Brown University Center for Computational Molecular Biology

Events

CCMB Distinguished Lectures 2006-2007

_______________________________________________________ Events

J. Craig Venter is one of leading scientists of the 21st century for his visionary contributions in genomic research. He is founder and president of the J. Craig Venter Institute and the J. Craig Venter Science Foundation. The Venter Institute conducts basic research that advances the science of genomics; specializes in high volume genome sequencing, and explores the ethical and policy implications of genomic discoveries and advances. The J. Craig Venter Science Foundation supports both the Venter Institute and The Institute for Genomic Research (TIGR), an affiliated research organization led by Claire M. Fraser, Ph.D. Venter founded TIGR in 1992.
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Craig Venter
J. Craig Venter Institute

Genomics: from Medicine to the Environment

Abstract: TBA

December 6th

A graduate of Columbia University, Professor Cooper also received the M.A. and Ph.D. degrees from that University. He spent a year at the Institute for Advanced Study and taught at the University of Illinois and Ohio State University before coming to Brown in 1958. A fellow of the American Physical Society, American Academy of Arts and Sciences, Member of the Natural Academy of Sciences, American Philosophical Society, Associate, Neurosciences Research Program, he was an Alfred P. Sloan Research Fellow from 1959 to 1966 and a Guggenheim Fellow in 1965-66. He has carried out research at various institutions including the Princeton Institute for Advanced Study, the European Organization for Nuclear Research (CERN) in Geneva, Switzerland. Professor Cooper is a Nobel Laureate, having been awarded the Nobel Prize in 1972 jointly with Bardeen and Schrieffer for their work on superconductivity. He is the Thomas J. Watson, Sr. Professor of Science at Brown, and Director of the Institute for Brain and Neural Systems.
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Leon Cooper
Thomas J. Watson, Sr. Professor of Physics, Brown University

Is Theory Possible in Neurosciences?

Abstract: TBA

December 6th

Dr. David L Barker is Vice President and Chief Scientific Officer at Illumina, Inc., in San Diego, California. Dr. Barker served from 1998 to 2000 as Vice President and Chief Science Advisor at Amersham Biosciences, now part of General Electric. From 1988 to 1998, Dr. Barker held senior positions, including Vice President of Research and Business Development, at Molecular Dynamics, Inc., until the acquisition of Molecular Dynamics by Amersham. He serves on the Boards of Directors of Excellin Life Sciences Inc., Cell Biosciences, and Microchip Biotechnologies, Inc. In his academic career, Dr. Barker conducted interdisciplinary research in neurobiology as a postdoctoral fellow at Harvard Medical School, Assistant Professor at the University of Oregon and Associate Professor at Oregon State University. Dr. Barker holds a BS with honors in Chemistry from the California Institute of Technology and a PhD in Biochemistry from Brandeis University.
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David Barker
Vice President and Chief Scientific Officer Illumina, Inc.

Capturing Common Variation
in the Human Genome on a Single Microarray

Abstract:
The International HapMap Project provided a framework for accessing all common variation in the human genome through SNP genotyping. The development of the Infinium® Assay has enabled true whole genome genotyping: One can now genotype more than 650,000 SNPs on a single microarray, enough to capture essentially all common human variation, at a cost per SNP three orders of magnitude less than six years ago. This methodology is being used by researchers around the world to genotype tens of thousands of patient samples in efforts to discover the genetic basis of common diseases such as cancers, heart disease, arthritis, and diabetes. Detailed scrutiny of many human genomes has revealed that both large and small deletions of genomic sequence are surprisingly frequent in "normal" genomes, and are commonplace in cancer cells. These variations can also be analyzed by SNP genotyping using appropriate software tools. The avalanche of data generated by whole genome genotyping presents challenges for computational biology, as valid associations to disease-causing genes are hidden among literally billions of data points generated by each study. In addition, further understanding will require the integration of genomic, epigenetic, and gene expression data by computational tools that reveal underlying mechanisms.

