Dr. Stephen Quake - 2012 $500,000 Lemelson-MIT Prize Winner

Mon, 04 Jun 2012 20:30:14 GMT

Profile of Dr. Stephen Quake, winner of the 2012 $500,000 Lemelson-MIT Prize for his revolutionary work in drug discovery, genome analysis and personalized medicine.

Whitehead director talks Y chromosome with Stephen Colbert

Thu, 29 Mar 2012 14:58:09 GMT

Whitehead Institute Director David Page appears on Comedy Central's The Colbert Report to engage in a little lively banter about the future of the human Y chromosome.

Paradigm Shifts: From Biology to Technology to Medical Applications

Wed, 16 Mar 2011 04:00:00 GMT

03/16/2011 1:30 PM KresgeRichard O. Hynes, PhD '71, Daniel K. Ludwig Professor for Cancer Research, Department of Biology; Investigator, Howard Hughes Medical Institute; Eric S. Lander, Professor of Biology ; Founding Director, Broad Institute of MIT and Harvard; Member, Whitehead Institute; Lee Hood, Affiliate Professor of Immunology, University of Washington; President, Institute of Systems Biology; Susan L. Lindquist, Professor of Biology, MITDescription: After years of working out the genetic and molecular machinery of cancer, scientists are gaining significant ground on the disease, and are on the verge of a new generation of diagnostic and therapeutic approaches. Three researchers who have spearheaded this biomedical revolution describe how increasingly fast and cost"effective technology has helped make sense of ever"growing data on different cancers, offering 'big picture' views that may lead not merely to more effective treatments, but to an entirely new kind of medical care. When exposed to environmental stress such as high temperatures, cells in all organisms respond with proteins called heat shock factors (HSFs), and endure all sorts of damage. Years ago, Susan Lindquist speculated that the stress response, an "ancient survival pathway," might have something to do with cancer. She set this work aside, until she was "enticed" by MIT and its multidisciplinary and computational approach to the disease. In recent studies, Lindquist has learned that a central protein, HSF1, promotes malignancy in many ways. She tested different strains of cancer cells from many MIT labs, and found that "cancer is aided and abetted by the stress response." In human breast cancer cells, for example, "the more deranged and metastatic and oncogenic the cell line is, the more it seems to depend on stress response," Lindquist says. Conversely, knocking out HSF1 can protect against cancer growth. With the help of the Broad Institute and its screening technology, Lindquist has explored 350 thousand compounds to see whether they inhibit or potentiate HSF1, and turned up herbal remedies that interfere with the stress response and slow the advance of some cancers. Only recently has it been possible to step back and get the big picture on cancer, says Eric Lander. This increasingly comprehensive perspective comes courtesy of Lander's own enterprises, including the Human Genome Project (1990"2003), and relentlessly improving DNA sequencing technology. MIT's own sequencing output has grown from 70 billion bases per year in 1999 to 125 billion bases, with the cost down 100 thousand fold _ "a stunning pace," concludes Lander, with major implications for cancer research. Lander has launched a cancer genome atlas that will assemble from hundreds of thousands of patient samples of normal and cancerous DNA, and permit the analysis of important cancer cell lines. He envisions the capacity to "knock out every gene in the genome" to build cellular models in order to predict "how a tumor will become resistant to drugs. "It's already time to start asking what is the standard of care for cancer patients," says Lander. "It should be soon for anybody that I loved that they could have this information." Leroy Hood figures he has participated in four paradigm changes in biomedical science, and is leading the charge on the fifth: the drive toward P4 medicine (for "predictive, preventive, personalized and participatory"). Hood was behind the automated DNA sequencer that made the Human Genome Project a reality, and has subsequently developed other devices for translating RNA, protein and other biological information. He says he came to realize that "cross"disciplinary biology was essential for the future," accompanied by a systems approach to disease. Hood imagines patients someday "surrounded by a cloud of virtual data points," which may be distilled to render "simple hypotheses about health and disease." With medicine increasingly an informational science, researchers will be able to map diseases as networks perturbed by precisely delineated genetic or environmental factors. Hood is developing a blood diagnostics system for detecting different types of disease, and developing genomes of families to track genes coding for these diseases. The ultimate goal: creating individualized patient "data spaces" in order to "deal with disease in powerful new ways," and to shift the future focus toward wellness. About the Speaker(s): Richard Hynes received his B.A. in biochemistry from the University of Cambridge, U.K., and his Ph.D. in biology from MIT. After postdoctoral work at the Imperial Cancer Research Fund in London, where he initiated his work on cell adhesion, he returned to MIT as a faculty member. Hynes is a fellow of the Royal Society of London, the American Academy of Arts and Sciences, and the American Association for the Advancement of Science, and a member of the National Academy of Sciences and the Institute of Medicine. He has received the Gairdner Foundation International Award for achievement in medical science and recently served as president of the American Society for Cell Biology.Host(s): Office of the President, MIT150 Inventional Wisdom

