DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/x5ds4f/the_year_in_human) has announced the addition of John Wiley and Sons Ltd's new book "The Year in Human and Medical Genetics: Inborn Errors of Immunity II" to their offering.

The genetic dissection of human primary immunodeficiency is expanding at full speed, in at least two directions. Some investigators pursue the dissection of well-known clinical phenotypes, for which the count of genetic etiologies seems to be endless, whereas others begin the search for inborn errors underlying new phenotypes, infectious and otherwise. The field of primary immunodeficiency is also expanding in other ways, with new therapeutic approaches, and with the care of patients in regions of the world where these diseases were unheard of less than a decade ago. The volume provides an overview of the field of medical genetics and its progress in 2011.

This volume focuses on new developments in primary immunodeficiencies" (PIDs), insights into PID pathophysiology, and PIDs in India and the Middle East. Volume I opens with a dialog between the volume editors on the definition of PIDs; additional papers in this volume focus on PIDs in Latin America, Eastern and Central Europe, North Africa, Turkey, Asia, Iran, and the South Pacific.

For more information visit http://www.researchandmarkets.com/research/x5ds4f/the_year_in_human

Source: John Wiley and Sons Ltd

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Research and Markets: The Year in Human and Medical Genetics: Inborn Errors of Immunity II

PHILADELPHIA Douglas C. Wallace, PhD, professor of Pathology and Laboratory Medicine, at the Perelman School of Medicine, University of Pennsylvania, is the recipient of the 2012 Genetics Prize of the Gruber Foundation. Wallace is a pioneering genetics researcher who founded the field of mitochondrial genetics in humans. He is also the director of the Center for Mitochondrial and Epigenomic Medicine at The Children's Hospital of Philadelphia.

Wallace is being honored with this prestigious international award for his groundbreaking achievements in understanding the role of mitochondriathe "power plants" of cellsin the development of disease and as markers for human evolution. He is also being honored for training and inspiring numerous pre- and postdoctoral students who have gone on to have distinguished careers of their own.

Wallace will receive the award on November 9 at the annual meeting of the American Society of Human Genetics in San Francisco. The Gruber Foundation, now based at Yale University, announced the Genetics Prize on June 28. The Foundation's Genetics Prize annually honors leading scientists for groundbreaking contributions to genetics research. The Peter and Patricia Gruber Foundation's International Prize Program honors contemporary individuals in the fields of Cosmology, Genetics, Neuroscience, Justice and Women's Rights, whose groundbreaking work provides new models that inspire and enable fundamental shifts in knowledge and culture. The Gruber Foundation's Genetics Prize, a gold medal and an unrestricted $500,000 cash award for fundamental insights in the field of genetics, was established in 2001.

"Douglas Wallace's contributions to our understanding of mitochondrial genetics have changed the way human and medical geneticists think about the role of mitochondria in human health and disease." said Elizabeth Blackburn, chair of the Selection Advisory Board to the Prize. Blackburn is the 2006 Gruber Genetics Prize laureate and shared the 2009 Nobel Prize in Physiology and Medicine.

Wallace began his research on mitochondrial biology 40 years ago, at a time when few people thought the study of mitochondria and its DNA (mtDNA) would have any significant applications for clinical medicine. In the late 1970s, Wallace demonstrated that human mtDNA is inherited solely through the mother. Using maternal inheritance as a guide, Wallace identified the first inherited mtDNA disease -Leber's hereditary optic neuropathy - and subsequently linked mtDNA mutations to a wide range of clinical symptoms, including deafness, neuropsychiatric disorders, cardiac and muscle problems, and metabolic diseases such as diabetes. Wallace also showed that mtDNA mutations accumulate in human tissue with age, and thus may play a role in age-related diseases, such as heart disease and cancer. In addition, he found that the levels of these age-related mtDNA mutations are higher in the brains of people with certain neurodegenerative diseases, including Alzheimer disease, Parkinson disease, and Huntington disease.

Wallace's research has also made a major contribution to the field of molecular anthropology. Using mtDNA variation, he has reconstructed the origins and ancient migrations of women, tracing all mtDNA lineages back some 200,000 years to a single African origin the so-called mitochondrial Eve.

Wallace holds the Michael and Charles Barnett Endowed Chair in Pediatric Mitochondrial Medicine at Children's Hospital. He is a member of the National Academy of Sciences, as well as the Academy's Institute of Medicine, and is also a member of the American Academy of Arts and Sciences. Wallace joined the Penn Department of Pathology and Laboratory Medicine in 2010 and previously held academic positions at Stanford University, at Emory University, where he chaired the Department of Genetics and Molecular Medicine, and most recently at the University of California Irvine, where he was Director of the Center for Molecular and Mitochondrial Medicine and Genetics.

For more information, read the Gruber Foundation news release.

The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 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 10 hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.

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Douglas Wallace to Receive Gruber Foundation 2012 Genetics Prize

Researchers are hoping to solve more indigenous health problems by overcoming barriers to genetic research in Aboriginal communities.

IT comes as the first research in almost a decade investigating genetic causes of disease in Aboriginal people is set to be released, after widespread opposition to the practice stymied research projects for years.