December 6th

M.D., D.T.M.H., CAPT, MC, USN (RET) has over 20 years of experience building and managing large, successful research and development programs. From 1987-2001 he was Director of the Malaria Program at the Naval Medical Research Center where he built a focused professional team of over 100 individuals in the United States and overseas working on all aspects of malaria research, but especially vaccine development and genomics. Dr. Hoffman and his team were leaders in the effort to sequence the P. falciparum genome and conducted the first studies in the world that showed that DNA vaccines elicited killer T cell responses in humans. In early 2001 Dr. Hoffman retired from the Navy and joined Celera Genomics as Senior Vice President of Biologics to create a program to utilize genomics and proteomics to produce new biopharmaceuticals. He established this program, organized the effort that successfully sequenced the genome of the mosquito responsible for most transmission of malaria in Africa, Anopheles gambiae, and left Celera in August 2002 to found Sanaria. He holds several professorships, and chairs or serves on multiple advisory boards. He is a past president of the American Society of Tropical Medicine and Hygiene, has edited two books on malaria vaccine development, been the author of more than 325 scientific publications, and has numerous patents. He received his B.A. from the University of Pennsylvania, M.D. from Cornell University Medical College, Diploma in Tropical Medicine and Hygiene from the London School of Hygiene and Tropical Medicine, and did residency training at the University of California, San Diego. He is board certified in Family Practice. In 2004 he was elected to membership in the Institute of Medicine of the National Academies.
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Stephen Hoffman
Chief Executive and Scientific Officer, Sanaria

The Journey from Genomics, Molecular Immunology and
DNA Vaccines to an Attenuated Whole Parasite Malaria Vaccine

Abstract:
Scientists have been working for more than 25 years to develop malaria vaccines. Modern, recombinant, subunit malaria vaccine development depends in large part on characterizing mechanisms of protective immunity and the antigen targets of these protective immune responses, and developing vaccine delivery systems that induce the required immune responses against the identified targets. The genomic sequences of Plasmodium falciparum and other malaria causing parasites and Homo sapiens have provided a wealth of information upon which to build experiments designed to characterize immune mechanisms and antigen targets, and optimize vaccine delivery systems. Translating this information into highly effective, sustainable malaria vaccines has been a difficult, expensive, long process. In fact only one P. falciparum protein which was discovered and shown to be protective using modern scientific methods, the circumsporozoite protein (PfCSP), has been shown to reproducibly elicit immune responses that prevent infection in humans. The magnitude and longevity of this protection is not comparable to the protection elicited by vaccines in general use for protecting against other infectious agents Because of the importance of malaria vaccine development, in parallel there are over 70 other approaches to subunit, modern, recombinant malaria vaccine development in progress. At Sanaria we are working on a completely different approach to malaria vaccine development. The goal is to develop a practically manufactured and administered, safe, non-toxic, effective, non-replicating, metabolically active whole parasite P. falciparum sporozoite vaccine. This approach is based on the fact that when the immunogens, radiation attenuated P. falciparum sporozoites, are administered via the bites of infected mosquitoes, they elicit immune responses that completely protect greater than 90% of human recipients against experimental P. falciparum challenge for at least 10 months. During the last 3 years we have demonstrated that it is feasible to immunize by a clinically practical route, produce adequate quantities of P. falciparum sporozoites, and produce a vaccine and release assays that meet regulatory standards and cost of goods requirements. Data describing this progress, and plans for cGMP manufacture, clinical testing, development, and licensing of an attenuated sporozoite vaccine designed to significantly reduce the 2700 to 8100 daily deaths in infants and children caused by malaria will be discussed.

December 6th

Jeffrey Skolnick is the Director of the Center for the Study of Systems Biology in the School of Biology at the Georgia Institute of Technology and the Georgia Research Alliance Eminent Scholar in Computational Systems Biology. He attended graduate school in Chemistry at Yale University, receiving a Ph.D. in Chemistry in polymer statistical mechanics. He then held a postdoctoral fellowship at Bell Laboratories. Next, he joined the faculty of the Chemistry Department at Louisiana State University, Baton Rouge. Then, he moved to Washington University, where he was subsequently appointed Professor of Chemistry. There he was also Director of the Institute of Macromolecular Chemistry at Washington University. He joined the Department of Molecular Biology of the Scripps Research Institute, where he held the rank of Professor. Among his awards is an Alfred P. Sloan Research Fellowship and he is a Fellow of the American Association for the Advancement of Science, a Fellow of the Biophysical Society, a Fellow of the St. Louis Academy of Science Recently, he moved to the Georgia Institute of Technology. He is the author of over 270 publications and has served on numerous editorial boards including Biophysical Journal, Biopolymers, Proteins, and the Journal of Chemical Physics. He is also a cofounder of an early stage structural proteomics company, GeneFormatics, and his software has been commercialized by Tripos. His current research interests are in the area of computational biology and bioinformatics. He has developed algorithms for the prediction of protein structure and folding pathways from protein sequence. In addition, he has been extensively involved in the simulation of membranes and membrane peptides. Most recently, he has developed approaches to predict protein function from amino acid sequence, to assign proteins to pathways, to predict protein-protein interactions, and to predict druggability that can be applied to entire genomes as well as in the development of tools for metabolic profiling and cancer diagnostics.
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Jeffrey Skolnick
Professor, Director, Center for the Study of Systems Biology, Georgia Tech