Technology Day 2001 - "Origins and Beyond: Our Place in the Cosmos"

Mon, 28 Feb 2011 16:31:21 GMT

The 2001 MIT Technology Day takse place on June 9, 2001, on the theme "Origins and Beyond: Our Place in the Cosmos." Featured speakers include Eric S. Lander, "The Human Genome and Beyond;" Claude R. Canizares, "The Origin of the Universe;" Maria T. Zuber, "Probing the Origin of the Planets from Spacecraft; " Charles R. Marshall, "On Palaeontology."The event is chaired by MIT President Charles M. Vest. [T10276, T10278, T10280]

The Human Genome and Cancer

Tue, 22 Jun 2010 17:14:52 GMT

Eric Lander - Broad Institute

Artificial Life: A global good or evil?
CIS audits the discovery

Wed, 02 Jun 2010 19:38:06 GMT

The Center's series Audit of the Conventional Wisdom continues with a look at the recent discovery out of the Venter laboratory: artificial life. Is this a global good or evil? Ken Oye, director of the Center's Program on Emerging Technologies and associate professor of political science and engineering systems, discusses the discovery from his MIT office on Friday, May 28, 2010.

Content and time approximates:
Intro
The significance of the discovery (1:40)
The reactions from NGOs, industry, media (4:01)
Potential applications, both near and long-term (5:06)
Potential risks (7:58)
Safety and security issues (12:12)
The bottomline (16:53)

How Can Engineers Contribute to the Fight Against Malaria?

Tue, 11 May 2010 04:00:00 GMT

05/11/2010 6:00 PM MuseumSubra Suresh, ScD '81, Dean, MIT School of Engineering; ; Monica Diez"Silva, Post"doctoral fellow, DMSE; David Quinn, Graduate student, Mechanical EngineeringDescription: Malaria has afflicted mankind from time immemorial, confounding many attempts at its eradication. Hundreds of millions now contract the disease annually, and between one and three million -- primarily children -- die from malaria each year. But thanks to an alliance with engineering, medical science has some powerful, new weapons in its arsenal that may ultimately prevail over malaria. From the labs of MIT Dean of Engineering Subra Suresh comes a fresh approach to the disease. The parasitic microbe that causes malaria affects the ability of red blood cells to contract, or deform, as they move through the body's thousands of blood vessels, delivering oxygen and removing CO2. Several years ago, Suresh had the insight that the infection could be viewed as "an engineering problem." With the recent deciphering of the malaria parasite genome, and new methods for measuring forces on individual molecules and cells, says Suresh, "We have some hope of asking a question that we did not have the hope of answering 10 years ago." Researchers can now minutely and systematically track how biochemical and environmental triggers lead to devastating changes in red blood cell deformability in malaria. Suresh has assembled an international group of researchers to investigate different pieces of this complex disease, which involves mosquitoes and humans, and multiple phases of infection. From the Institut Pasteur Suresh recruited microbiologist Monica Diez"Silva, who is exploring how Plasmodium falciparum (the parasite responsible for the most severe form of malaria) produces mechanical changes inside infected red blood cells. This microorganism churns out thousands of merozoites that enter the cells, making them stick to each other and to the walls of blood vessels. They become so rigid that they can't squeeze easily through blood vessels, compromising circulation. Diez"Silva is especially concerned with infected cells that invade the brain. Another Suresh group member, mechanical engineer David Quinn, developed a home"made optic system to trap and stretch red blood cells. He learned that in the late stages of malaria infection, the membranes of these cells increase in stiffness by a factor of 50. He is also using microfluidics to model the flow of infected and uninfected red blood cells -- an "engineered obstacle course" -- which may some day yield a portable diagnostic tool. Suresh hopes his team's work will lead to a host of analytic and therapeutic aids for malaria. They have already made a great leap with the discovery of a Plasmodium falciparum gene that codes for a protein reducing the deformability of red blood cells. This same protein, they learned, also has greater impact when body temperature rises _ typical of high fever episodes in malaria. With research partners in Singapore, the Suresh group is working on a humanized mouse model in which different genes of the Plasmodium parasite are removed to see how they affect the disease. Some day, it might be possible to kill key parasite proteins in mosquitoes by widespread spraying, effectively defanging the disease. But Suresh warns, "We are very far away from therapeutic success. Mosquitoes adapt faster than we can study malaria." About the Speaker(s): Subra Suresh joined the MIT faculty from Brown University in 1993. He has served as the head of the Department of Materials Science and Engineering at MIT, and became Dean of the School of Engineering in 2007. His current research focuses on the mechanical responses of single biological cells and molecules and their implications for human health and diseases. Suresh has published more than 210 articles in journals, and is co"inventor of 14 U.S. and international patents. Suresh is a member of the National Academy of Engineering, the American Academy of Arts and Sciences, and the Indian National Academy of Engineering. His honors include the Gordon Moore Distinguished Scholar award from CalTech, the Brahm Prakash Visiting Professorship from the Indian Institute of Science, selection by the Institute for Scientific Information as one of the most highly cited researchers in Materials Science, the Clark B. Millikan Visiting Professorship at CalTech, the TFR Swedish National Chair in Engineering from the Royal Instiute of Technology, Stockholm and the Distinguished Alumnus Award from Indian Institute of Technology, Madras. Host(s): Office of the Provost, MIT Museum