Melbourne University anthropologist Emma Kowal said research into genetic associations between diabetes and middle-ear infections would shortly be published, while studies into heart disease, kidney disease and vulval cancer started in the past two years.

Dr Kowal, writing in the Medical Journal of Australia on Monday, said ethical concerns around indigenous genetic research internationally - such as its potential to inadvertently reinforce racial stereotypes - had contributed to Australian projects losing or being rejected funding.

"What we've seen in the past couple of years is that tide of opinion start to reverse," Dr Kowal told AAP.

Dr Kowal, from the university's School of Social and Political Sciences, said Australian guidelines needed to be developed for ethical genetic research in indigenous communities.

Similar guidelines had been developed in Canada, including specific guidance on how biospecimens should be collected, stored and used, Dr Kowal said.

Guidelines should also include how to effectively communicate genetic concepts to Aboriginal communities.

Australia's national research body for Aboriginal and Torres Strait Islander health, the Lowitja Institute, hosted discussions between the research and indigenous communities in the past two years.

As a result, a team of indigenous and non-indigenous researchers and geneticists formed a group to develop the Australian guidelines.

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Genetics 'could improve' Aboriginal health

Newswise Douglas C. Wallace, Ph.D., director of the Center for Mitochondrial and Epigenomic Medicine at The Childrens Hospital of Philadelphia, will receive the 2012 Genetics Prize of The Gruber Foundation. This prestigious international awarda $500,000 prizerecognizes Wallaces pioneering scientific investigations of the wide-ranging role of mitochondria in the development of disease and as markers of human evolution. Mitochondria are the tiny power plants within the cytoplasm of animal and plant cells.

Wallace will receive the award on November 9 at the annual meeting of the American Society of Human Genetics in San Francisco. The Gruber Foundation, now based at Yale University, announced the Genetics Prize on June 28. The Foundations Genetics Prize annually honors leading scientists for groundbreaking contributions to genetics research.

Philip R. Johnson, MD, chief scientific officer at The Childrens Hospital of Philadelphia, acknowledged Wallaces achievements, saying, The Childrens Hospital of Philadelphia Research Institute is privileged to number Douglas Wallace among our research leaders. His commitment to the field of mitochondrial genetics and his pioneering nature embody the mission of research at CHOP, and his research and leadership are shaping the way we approach therapies for genetic disorders previously considered beyond treatment.

Douglas Wallaces contributions to our understanding of mitochondrial genetics have changed the way human and medical geneticists think about the role of mitochondria in human health and disease, said Dr. Elizabeth Blackburn, chair of the Selection Advisory Board to the Prize. Blackburn, who shared the 2009 Nobel Prize in Physiology or Medicine, also received the Gruber Genetics Prize in 2006.

Wallace, who came to The Childrens Hospital of Philadelphia in 2010 to launch the Center for Mitochondrial and Epigenomic Medicine, first achieved prominence in the 1970s as the leader of a research team at Stanford University that defined the genetics of mitochondrial DNA. This DNA resides within each mitochondrion, as distinct from the more familiar nuclear DNA inside chromosomes. His group showed that human mitochondrial DNA is inherited exclusively from the mother.

This discovery, coupled with other findings, allowed the researchers to reconstruct ancient human migration patterns over hundreds of millennia, a major contribution that bridges genetics and anthropology. Wallace and colleagues also have linked mutations in mitochondrial DNA to a broad range of human diseases, including types of blindness, deafness, metabolic disorders such as diabetes, neuropsychiatric conditions, and age-related diseases such as heart disease and cancer.

The Center for Mitochondrial and Epigenomic Medicine at Childrens Hospital researches mitochondrial dysfunction in many clinical problems, and also focuses on preclinical studies relevant to developing therapies for mitochondrial diseases, for which few effective clinical treatments currently exist.

Wallace holds the Michael and Charles Barnett Endowed Chair in Pediatric Mitochondrial Medicine at Childrens Hospital and also is a professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. He is a member of the National Academy of Sciences, the nations premier organization of leading researchers, as well as the Academys Institute of Medicine, and is also a member of the American Academy of Arts and Sciences.

About The Childrens Hospital of Philadelphia: The Childrens Hospital of Philadelphia was founded in 1855 as the nations first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals and pioneering major research initiatives, Childrens Hospital has fostered many discoveries that have benefited children worldwide. Its pediatric research program is among the largest in the country, ranking third in National Institutes of Health funding. In addition, its unique family-centered care and public service programs have brought the 516-bed hospital recognition as a leading advocate for children and adolescents. For more information, visit http://www.chop.edu.

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Dr. Douglas Wallace to Receive Gruber Foundation 2012 Genetics Prize

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

Contact: Sara Hrera media@gruberprizes.org 203-432-6231 Yale University

Douglas C. Wallace, PhD, a pioneering genetics researcher who founded the field of mitochondrial genetics in humans, will receive the 2012 Genetics Prize of The Gruber Foundation. Wallace is being honored with this prestigious international award for his groundbreaking achievements in helping science understand the role of mitochondriathe "power plants" of cellsin the development of disease and as markers for human evolution.