Prediction of Protein Structure, Function
and Druggability on a Proteomic Scale

Abstract: TBA

December 7th

Dr. King is Professor of Molecular Biology at MIT, and an authority on the genes and proteins of micro-organisms. Prof. King was a founder of the Council for Responsible Genetics and Co-Chair of its Committee on the Military Use of Biological Research.
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Jonathan King
Professor of Molecular Biology, MIT

Why deciphering the Amino Acid Sequence Rules for Protein Folding is so difficult: The Case of the Beta-sheet Fold

Abstract: TBA

December 7th

Dr. Pevzner is Ronald R. Taylor Chair professor of Computer Science and ZDirector of the Center for Algorithmic and Systems Biology at University of California, San Diego. He holds Ph.D. (1988) from Moscow Institute of Physics and Technology, Russia. Dr. Pevzner has authored graduate textbook "Computational Molecular Biology: An Algorithmic Approach" in 2000 and undergraduate textbook "Introduction to Bioinformatics Algorithms" in 2004 (jointly with Neal Jones). He was named Howard Hughes Medical Institute Professor in 2006.
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Pavel A. Pevzner
Ronald R. Taylor Professor of Computer Science, UCSD

The Third Rebuttal of the Random Breakage Theory

Abstract:
Rearrangements are genomic "earthquakes" that change the chromosomal architectures. The fundamental question in molecular evolution is whether there exist "chromosomal faults" where rearrangements are happening over and over again. In 1984 Nadeau and Taylor proposed Random Breakage Model (RBM) of chromosome evolution that recently caused a controversy. RBM postulates that rearrangements are "random", and thus there is no rearrangement hot-spots in mammalian genomes. It was embraced by biologists from the very beginning (due to its prophetic prediction power) but in 2003 was refuted by Pevzner and Tesler who gave a non-constructive argument against RBM using a combinatorial theorem. They further proposed Fragile Breakage Model that postulates that mammalian genomes represent a mosaic of fragile and solid regions. However, the rebuttal of RBM caused a controversy and shortly after Pevzner-Tesler work was published, Sankoff and Trinh, 2004 gave a rebuttal of the rebuttal of RBM. Sankoff and Trinh, 2004 did not question the validity of combinatorial arguments in Pevzner and Tesler, 2003 but instead argued that the synteny block generation algorithm is parameter-dependent and that rebuttal of RBM is more subtle than it may look like at the first glance. Recently, Peng et al., 2006 re-examined the Sankoff-Trinh arguments and demonstrated that they fell victims to their inaccurate synteny block generation algorithm that fails even on small toy examples. They further demonstrated that if Sankoff and Trinh had fixed these problems and chosen realistic parameters, their arguments against Pevzner and Tesler, 2003 would disappear. Sankoff, 2006 recently acknowledged the flaw in Sankoff and Trinh, 2004 but still appeared reluctant to acknowledge the validity of the Pevzner-Tesler rebuttal of RBM, this time arguing that a larger set of rearrangement operations (e.g., transpositions) may explain the "fragile regions" and that the "block deletion" argument in Sankoff and Trinh, 2004 is still valid. In this talk we give a rebuttal of the rebuttal (Sankoff, 2006) } of the rebuttal (Peng et al., 2006) of the rebuttal (sankoff and Trinh, 2004) of the rebuttal (Pevzner and Tesler, 2003) of RBM.

December 7th

Dr. Shaw is the chief scientist of D. E. Shaw Research and a senior research fellow at the Center for Computational Biology and Bioinformatics at Columbia University. He and his research group are currently involved in the design of massively parallel machine architectures and algorithms for high-speed molecular dynamics simulations, and in the use of such simulations to study biomolecular systems of interest from both a scientific and a pharmaceutical perspective.
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David E. Shaw
Chief Scientist, D. E. Shaw Research;
Center for Computational Biology and Bioinformatics, Columbia University