Lunch with a Laureate: Robert Horvitz

Tue, 27 Apr 2010 04:00:00 GMT

As an undergraduate at MIT, Robert Horvitz did not take a biology course until his senior year.

Autism: What Do We Know, What Do We Need?

Wed, 02 Dec 2009 05:00:00 GMT

"I'll give you the 30,000 foot view of autism."

New Frontiers in Schizophrenia and Bipolar Disorder Research

Mon, 04 May 2009 04:00:00 GMT

05/04/2009 3:00 PM 46"3002Ed Scolnick, Director, Psychiatric Disease Program and the Stanley Center for Psychiatric Research, Broad InstituteDescription: In contrast to cardiovascular disease, few breakthrough remedies for psychiatric illness have emerged in the past half century. Edward Scolnick lays blame for this dismal situation on barriers to understanding the genetic basis behind such illnesses. But the research drought may be over, as the current revolution in human genetics opens wide a door into the molecular biology and brain physiology behind diseases like schizophrenia and bipolar disorder. These common, chronic and disabling mental illnesses are complex, involving abnormal behaviors that vary in expression. They have also lacked the kind of quantitative tests that enable precise diagnosis. While science has demonstrated that the single biggest risk factor for both schizophrenia and bipolar disorder is genetic, it has not been able to design tools for exploring how the genetics relates to the evolution of the disease in people. But just in the last two years, with the sequencing of the human genome and maps of human genetic variation, ignorance has given way to major findings. In schizophrenia and bipolar disease, researchers have discovered that gene deletions and duplications (called copy number variants) cause significant brain circuit mischief. They've also learned there are gene variants common to both diseases, as well as clusters of genes that malfunction. Scolnick describes diverse research at MIT, proceeding at a "breakneck pace," that uses this genetic information "to delve into the malfunctioning of brain circuits." Scientists have applied functional magnetic resonance imaging to compare the brains of ordinary people and schizophrenia patients, and discovered that the schizophrenic's brain in a resting state is hyperactive. Other researchers found that schizophrenics generate the gamma brainwaves involved with higher mental activities in a different manner than control subjects. Another MIT lab has begun to manipulate specific brain circuits using optical technology -- shining different wavelengths of light at special interneurons that regulate the firing of other neurons, and which are postulated to have a critical role in the malfunctioning of schizophrenics' brains. Two other MIT labs are examining the biochemical disruptions due to altered genes, and developing "safe, specific chemical inhibitors" that might yield potential treatments for schizophrenia and bipolar illnesses. In Japan, researchers are growing stem cells into brain cells, which may lead to precise experiments that relate genetic problems to malfunctions in brain wiring. Indeed, adding up this research, a central biochemical pathway central to the pathogenesis of psychogenic illness seems to be emerging, knowledge that "can be exploited to understand illness and to find drug treatments." About the Speaker(s): At the Broad Institute, Edward Scolnick works to identify risk genes for bipolar disorder and schizophrenia. From 1982"2003, Scolnick served as president of Merck Research Laboratories; executive vice president for science and technology at Merck & Company, Inc; executive director and vice president in the department of virus and cell biology and senior vice president for basic research at Merck Research Laboratories. Prior to joining Merck, he worked at the National Cancer Institute where he demonstrated the cellular origin of sarcoma virus oncogenes in mammals and defined specific genes that cause human cancer. He also worked at the National Heart Institute. Scolnick was elected to the National Academy of Sciences in 1984 and to the American Academy of Arts and Sciences in 1993. He became a member of the Institute of Medicine in 1996 and served on the Board of Directors of Merck & Co., Inc. from 1997 to 2002. He recently was selected as Regents' Lecturer, University of California at Berkeley, Frank H.T. Rhodes Class of '56 University Professor at Cornell University, and appointed to the Board of Visitors at the University of Pittsburgh School of Medicine. He currently serves on the board of directors for Millipore Corporation; Renovis, Inc.; and TransForm Pharmaceuticals, Inc.; and on the Medical and Scientific Advisory Board for MPM Capital. He was a member of the FDA Science Board from 2000 to 2002. Scolnick holds an A.B. from Harvard College and an M.D. from Harvard University Medical School. Host(s): School of Science, Department of Brain and Cognitive Sciences