He will receive the award November 9 in San Francisco at the Annual Meeting of the American Society of Human Genetics, where he will also deliver a lecture titled "A Bioenergetic Perspective on Origins, Health, and Disease".

"Douglas Wallace's contributions to our understanding of mitochondrial genetics have changed the way human and medical geneticists think about the role of mitochondria in human health and disease," said Elizabeth Blackburn, chair of the Selection Advisory Board to the Prize. Blackburn is the 2006 Gruber Genetics Prize laureate and shared the 2009 Nobel Prize in Physiology and Medicine.

Wallace began his research on mitochondrial biology 40 years ago, at a time when few people thought the study of mitochondria and its DNA (mtDNA) would have any significant applications for clinical medicine. In the early 1970s, Wallace and associates demonstrated that the mtDNA coded for heritable traits by developing the cybrid transfer technique and showing that chloramphenicol resistance was cytoplasmically inherited. This system permitted them to delineate the characteristics of cytoplasmic genetics. Then in the late 1970s, Wallace demonstrated that the human mtDNA is inherited solely through the mother. Using maternal inheritance as a guide, Wallace identified the first inherited mtDNA disease, Leber's hereditary optic neuropathy (LHON), and subsequently linked mtDNA mutations to a wide range of clinical symptoms, including deafness, neuropsychiatric disorders, cardiac and muscle problems, and metabolic diseases such as diabetes. Wallace also showed that mtDNA mutations accumulate in human tissue with age, and thus may play a role in age-related diseases, such as heart disease and cancer. In addition, he found that the levels of these age-related mtDNA mutations are higher in the brains of people with certain neurodegenerative diseases, including Alzheimer disease, Parkinson disease and Huntington disease.

Wallace's research has also made a major contribution to the field of molecular anthropology. Using mtDNA variation, he has reconstructed the origins and ancient migrations of women, tracing all mtDNA lineages back some 200,000 years to a single African originthe so-called mitochondrial Eve.

"The impact of Doug Wallace's visionary research has been remarkable," said Huda Zoghbi, a member of Selection Advisory Board and the 2011 laureate of the Gruber Neuroscience Prize. "His discovery of the first mtDNA mutations in humans opened up the field of mitochondrial genetics and demonstrated the role of mitochondria in many human diseases. It's an extraordinary legacyand he is richly deserving of this award."

###

By agreement made in the spring of 2011 The Gruber Foundation has now been established at Yale University.

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$500,000 Gruber Foundation Genetics Prize goes to Philadelphia scientist

LEXINGTON, Mass. & NUREMBERG, Germany--(BUSINESS WIRE)--

RainDance Technologies, Inc., the Digital Biology Company, today announced the introduction of its new RainDrop Digital PCR System to the European genetics research market. Attendees of the annual European Society of Human Genetics (ESHG) meeting in Nuremberg, Germany have the opportunity to see demonstrations of the system, which establishes new performance standards in sensitivity, multiplexing and absolute quantitation in PCR analysis.

Capable of generating more than a billion reactions in a single day, the RainDrop System transforms the performance of molecular assays by enabling digital answers across a number of important applications including low-frequency tumor allele detection, gene expression, copy number variation, and SNP measurement. Since each droplet encapsulates a single molecule, researchers can quickly determine the absolute number of specific target DNA and compare that to the background wild-type DNA. The RainDrop System also shifts the current digital PCR (dPCR) paradigm from a single-color-per-marker approach to a two color with varying probe intensity method that is capable of multiplexing up to 10 markers.

With the introduction of the RainDrop System at ESHG, we have officially ushered in the next generation of PCR for European researchers, said Mark Dronsfield, Ph.D., European Sales Director at RainDance. Europe is home to a number of the worlds leading research organizations and we are already actively engaged with many of them who are interested in bringing the power of a billion reactions with digital answers to their projects.

In a recent Lab on a Chip paper, scientists from Universit de Strasbourg and Universit Paris Descartes, used the RainDance dPCR technology to detect a single mutated copy of KRAS in a background of 200,000 wild-type copies. By processing reactions in millions of picoliter droplets, the platform improved sensitivity by two orders of magnitude compared to existing technologies.

RainDance will be showcasing the new RainDrop System at ESHG in booth #418. For more information, please visit: http://www.RainDanceTech.com/ESHG.

About RainDance Technologies

RainDance Technologies, the Digital Biology Company, is pioneering the use of high-throughput picodroplet-based analysis in human health and life science research. The company's core RainStorm technology generates millions of discrete droplets that can encapsulate a single molecule, cell or reaction and be digitally analyzed and sorted one at a time. The power, precision and simplicity of picodroplets enable researchers to answer complex questions with unprecedented sensitivity and quantitation. The complete RainDance solution includes automated instrumentation, customizable bioinformatics and high-value consumables and reagents for applications including targeted next-generation DNA sequencing, methylation, digital PCR. Based in Lexington, Massachusetts, the company supports scientists around the world through its international sales and support operations and a global network of distributors and service providers. For more information, please visitwww.RainDanceTech.com.

The RainDance products are for research use only. Not for use in diagnostic procedures.

RainDance Technologies, the RainDance Technologies logo, RainDrop, RainStorm, and Digital Biology are trademarks of RainDance Technologies, Inc. All other brands may be trademarks of their respective holders.