New Architectures for a New Biology

Abstract:
Some of the most important outstanding questions in the fields of biology, chemistry, and medicine remain unsolved as a result of our limited understanding of the structure, behavior and interaction of biologically significant molecules. The laws of physics that determine the form and function of these biomolecules are well understood. Current technology, however, does not allow us to simulate the effect of these laws with sufficient accuracy, and for a sufficient period of time, to answer many of the questions that biologists, biochemists, and biomedical researchers are most anxious to answer. This talk will describe the current state of the art in biomolecular simulation and explore the potential role of high-performance computing technologies in extending current capabilities. Efforts within our own lab to develop novel architectures and algorithms to accelerate molecular dynamics simulations by several orders of magnitude will be described, along with work by other researchers pursuing alternative approaches. If such efforts ultimately prove successful, one might imagine the emergence of an entirely new paradigm in which computational experiments take their place alongside those conducted in "wet" laboratories as central tools in the quest to understand living organisms at a molecular level, and to develop safe, effective, precisely targeted medicines capable of relieving suffering and saving human lives.

December 7th

Dr. Kronstadt was graduated from Brown University in 1967, and received his Ph.D. in mathematics from Harvard University in 1973. He was T. H. Hildebrandt Assistant Professor of mathematics at the University of Michigan from 1973 to 1978, where he conducted research in the area of several complex variables and functional analysis. He joined the Computer Science department of the IBM T. J. Watson Research Center in 1978. From 1978 to 1983 he helped develop software and architectural extensions for the Yorktown Simulation Engine (YSE). In 1983, he joined the VLSI Systems group, and became manager of that group in June 1983. In that capacity he was involved in the design and specification of a number of high performance experimental RISC microprocessors, as well as the development of a standard cell design system. From 1986 to 1988 he was manager of the Microsystems, Analysis and Design Department with responsibility for experimental microprocessor design, advanced VLSI chip design, and circuit design and analysis tools. After an assignment to the Research Division Technical Planning Staff, he became manager of the RISC Systems Department in January, 1990. Subsequently he was named Director of Advanced RISC Systems in January, 1994, Director of Personal Systems Solutions in May, 1995. Responsibilities in these positions included, PowerPC based architecture, microprocessor design, compilers and operating systems, the IBM Anti-virus product, development of advanced handwriting recognition techniques and prototypes, development of MPEG encoding and decoding hardware and software, and the development of wireless and mobile computing environments. In 1996, Dr. Kronstadt became Director of VLSI Systems where his responsibilities continue to include development of the PowerPC architecture, research in microprocessor implementation and micro-architecture, as well as CAD development. Since 2004, he has been Director of Exploratory Server Systems and the Director of the Deep Computing Institute, with responsibility for advanced operating systems research, highly performance computing architectures including BlueGene, and emerging high performance applications including computational biology. Dr. Kronstadt is a member of the IBM Academy of Technology and was awarded two IBM Outstanding Technical Achievement awards for his work on the YSE software. He holds three patents in microprocessor design, and is a Fellow of the IEEE.
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Eric Kronstadt
IBM Academy of Technology

Tools of the Trade: The next Generation of Supercomputers

Abstract:
By the end of the next decade projections point to consumer "appliances" with nominal compute capability equivalent to high end supercomputers of today and supercomputers with raw performance capabilities approaching three orders of magnitude more powerful than today's fastest supercomputers. Of course projections this far out in time must always be taken with several grains of salt. In this talk I will try to say something sensible about them. Are the projections achievable? How might they be achieved? And, more importantly what might we do with these capabilities? (i.e. So what?)

December 7th

Professor Johnson was awarded a Young Investigator's (FIRST) Award from the NIH in 1992, the NSF National Young Investigator (NYI) Award in 1994, and the NSF Presidential Faculty Fellow (PFF) award from President Clinton in 1995. In 1996 he received a DOE Computational Science Award and in 1997 received the Par Excellence Award from the University of Utah Alumni Association and the Presidential Teaching Scholar Award. In 1999, Professor Johnson was awarded the Governor's Medal for Science and Technology from Governor Michael Leavitt. In 2003 he received the Distinguished Professor Award from the University of Utah. In 2004 he was elected a Fellow of the American Institute for Medical and Biological Engineering (AIMBE) and in 2005 he was elected a Fellow of the American Association for the Advancement of Science (AAAS).
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Christopher Johnson
Director, Scientific Computing and Imaging Institute, Utah University

Computational Bioimaging and Visualization:
Challenges and Opportunities

Abstract:
The next decades will see an explosion in the use and the scope of biological imaging and the fuel for this fire will be computing and visualization. In my opinion, advanced, multimodal imaging techniques, powered by new computational methods, will change the face of biology and medicine. Advances in computational modeling, imaging, and simulation allow researchers to build and test models of increasingly complex phenomena and thus to generate unprecedented amounts of data. These advances have created the need to make corresponding progress in our ability to understand large amounts of data and information arising from multiple sources. In fact, to effectively understand and make use of the vast amounts of information being produced is one of the greatest scientific challenges of the 21st Century. Increases in imaging and computation offer views of biological complexity in progressively greater depth and detail, while such visualizations gradually become cheaper, faster, and easier to use. In this talk, I will present I will provide several examples of state-of-the-art computational bioimaging and visualization research and then go on to discuss future research challenges and opportunities.