New Lessons in Cancer Research

Wed, 24 Oct 2007 04:00:00 GMT

10/24/2007 6:00 PM MuseumJacqueline Lees, SM '86, PhD '90, Associate Director, Center for Cancer Research and Professor, Dept of BiologyDescription: Cancer is a conniving enemy. Try to kill it off through surgery or chemotherapy, and it finds a way to sneak back in. Jacqueline Lees tells an engaged Soap Box audience what insights and tools research now offers in the longstanding battle against this relentless disease. Big gains have come from molecular study of tumors at different stages, Lees says. It often takes many years for a cancerous cell to develop into a dangerous tumor, one that can yield metastases. There might be six phases of development over 15 years in a cancer's evolution, and scientists have formed a good understanding of what these different lesions look like in various cancers, and how they behave. Lees calls this process -actually a beautiful example of evolution," since the cell that mutates and begins to divide uncontrollably evolves to become more successful relative to other cells in the tissue. Other research focuses on the genetic basis of cancers. Two -flavors" of genes appear responsible for provoking cancerous changes in cells: oncogenes and tumor suppressor genes. It may be possible to intervene along the genetic pathways underlying cancer growth, says Lees. Her own work, involving mutant mice and zebrafish, hopes to identify the mechanisms involved in specific kinds of tumors, and to figure out ways of inhibiting cancer cell growth. Understanding the nature of specific cancers might help prevent treating people with chemical agents that don't work for their kind of cancer, and that actually increase their tumor's growth. With the advent of fast and inexpensive genetic screens, it may soon be possible to determine whether each of us carries genes that predispose us toward certain kinds of cancers. But Lees questions the universal adoption of DNA testing, not just because of privacy concerns, but because there may very well be no known cure if a predisposition to disease is found. -If we sequenced every baby, and said you're highly predisposed to a cancer, and there's nothing we can do, would that be information people want to have?" Lees wonders. -If we could find a rapid way to sequence small subsets of genome, identify people with high risk and we could treat them if we knew they had those diseases, there'd be an argument for that, much as we do testing for diseases where we know can intervene if find children carrying them," says Lees. About the Speaker(s): Jacqueline Lees'research is focused on identifying the proteins and pathways that play a key role in tumorigenicity and establishing the mechanism of their action in both normal and tumor cells. Her lab uses a combination of molecular and cellular analyses, mutant mouse models and genetic screens in zebrafish. Lees received her Ph.D. in 1990 from the University of London.Host(s): Office of the Provost, MIT Museum

Zebrafish and Cancer: What's the Connection?