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RainDance Technologies Unveils Digital PCR Platform to European Market

ZURICH, Switzerland--(BUSINESS WIRE)--

Myriad Genetics GmbH announced today that a presentation entitled Current Variant of Uncertain Significance Rates in BRCA 1/2 and Lynch Syndrome (MLH1, MSH2, MSH6, PMS2, EPCAM) Testing, was presented today at the European Human Genetics Conference in Nurnberg, Germany. The study highlights Myriads best-in-class variant classification process and variant of uncertain significance rate.

Researchers analyzed the variant of uncertain significance rate for the BRACAnalysis test (BRCA 1 and BRCA 2 genes) test as well as the COLARIS test (MLH1, MSH2, MSH6, PMS2 and EPCAM genes). From 2002 to 2012, Myriads overall uncertain variant rate decreased due to significant investments made in the development and application of improved processes and statistical techniques and the implementation of a targeted program designed to gather data on family members. Across all ancestries, the BRCA 1 and BRCA 2 variant of uncertain significance rate declined from 12.8% to 2.9%. Further, the variant of uncertain significance rate for Lynch syndrome, a test analyzing the MLH1, MSH2, MSH6, and EPCAM genes, declined to 6.6% in 2012. The variant of uncertain significance for PMS2 gene test, also for Lynch Syndrome, was 4.0%.

This data underscores the importance of a world-class variant classification program as well as the high level of accuracy and sensitivity of Myriads genetic tests. Further, through the investment in research and development for its existing tests, the Company has deepened its understanding of variants and variant classification. Myriad continues to invest furthering this knowledge base in an effort to provide best-in-class testing to patients globally.

Current tests available in Europe have a very high variant of uncertain significance rate, often 25 to 30 percent, stated Gary King, Executive Vice President of International Operations at Myriad. We are pleased to bring Myriads technology and variant classification program to Europe, to enhance the quality of genetic testing available to patients and physicians.

About Myriad Genetics GmbH

Myriad Genetics GmbH is the international headquarters of Myriad Genetics, Inc., a global molecular diagnostic company. The Company is 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 nine molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a focus on improving an individual's decision making process for monitoring and treating disease. 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.

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 Companys variant classification program; and the Companys strategic directives under the caption About Myriad Genetics. These forward-looking statements are based on managements 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 Presents Variant of Uncertain Significance Rates at European Human Genetics Conference 2012

Public release date: 24-Jun-2012 [ | E-mail | Share ]

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

Nuremberg, Germany: The use of genome-wide array analysis[1] in parents whose children are suspected of having a genetic disease shows that the parents frequently also have previously undetected genetic abnormalities, a researcher from The Netherlands told the annual conference of the European Society of Human Genetics today (Sunday). Being aware of this is important to parents because it means that their risk of having another affected child is significantly increased.

Dr. Nicole de Leeuw, a clinical laboratory geneticist in the Department of Human Genetics of the Radboud University Nijmegen Medical Centre in Nijmegen, and colleagues performed genome-wide SNP[2] array analysis in 6,500 patients and 1,874 parents. The patients had intellectual disability and/or congenital abnormalities, and the parents of those in whom an aberration was detected were tested in a similar way to determine whether they had the same aberration as their child. Mosaic aberrations, where both genetically normal and abnormal cells are present in an individual, were not only found in one in every 300 patients, but in one in every 270 parents as well. "These abnormalities occurred more frequently than we had expected", said Dr. de Leeuw. "Armed with this knowledge, we can try to understand not only why, but also how genetic disease arises in individuals, and this can help us to provide better genetic counselling."

Analysis of patients' genomes showed 6.5% de novo (spontaneously arising) genomic imbalances, 9.1% of rare, inherited imbalances, and 0.8% of X-linked abnormalities. Moreover, with the additional data from their SNP array test results, the researchers were able to subsequently find pathogenic mutations in recessive disease genes, uniparental disomies (where a single chromosome is doubled leading to two genetically identical ones), and mosaic aneuploidies (an extra or missing chromosome in some of the cells of the body) in about 30 patients.

"In at least seven families, these findings meant that what we had thought of as a spontaneously arising, non-inherited genetic abnormality in a child was in fact already present in some form in the parent", said Dr. de Leeuw. "Furthermore, when we tested in different cell lines for example, DNA from blood and that from a mouth swab we often found that results varied. This is because mosaic aberrations can occur in cells in some organs and not in others, and underlines the importance of not just relying on one type of cell line for this kind of genetic diagnosis."

In two cases these tissue-dependent differences changed over time, and the researchers believe that this was due to an attempt by the body to correct and rescue the situation. "Such rescue attempts are best known in cases of trisomy, where there are three chromosomes instead of two in a cell, or monosomy, where there is only one. In both these cases, the body may try to correct the situation by respectively deleting or adding (doubling) a chromosome. Such rescue mechanisms may be more common than we expected, and by using genome-wide SNP array analysis it will help us to reveal them. For some patients, it would be particularly interesting if we could test multiple samples of these patients over time", said Dr. de Leeuw.