December 8th

Jeremy Smith has led research groups in biomolecular simulation in three different countries: first a 15-strong group in Paris at the French Atomic Energy Commission, then a 30-strong group at the University of Heidelberg in Germany, and now as Director of the Center for Molecular Biophysics at UT/ORNL. He specializes in high-performance computer simulation and neutron scattering experiments on protein dynamics. He is the author of over 200 papers in these fields. A press reports on his appointment in Tennessee can be found at http://www.tennessee.edu/news/article.php?id=3692.
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Jeremy Smith
Director of the Center for Molecular Biophysics, UT/ORNL

Dynamics of Protein Binding, Reaction and Structural Change

Abstract: TBA

December 8th

Dr. Yewdell is Chief of the Cellular Biology Section, Laboratory of Viral Diseases in the National Institute of Allergy and Infectious Diseases.
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Jonathan W. Yewdell
National Institute of Allergy and Infectious Diseases

Gained in Translation:
The Immunoribosome Hypothesis of Immunosurveillance

Abstract:
The major histocompatibility complex (MHC) class I immunosurveillance system plays a critical role in host defense to intracellular pathogens and tumors. In 1996, to explain the rapid presentation of viral proteins to CD8+ T cells, Jack Bennink, Luis Anton and I proposed that peptides presented by MHC class I molecules derive from defective ribosomal products (DRiPs), which we defined as polypeptides arising from in-frame translation that fail to achieve native structure owing to inevitable imperfections in transcription, translation, post-translational modifications or protein folding. Based on evidence accrued over the past decade, it appears that DRiPs are the the predominant source of class I peptid ligands generated from viral and cellular proteins. In this talk I will discuss this evidence, the recent controversy over the fraction of newly synthesized proteins that are rapidly degraded by proteasomes, and will add a new twist to the DRiP hypothesis that posits that cells possess specialized machinery,possibly in the form of 'immunoribosomes', to couple protein synthesis to antigen presentation.

Bio:
I grew up in Eastchester, NY, just a few miles from New York City (well, the Bronx anyway). I majored in biochemistry at Princeton University, graduating in 1975. I got hooked on research during my senior thesis with Arnie Levine, who had me studying immune rejection of adenovirus transformed cells. Though our approach was hopelessly naive (reverberations of Z & D's discovery in Australia had yet to hit), I developed an interest in immune recognition of virus-infected cells that would become the major focus of my Ph.D. dissertation and career. I owe a lot to Art Levinson, then a Ph.D. student, who took me under his wing and conveyed his boundless enthusiasm for science and the importance of critical thinking. I obtained my Ph.D. in 1981 from the University of Pennsylvania. I worked with Walter Gerhard at the Wistar Institute, who was the first to generate anti-viral monoclonal antibodies. I contributed to Walter's grand project of antigenic mapping of influenza virus hemagglutinin with monoclonal antibodies, and also generated and characterized monoclonal antibodies to other viral proteins. During the same period, I managed to learn as little medicine as possible to meet the requirements for a M.D. degree (1981). A one-year post-doc at Imperial College (London, UK) with David Lane, the co-discoverer of p53 (along with Arnie Levine [small world!]) taught me the importance of cell biology and particularly the power of microscopy. Returning to the Wistar Institute as a newly minted Assistant Professor in 1983, I re-initiated the collaboration with Jack Bennink (also on the Wistar faculty by then) that began in 1981 when we provided the 1st demonstration of CTL recognition of internal proteins of a non-transforming virus. We mapped the influenza virus antigens recognized by mouse CTLs, and provided the initial description of immunodominance at the level of individual viral gene products. At the same time I was using mAbs to study the conformational alterations in flu HA during viral penetration and HA biogenesis. Our last discovery at Wistar was that the cytosol is the portal to the class I processing pathway. In 1987, Jack and I were recruited by Bernie Moss to NIAID where we set up a joint lab, first in a new satellite facility in Rockville, moving four years later to the main campus in Bethesda. We were fortunate to attract the first of what would become a wonderful group of hard working and talented post-doctoral fellows. In Rockville, our team discovered the effects of brefeldin A on Golgi to ER trafficking and antigen presentation, the lack of COOH-terminal trimming of antigenic peptides, and the ability of viral proteins to block antigen presentation. In Bethesda, we discovered NH2-terminal trimming of peptides in the ER, the role of DRiPs in generating antigenic peptides, the contribution of the myriad factors that contribute to immunodominance, the dependence of cross-priming on proteasome substrates, the involvement of the ubiquitin-proteasome pathway in HIV morphogenesis, and PB1-F2, the 11th influenza A virus gene product.

