injection site reactions, all treated with conservative local therapies.

Anecdotally, three patients with cancer recurrence after receiving algenpantucel-L obtained complete radiographic responses with the use of subsequent chemotherapy. As of May 16, 2012, all three patients remain in remission with no evidence of disease for periods ranging from six to 36 months. "We are presenting data from three different HyperAcute products at ASCO this year and each of these has generated intriguing data that provide insights into the activity and mechanisms associated with the treatment of patients with HyperAcute immunotherapies," stated Dr. Charles Link, CEO and Chief Scientific Officer of NewLink Genetics. "These observations include survival advantages that improve over time, objective responses, novel immunological findings and chemosensitization."

About the Phase 2 Study

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NewLink Genetics Reports Two- and Three-Year Overall Survival Data From Its Phase-2 HyperAcute(R) Pancreas ...

SANTA MONICA, Calif. & BOTHELL, Wash.--(BUSINESS WIRE)--

Agensys, Inc., an affiliate of Tokyo-based Astellas Pharma Inc., and Seattle Genetics, Inc. (SGEN) today announced interim data from a phase I clinical trial evaluating ASG-5ME for the treatment of castration-resistant prostate cancer (CRPC). ASG-5ME is an antibody-drug conjugate (ADC) targeting the SLC44A4 antigen that is being co-developed by both companies for the treatment of solid tumors. The data are being presented at the American Society of Clinical Oncology (ASCO) annual meeting being held June 1-5, 2012 in Chicago, IL.

SLC44A4 is an attractive target in prostate cancer and is present in the majority of patients with both localized and metastatic disease, said Leonard Reyno, M.D., Senior Vice President and Chief Medical Officer of Agensys. The current Phase I data demonstrates the tolerability of this antibody drug conjugate and further evaluation of safety and antitumor activity in patients with castration resistant prostate cancer is ongoing.

It is encouraging to observe these preliminary data with ASG-5ME in prostate cancer, a disease for which late-stage patients need additional therapeutic options, said Jonathan Drachman, M.D., Senior Vice President, Research and Translational Medicine of Seattle Genetics. In addition to prostate cancer, our two companies are continuing to evaluate the potential use of ASG-5ME in other solid tumor indications. In parallel, we are collaborating with Agensys to co-develop ASG-22ME, an ADC targeting Nectin-4 for solid tumors.

Phase 1 trial of ASG-5ME in metastatic castration-resistant prostate cancer (CRPC) (Abstract #4568) ASG-5ME is being evaluated in a single-agent phase I clinical trial to determine the maximum tolerated dose (MTD) and to assess the safety, pharmacokinetic profile and antitumor activity of escalating doses of ASG-5ME. At the time of data analysis, 26 patients were enrolled. The median age of the patients was 69.5 years and the median baseline prostate-specific antigen (PSA) level was 82.25.

Key findings, presented by Dr. Michael Morris from Memorial Sloan Kettering Cancer Center in New York, NY, and clinical investigator on the study include:

The phase I trial is ongoing, with enrollment to two expansion cohorts in chemotherapy nave and chemotherapy exposed CRPC patients planned.

Seattle Genetics and Agensys recently completed enrollment in a phase I pancreatic cancer trial of ASG-5ME dosed weekly. The companies plan to evaluate ASG-5ME in patients with gastric cancer based on preclinical expression data.

About ASG-5ME ASG-5ME is an ADC composed of a fully human antibody directed to SLC44A4, a solute carrier antigen family member identified by Agensys to be overexpressed in epithelial cancers, including more than 80 percent of samples derived from patients with prostate, pancreatic and gastric cancers. The antibody is attached to monomethyl auristatin E (MMAE) via an enzyme-cleavable linker using Seattle Genetics proprietary technology. The ADC is designed to be stable in the bloodstream, but to release MMAE upon internalization into SLC44A4-expressing tumor cells, resulting in targeted cell-killing.

Seattle Genetics and Agensys are co-developing and will globally co-commercialize and share profits on a 50:50 basis for ASG-5ME and ASG-22ME. Seattle Genetics also has an option for 50:50 cost and profit-sharing of a third ADC program at the time of investigational new drug submission.

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Agensys and Seattle Genetics Announce Interim Phase I Data from ASG-5ME Clinical Trial for Prostate Cancer

The IPO said it was changing its approach to the consideration for patentability of inventions in the human genetics field following a recent interpretation of EU laws by the European Court of Justice (ECJ).

In October last year the ECJ ruled that, under the terms of the EU Biotech Directive, inventions are said to have used human embryos if they require human embryos to be destroyed at any stage, including "long before the implementation of the invention", and even if the claims for the invention do not mention any use of human embryos at all, the IPO said.