The majority of genetic diseases are not treatable, but in some cases a special diet may reduce the severity of the symptoms ,for example, in phenylketonuria (PKU) or in coeliac disease, in others the same can be obtained by periodic examination of certain organs (for example in Down syndrome or Marfan syndrome). Sometimes hormone treatment will be of benefit to the patient, for example growth hormone treatment in Turner syndrome. For most patients with a genetic disorder, there is no cure, but knowing the genetic cause of their disease may help and improve the care for these patients through knowledge about other patients with the same disease. And if the family is at risk of a genetic disease, couples considering having children can be better informed as to their options, the researchers say.

"By using genome-wide array analysis to look for imbalances in the human genome, we will uncover more and more accurate findings in patients. This will not only increase our knowledge of genetic disorders and the human genome in general, but if we can also collect the clinical features of these patients in a structured and uniform way, the information will become increasingly valuable. Fortunately, this is becoming easier due to advances in tools and software applications, and many professionals in the academic and commercial world have agreed to collaborate in order to substantially increase the genotype/phenotype collection and make these anonymised data publicly available to medical professionals in order to improve patient care worldwide", Dr. de Leeuw concluded.

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Genome-wide analysis shows previously undetected abnormalities in parents of affected children

June 22, 2012 - 18:47 AMT

PanARMENIAN.Net - Clues to the origins of the Queen of Sheba legend are written in the DNA of some Africans, according to scientists, BBC News said.

Genetic research suggests Ethiopians mixed with Egyptian, Israeli or Syrian populations about 3,000 years ago. This is the time the queen, mentioned in great religious works, is said to have ruled the kingdom of Sheba.

The research, published in The American Journal of Human Genetics, also sheds light on human migration out of Africa 60,000 years ago.

According to fossil evidence, human history goes back longer in Ethiopia than anywhere else in the world. But little has been known until now about the human genetics of Ethiopians.

Professor Chris Tyler-Smith of the Wellcome Trust Sanger Institute in Cambridge, UK, a researcher on the study, told BBC News: "Genetics can tell us about historical events.

"By analysing the genetics of Ethiopia and several other regions we can see that there was gene flow into Ethiopia, probably from the Levant, around 3,000 years ago, and this fits perfectly with the story of the Queen of Sheba."

More than 200 individuals from 10 Ethiopian and two neighbouring African populations were analysed in the largest genetic investigation of its kind on Ethiopian populations.

About a million genetic letters in each genome were studied. Previous Ethiopian genetic studies have focused on smaller sections of the human genome and mitochondrial DNA, which passes along the maternal line.

Dr Sarah Tishcoff of the Department of Genetics and Biology at the University of Pennsylvania, said Ethiopia would be an important region to study in the future.

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Africans’ DNA holds clue to Queen of Sheba tale

London, June 22 (ANI): Scientists say that clues to the origins of the Queen of Sheba legend are written in the DNA of some Africans.

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Africans' DNA holds clues to origins of Queen of Sheba tale

June 22, 2012

UK researchers studying the genomes of Ethiopian people have discovered similarities to those of populations in Israel and Syria, proving genetic evidence that may support the tale of the legendary Queen of Sheba.

Ethiopians are described by representatives of the Wellcome Trust Sanger Institute, one of the organizations involved in the study, as one of the most genetically diverse cultures in the world. By studying their DNA, the researchers detected mixing from some Ethiopians and non-Africans dating back to approximately 3,000 years ago.

The origin and date of this genomic admixture, along with previous linguistic studies, is consistent with the legend of the Queen of Sheba, who according to the Ethiopian Kebra Nagast book had a child with King Solomon from Israel and is mentioned in both the Bible and the Quran, the Institute said in a press release.

As part of their work, which is detailed in the American Journal of Human Genetics, the scientists studied the DNA of more than 200 subjects from 10 Ethiopian and two neighboring African populations, Helen Briggs of BBC News reported on Thursday. Approximately one million genetic letters in each genome were analyzed in what is being called the largest Ethiopian-centered genetic investigation of its kind.

We found that some Ethiopians have 40 percent to 50 percent of their genome closer to the genomes of populations outside of Africa, while the remaining half of their genome is closer to populations within the African continent, study co-author Toomas Kivisild of the University of Cambridge said, according to HealthDay News reports. We calculated genetic distances and found that these non-African regions of the genome are closest to populations in Egypt, Israel and Syria, rather than to the neighboring Yemeni and Arabs.

Likewise, Dr. Chris Tyler-Smith of the Wellcome Trust Sanger Institute, co-lead author of the study, told Briggs, Genetics can tell us about historical events By analyzing the genetics of Ethiopia and several other regions we can see that there was gene flow into Ethiopia, probably from the Levant, around 3,000 years ago, and this fits perfectly with the story of the Queen of Sheba.

The experts did tell BBC News that there was some doubt regarding the absolute accuracy of the dating, and that there was a possible margin of error of a couple of hundred years plus or minus the 3,000 years estimate. They added that they plan to analyze all three billion genetic letters of the DNA contained within the genomes of individual Ethiopians in order discern more about the diversity and evolution of human genetics.