I am extremely grateful to NIAID for paying me to do a job I would do for free had I invested early in Enron and sold at just the right time.

December 8th

Dr. Altshuler's laboratory aims to characterize and catalogue patterns of human genetic variation, and to apply this information to understand the inherited contribution to common diseases. Dr. Altshuler was a leader in the SNP Consortium and International HapMap Consortium, public-private partnerships that created genome-wide maps of human genetic diversity that now guide the design and interpretation of genetic association studies. Dr. Altshuler's group has also contributed to identifying the role of common genetic variants in type 2 diabetes, prostate cancer, and lupus. Dr. Altshuler is a Clinical Scholar in Translational Research of the Burroughs Wellcome Fund, a Charles E. Culpeper Medical Scholar, and winner of the Stephen Krane Award of the Massachusetts General Hospital. He received the Richard and Susan Smith Pinnacle Award of the American Diabetes Association, and the "Freedom to Discover" Award from the Foundation of Bristol-Myers Squibb. He is a member of Advisory Boards at The National Institutes of Health, The Doris Duke Charitable Foundation, The Juvenile Diabetes Research Foundation, The Wellcome Trust and Merck Research Laboratories, on the Editorial Board of Annual Reviews of Human Genetics and Genomics, and the Board of Reviewing Editors at Science. Professor Altshuler is one of four Founding Members and Director of the Program in Medical and Population Genetics of The Broad Institute of Harvard and MIT, a unique research collaboration of Harvard, MIT, The Whitehead Institute, and the Harvard Hospitals.
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David Altshuler
Broad Institute of Harvard and MIT

Human Genome Sequence Variation
and the inherited Basis of Disease

Abstract:
Despite great progress in medical science much remains to be learned about the pathophysiological processes that underlie disease risk in the general population, and to identify those genes whose products, if modulated by a therapeutic intervention, might effectively prevent or treat disease. As family history is one of or the strongest risk factor for nearly all human diseases, and given great progress in knowledge of and tools for studying the human genome, human genetics offers a promising approach to expand our knowledge of human diseases mechanisms. Until recently, studies of human genetics were limited to family-based linkage studies, and to candidate gene association studies, neither of which have proven generally successful in studies of complex, common diseases. While linkage studies were genome-wide, and thus could discover novel information about disease mechanisms, association studies were previously limited to preconceived hypotheses about which genes might be responsible. It has recently become possible to systematically test common genetic variants for association to disease. The HapMap Project provides a guide for the design and interpretation of linkage disequilibrium-based association studies. Affordable genome-wide genotyping technologies enable whole-genome association studies in large clinical samples. Copy number polymorphisms (CNPs) are similiarly being catalogued, and next-generation microarray technologies make it possible simultaneously to genotype SNPs and CNPs genome-wide. Robust and reproducible SNP associations have already provided novel insights into common diseases such as type 1 and type 2 diabetes, prostate cancer, age related macular degeneration, Alzheimer's disease, deep venous thrombosis, inflammatory bowel disease, rheumatoid arthritis, and systemic lupus erythematosis, as well as into quantitative traits such as hyperlipidemia, and QT intervals on the ECG. Whole genome association studies in a variety of diseases will soon provide a more complete picture of the role of common SNPs and CNPs in human disease, providing insight into disease mechanisms, new pathways as targets for therapeutic intervention and disease prevention, and clues about the evolutionary history of common human diseases.

December 8th

Eric Davidson, Ph.D.
California Institute of Technology

Title: TBA

Abstract: TBA

John Reynders
Chief Information Officer, Eli Lilly and Company

Title: TBA

Abstract: TBA

Ellen Rothenberg, PhD
California Institute of Technology

Title: TBA

Abstract: TBA

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