The Biotech Directive states that an element isolated from the human body can be protected by a patent even if the structure of that element is identical to that of a natural element and its industrial application is disclosed in the patent. The Biotech Directive further states that "uses of human embryos for industrial or commercial purposes" shall be considered unpatentable.

The IPO updated its guidance on inventions involving human embryonic stem cells on the basis of the ECJ's findings. It said that because the UK's Patents Act implements the Biotech Directive, that the ECJ's interpretation of provisions of that Directive was binding on it.

"The Office practice will now recognise that where the implementation of an invention requires the use of cells that originate from a process which requires the destruction of a human embryo, the invention is not patentable according to [the Patents Act]," it said. "For example, where the implementation of the invention requires the use of a human embryonic stem cell line the establishment of which originally required the destruction of a human embryo, the invention is not patentable."

The IPO said that inventions that involve human stem cells that do not emanate from human embryos can still be patented, providing they "satisfy the normal requirements for patentability" and that the ECJ's ruling had also "confirmed that inventions that are for therapeutic or diagnostic purposes that are applied to and useful to the human embryo are not excluded from patentability."

The ECJ had been ruling on the meaning of the term 'human embryo' in its case last year. It said that any organism that is "capable of commencing the process of development of a human being" should be considered a human embryo and gave examples where both fertilised and non-fertilised human ovums would be said to constitute human embryos. It also left it to national courts to decide "in light of scientific developments" whether a stem cell obtained at the blastocyst stage, which is a very early stage of development, constitutes a human embryo within the meaning of the Biotech Directive.

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Patents will not be granted to inventions that result from human embryo destruction, IPO says

Public release date: 30-May-2012 [ | E-mail | Share ]

Contact: NIDA Press Team media@nida.nih.gov 301-443-6245 NIH/National Institute on Drug Abuse

Genetics can help determine whether a person is likely to quit smoking on his or her own or need medication to improve the chances of success, according to research published in today's American Journal of Psychiatry. Researchers say the study moves health care providers a step closer to one day providing more individualized treatment plans to help patients quit smoking.

The study was supported by multiple components of the National Institutes of Health, including the National Institute on Drug Abuse (NIDA), the National Human Genome Research Institute, the National Cancer Institute, and the Clinical and Translational Science Awards program, administered by the National Center for Advancing Translational Sciences.

"This study builds on our knowledge of genetic vulnerability to nicotine dependence, and will help us tailor smoking cessation strategies accordingly," said NIDA Director Nora D. Volkow, M.D. "It also highlights the potential value of genetic screening in helping to identify individuals early on and reduce their risk for tobacco addiction and its related negative health consequences."

Researchers focused on specific variations in a cluster of nicotinic receptor genes, CHRNA5-CHRNA3-CHRNB4, which prior studies have shown contribute to nicotine dependence and heavy smoking. Using data obtained from a previous study supported by the National Heart Lung and Blood Institute, researchers showed that individuals carrying the high-risk form of this gene cluster reported a 2-year delay in the median quit age compared to those with the low-risk genes. This delay was attributable to a pattern of heavier smoking among those with the high risk gene cluster. The researchers then conducted a clinical trial, which confirmed that persons with the high-risk genes were more likely to fail in their quit attempts compared to those with the low-risk genes when treated with placebo. However, medications approved for nicotine cessation (such as nicotine replacement therapies or bupropion) increased the likelihood of abstinence in the high risk groups. Those with the highest risk had a three-fold increase in their odds of being abstinent at the end of active treatment compared to placebo, indicating that these medications may be particularly beneficial for this population.

"We found that the effects of smoking cessation medications depend on a person's genes," said first author Li-Shiun Chen, M.D., of the Washington University School of Medicine, St. Louis. "If smokers have the risk genes, they don't quit easily on their own and will benefit greatly from the medications. If smokers don't have the risk genes, they are likely to quit successfully without the help of medications such as nicotine replacement or bupropion."

According to the Centers for Disease Control and Prevention, tobacco use is the single most preventable cause of disease, disability, and death in the United States. Smoking or exposure to secondhand smoke results in more than 440,000 preventable deaths each year -- about 1 in 5 U.S. deaths overall. Another 8.6 million live with a serious illness caused by smoking. Despite these well-documented health costs, over 46 million U.S. adults continue to smoke cigarettes.

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The study can be found at: http://ajp.psychiatryonline.org/article.aspx?articleID=1169679. For information on tobacco addiction, go to: http://www.drugabuse.gov/drugs-abuse/tobacco-addiction-nicotine. For more information on tools and resources to help quit smoking, go to: http://www.smokefree.gov/.

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Odds of quitting smoking affected by genetics