Our research gives insights into important evolutionary questions, Dr. Tyler-Smith said in a statement. We see imprints of historical events on top of much more ancient prehistoric ones that together create a region of rich culture and genetic diversity. The next step for our research has to be to sequence the entire genomes, rather than read individual letters, of both Ethiopian people and others to really understand human origins and the out-of-Africa migration.

Source: redOrbit Staff & Wire Reports

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Ethiopian Genetics Could Verify 'Queen of Sheba' Legend

21 June 2012 Last updated at 12:17 ET By Helen Briggs BBC News

Clues to the origins of the Queen of Sheba legend are written in the DNA of some Africans, according to scientists.

Genetic research suggests Ethiopians mixed with Egyptian, Israeli or Syrian populations about 3,000 years ago.

This is the time the queen, mentioned in great religious works, is said to have ruled the kingdom of Sheba.

The research, published in The American Journal of Human Genetics, also sheds light on human migration out of Africa 60,000 years ago.

According to fossil evidence, human history goes back longer in Ethiopia than anywhere else in the world. But little has been known until now about the human genetics of Ethiopians.

Professor Chris Tyler-Smith of the Wellcome Trust Sanger Institute in Cambridge, UK, a researcher on the study, told BBC News: "Genetics can tell us about historical events.

"By analysing the genetics of Ethiopia and several other regions we can see that there was gene flow into Ethiopia, probably from the Levant, around 3,000 years ago, and this fits perfectly with the story of the Queen of Sheba."

This paper sheds light on the very interesting recent and ancient population history of a region that played an important role in both recent and ancient human migration events

Lead researcher Luca Pagani of the University of Cambridge and the Wellcome Trust Sanger Institute added: "The genetic evidence is in support of the legend of the Queen of Sheba."

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DNA clues to Queen of Sheba tale

Public release date: 20-Jun-2012 [ | E-mail | Share ]

Contact: Ruthann Richter richter1@stanford.edu 650-725-8047 Stanford University Medical Center

STANFORD, Calif. Genetics play a significant role in determining which patients will suffer the most from the disturbing side effects of opiates, commonly prescribed painkillers for severe to moderate pain, according to a new Stanford University School of Medicine study, which pinpoints nausea, slowed breathing and potential for addiction as heritable traits.

"One of the most hated side effects of these opiates, nausea, is strongly inherited," said Martin Angst, MD, professor of anesthesia and one of two principal investigators for the new study, which explores individual variations in the response to opiate use. The study will be published online June 20 in Anesthesiology. Genetics also play a likely role in determining which patients will suffer from itchiness and sedation associated with the use of these powerful medications, which include morphine, methadone and oxycodone.

"The study is a significant step forward in efforts to understand the basis of individual variability in response to opioids and to eventually personalize opioid treatment plans for patients," said Angst, director of the Stanford Human Pain Research Laboratory. "Our findings strongly encourage the use of downstream molecular genetics to identify patients who are more likely or less likely to benefit from these drugs to help make decisions on how aggressive you want to be with treatment, how carefully you monitor patients and whether certain patients are suitable candidates for prolonged treatment."

Treatment with opiates, also known as narcotics, is tricky because of this variability in drug response. Certain patients may require 10 times the amount of these painkillers to get the same level of pain relief as others. In fact, in some patients the occurrence of side effects may prevent the use of opioids for effectively alleviating pain. Side effects such as nausea or sedation can be debilitating to some, while nonexistent for others. Similarly, some patients can take medications for months with little addiction potential, while others are at risk within weeks.

Millions of U.S. patients are prescribed opiates for pain each year. A better understanding of the potential risk of side effects motivated the researchers to explore individual variation in pairs of identical and fraternal twins, Angst said. The study was prompted by past genetic studies in animals that have shown a strong genetic component in the response to opiates.

"We rely heavily on narcotics as the cornerstone medication for the relief of pain," said Angst. "Yet we don't know the answers to fundamental questions, such as why some people 'like' narcotics more than others drug liking and disliking could be key in determining addiction potential."

Researchers recruited 121 twin pairs for the randomized, double-blinded and placebo-controlled study. Pain sensitivity and analgesic response were measured by applying a heat probe and by immersing a hand in ice-cold water, both before and during an infusion of the opiate alfentanil, a short-acting painkiller prescribed by anesthesiologists. The team also compared individual variations in levels of sedation, mental acuity, respiratory depression, nausea, itch, and drug-liking/disliking a surrogate measure of addiction potential between identical twins, non-identical twins and non-related subjects. This provided an estimate of the extent to which variations in responses to opiates are inherited. For example, the finding that identical twins are more similar in their responses to opiates than non-identical twins suggested inheritance plays a significant role.

Heritability was found to account for 30 percent of the variability for respiratory depression, 59 percent of the variability for nausea and 36 percent for drug disliking. Additionally, up to 38 percent for itchiness, 32 percent for dizziness and 26 percent for drug-liking could be due to heritable factors. An earlier study published by the same researchers in the March issue of Pain reported that genetics accounted for 60 percent of the variability in the effectiveness of opiates in relieving pain.

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Stanford study shows opiates' side effects rooted in patients' genetics

By Rick Nauert PhD Senior News Editor Reviewed by John M. Grohol, Psy.D. on June 20, 2012

It may seem a long way from zebrafish to humans, buta team of MIT biologists is investigating the genetic basis ofautism, schizophrenia and other human brain disorders by focusing on the freshwater minnow.

As it happens, the zebrafish has long been studied as a model for brain development from molecular, genetic and neuroscience perspectives. In a new study, the researchers set out to explore a group of about two dozen genes known to be either missing or duplicated in about 1 percent of autistic patients.

Although most of the genes functions were unknown, researchers discovered that nearly all of them produced brain abnormalities when deleted in zebrafish embryos.

The findings should help researchers pinpoint genes for further study in mammals, said Dr. Hazel Sive, a professor of biology and associate dean of MITs School of Science.

Autism is thought to arise from a variety of genetic defects; this research is part of a broad effort to identify culprit genes and develop treatments that target them.

Thats really the goal to go from an animal that shares molecular pathways, but doesnt get autistic behaviors, into humans who have the same pathways and do show these behaviors, said Sive.

Sive and her colleagues described their findings in a recent paper in the online edition of the journal Disease Models and Mechanisms.

Sive recalls that some of her colleagues chuckled when she first proposed studying human brain disorders in fish, but it is actually a logical starting point, she said.

Brain disorders are difficult to study because most of the symptoms are behavioral, and the biological mechanisms behind those behaviors are not well understood, she said.

More here:

Zebrafish to Man, Tracking the Genetics of Autism

The European Society of Human Genetics is condemning the use of genetic testing to establish "ethnic purity," as was suggested by a member of the Hungarian far-right Jobbik party. In a press release, ESHG says that Hungarian genetic testing company Nagy Gn scanned 18 positions in a member of parliament's genome for variants that are supposedly characteristic of Roma and Jewish origins to prove that he does not have Roma or Jewish roots. "The use of genetic testing to establish racial origins for political purposes is not only scientifically foolish, but also unethical and should be condemned," ESHG says, calling the testing "ethically unacceptable." ESHG President Joerg Schmidtke called the situation a "gross distortion of the values of genetic testing" and condemned the use of the technology to "promote hatred" rather than help the sick. Bla Melegh, president of the Hungarian Society of Human Genetics, added that the society was "shocked" to hear that any lab was willing to do the testing, and has asked the Hungarian government to prosecute the company under a 2008 law meant to protect against the abuse of genetic testing.

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Not What It's For

Newswise BETHESDA, MD June 18, 2012 -- In cancer, the genome is shot to hell," Columbia University cell biologist I. Bernard Weinstein, M.D., famously said in 1989. Since then, researchers have catalogued the mutations that drive many human cancers. But since cancer takes years to develop, experiments on shorter-lived species have been critical in developing new diagnostics and therapeutics. Scientists who work on human cancer and those who use other species as stand-ins for humans will get together June 17-20, 2012 at the Genetics Society of Americas (GSAs) Model Organism to Human Biology (MOHB): Cancer Genetics Meeting at the Omni Shoreham Hotel in Washington, D.C.

Unlike a single-gene disease inherited through either sperm or egg, the genetic changes of cancer strike somatic (from the Greek soma meaning body) cells including those cells that make up internal organs. In affected organs, these somatic cells may have an underlying susceptibility mutation present. Once a cancer begins, an oncogene, a gene that has the potential of causing cancer, is turned on or a tumor suppressor turned off and other changes ensue. The changing nature of cancer explains why treating the disease requires staying steps ahead.

Animal models have been instrumental for working out the pathways through which all human solid tumors form. Current knowledge of cancer genes is a tribute to the basic research that has been performed over the past four decades, the majority of it in model systems, Bert Vogelstein, M.D., director, Ludwig Center at Johns Hopkins University and Investigator, Howard Hughes Medical Institute said. Dr. Vogelstein, a keynote speaker at the MOHB: Cancer Genetics Meeting has identified the sequence of genetic changes behind colorectal cancer.

Looking at the big picture, Eric Green, M.D., Ph.D., director of the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH) and another speaker at the MOHB: Cancer Genetics meeting said, Cancer is a disease of the genome. The more knowledge we gain about the structure and function of genomes, the more we will be able to learn about the genomic changes responsible for different types of cancer.

The cancer-genome connection is why NHGRI began partnering with the National Cancer Institute in 2005 to create The Cancer Genome Atlas, which will describe the genomes of 20 cancer types.

Quite a varied group of organisms have taught us about human cancers, explained Phil Hieter, Ph.D., (University of British Columbia), President of the GSA, Each model organism has its own advantages and disadvantages for the study of a particular process. The aggregate is much more powerful, so it makes great sense to shuttle among species in studying the mechanisms and mutations associated with cancer. Thats what this conference is all about.

Thanks to evolution, the cancers of model organisms reflect derangement in many of the same genes and pathways that fuel human cancers. The model organism Encyclopedia of DNA Elements (modENCODE) project, begun in 2009, is identifying the genetic controls of two popular model organisms: the roundworm Caenhorhabditis elegans and the fruit fly Drosophila melanogaster. ModENCODE has greatly advanced our knowledge of genome function in model systems, which is foundational knowledge for deciphering the biological consequences of cancer-associated genomic changes, said Dr. Green, who will discuss it at the meeting.

The mini-modENCODE Symposium being held at GSAs MOHB: Cancer Genetics Meeting will be followed by a symposium on June 20-21 hosted by NHGRI at the NIH campus to celebrate the projects accomplishments as it draws to completion this year. For more information about the NHGRI symposium, please see http://www.genome.gov/27548680.

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. 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 journal, 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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Genetics Meeting Surveys the Cancer Genome Landscape

Migration from Earth: Human Evolution and Space Colonization

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Migration from Earth: Human Evolution and Space Colonization

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Published on Jun 17, 2012

From left: NCCS-Vari Translational Research Laboratory director Teh Bin Tean, NCCS-Vari lab researcher Ong Choon Kiat and head of the computational systems biology and human genetics laboratory at Duke-NUS, Associate Professor Steve Rozen. They are part of the team that has made waves in cancer research, especially in cancers prevalent in the region. -- ST PHOTO: NG SOR LUAN

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Doctors, scientists making waves in united fight

Newswise BETHESDA, MD June 15, 2012 A transparent member of the minnow family is providing researchers at Weill Cornell Medical College in New York City with insight into human melanoma a form of skin cancer that may lead to new or repurposed drug treatments, for skin and other cancers.

The experiments will be reported at the Model Organisms to Human Biology: Cancer Genetics Meeting, June 17-20, 2012, at the Omni Shoreham Hotel in Washington, D.C., which is sponsored by the Genetics Society of America. The meeting will bring together investigators who study cancer-relevant biology in model organisms such as fruit flies, yeast, fungi, worms, and mice with investigators studying human cancer. Each session includes both speakers from the model organism research community and those focusing on human cancer research.

Each year in the United States, 8,700 people die from malignant melanoma. Yariv Houvras, MD, PhD, at Weill Cornell Medical College and Craig Ceol, PhD, at the University of Massachusetts Medical School, along with their colleagues, discovered that a previously-identified human gene, SETDB1, accelerated the progression of cancer when a copy of the gene was inserted into the zebrafish genome. This led researchers to believe that this gene may have a similar effect in humans. In fish with the human SETDB1 gene, melanomas appear earlier and spread faster, which is easily seen through the transparent skin of the zebrafish.

Zebrafish are valuable models for people. Their generation time is three to four months, and each female lays hundreds of eggs every two to three days. In addition, researchers can easily manipulate its genes, many of which have human counterparts, and they can even see inside the developing embryos because they are transparent.

In the work that will be presented at the meeting on Monday, June 18, the researchers used the fish to probe a part of human chromosome 1 that is involved in melanoma. In humans, cancer gets underway when a sequence of genes mutate, including a key gene called BRAF. About 60 percent of human melanomas have a specific BRAF mutation, and a drug targeting mutant BRAF, Vemurafenib, was approved by the Food and Drug Administration (FDA) last year for the treatment of patients with metastatic melanoma. Its not unusual for cancers to have multiple genetic mutations, so the researchers reasoned that additional genes found in the amplified region on chromosome 1 could also drive melanoma.

And thats where the zebrafish came in. The researchers delivered SETDB1 into single-cell zebrafish embryos that already had BRAF mutations, and the resulting adult fish had the human gene in every melanocyte. They discovered that SETDB1 is a master regulator, playing an important role in the regulation of many other genes and accelerating the cancer. SETBD1 acts by altering regions of the genome using a biochemical process called methylation, and in doing so prevents many genes from being turned on and making their appropriate protein products.

Methylation of chromatin is an epigenetic change that is, it doesnt alter the underlying DNA sequence. SETDB1 acts by binding to DNA and changing the methylation pattern, which it does at several thousand places in the human genome, according to the studies performed by Dr. Houvras and colleagues.

This is a very exciting area. Many new connections are being made between chromatin-modifying enzymes and cancer, Dr. Houvras explains. The FDA has already approved a drug that inhibits DNA methylation, Decitabine, for a blood disorder called myelodysplasia. Within the next few years drugs that inhibit histone methylation will be tested in clinical trials. These drugs may target SETDB1 and other histone methyltransferases and help treat specific cancers that rely on these pathways, Dr. Houvras notes.

The zebrafish may be easy to work with, however this project was anything but. The researchers scaled up their experiments to follow several thousand fish for six months. They performed over 35,000 individual observations, Dr. Houvras says, as they watched fish develop melanomas individually.

The role of SETDB1 in the cancer isnt black-and-white. In humans its highly expressed in 5 percent of normal melanocytes, in 15 percent of benign nevi, and in 70 percent of malignant melanomas. Moles that overexpress the gene may be more likely to progress to cancer, the researchers speculate which could be very useful information, and all thanks to the zebrafish.

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Fish Shed Light on Human Melanoma

BRUSSELS, June 14 (UPI) -- European geneticists have condemned the use of genetic testing by a Hungarian politician intended to establish his "racial purity."

The European Society of Human Genetics, which promotes research in basic and applied human and medical genetics, said 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.

"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," Joerg Schmidtke, president of ESHG, said in a release from the society.

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

"The test proves nothing," Schmidtke said. "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."

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Geneticists condemn 'racial purity' test