Tue, 19 Sep 2006 04:00:00 GMT

09/19/2006 6:00 PM MuseumNancy Hopkins, Amgen, Inc. Professor of BiologyDescription: Through her rapport with the zebrafish, Nancy Hopkins has made large contributions to the fields of developmental biology and cancer research. But her model organism, and to some degree her particular slant on molecular biology, were a matter of serendipity, as she relates to this MIT Museum audience. When Hopkins was 10, her mother developed a form of mild cancer, terrifying to her, but also a catalyst for her interest in medical research. Later in college, after a lecture about DNA by James Watson, Hopkins realized that -the secret of life was being placed in front of you, that molecular biology someday had the potential to explain everything worth knowing: the meaning of life, why I looked like my mother..." After obtaining a Ph.D. in molecular biology, Hopkins was determined to enter the field of cancer research, although colleagues warned it would be the -end of my career." Fortunately for her, Richard Nixon was just as energized about finding cures for cancer, and poured money into the field. Even better, scientists had begun to make some key discoveries about the source of some cancers. After years working on viruses and oncogenes, Hopkins -thought it would be fun to move on to something else." On sabbatical in Germany to study the genetics of behavior, she encountered zebrafish in her colleague's lab. The evolution of the zebrafish from fertilized egg to adult occurs in five days, and Hopkins found it a perfect subject for studying an organism's early development. In her own words, she came back to MIT completely obsessed with finding all the genes -that make things work properly" in the zebrafish. After years of painstaking study, Hopkins and her team figured out how to remove one gene at a time from the zebrafish (with its 20,000-25,000 genes), in order to understand what those genes did. She built 4,200 fish tanks with almost 100 thousand fish, and ended up with 550 mutant lines of fish. Then -a funny thing happened to bring me back to cancer," says Hopkins. A lab assistant noticed some fish were developing tumors. She screened 17 mutant lines and found a family of cancer genes that appeared comparable to a group of human cancer genes. This discovery may explain the genetic basis for other human tumors. As she continues work with her fish, Hopkins embraces new and faster technologies to accomplish genetic screens, as well as better detection and imaging capability. -I look forward to the day when I can just sit at home and do experiments with existing data," she says. About the Speaker(s): Nancy Hopkins earned widespread recognition for cloning vertebrate developmental genes. Using a techniqe called insertional mutagenesis -- designed for such invertebrate animals as the fruit fly -- Hopkins's laboratory has cloned hundreds of genes that play a role in creating a viable fish embryo. Hopkins' research earned her 1998 election to the American Academy of Arts and Sciences and 1999 election to the Institute of Medicine. She speaks frequently about gender equity issues in science. Hopkins obtained a B.A. from Radcliffe College in 1964 and a Ph.D. from the department of Molecular Biology and Biochemistry at Harvard University in 1971. Host(s): Office of the Provost, MIT Museum

Immunology and Cancer

Thu, 08 Jun 2006 04:00:00 GMT

06/08/2006 9:00 AM 46-3002Jianzhu Chen, Cottrell Professor of Biology;; Professor of ImmunologyDescription: Jianzhu Chen lays out the thorny challenges of harnessing the immune system to fight cancer. He starts with the basics: how the body employs two levels of defense against pathogens: native and adaptive immunity. The latter type of protection specifically interests Chen, because it can recognize and remember -an almost unending number" of specific pathogens, both inside and outside cells. B cells, produced in the bone marrow, can generate antibodies for clearing out bacteria, and T cells, originating in the thymus, go after viruses and other intracellular threats. They work by identifying an antigen (foreign substance) and expressing receptors -- cell surface proteins -- that bind to those antigens. Early on, the immune system learns to distinguish between what is self and what is a pathogen. It develops, says Chen, -layers of self-tolerance," without which the body might launch an assault on itself. But cancers can manipulate this useful feature of the immune system. Some tumors express chemicals, or summon naturally occurring suppressor cells in order to prevent T-cells from attacking them. So, says Chen, to mount an immune response against cancer, says Chen, you -need to induce a response against the selfãyou have to overcome the built-in tolerance mechanism of the immune system." Chen sees evidence of the possibility of overcoming -tumor-induced tolerance." For instance, some tumors spontaneously shrink, and there's an accumulation of immune cells at tumor sites. Researchers are focusing on three areas: using antibodies or T cells in cancer therapy; developing a therapeutic vaccine that would induce cancer specific antibodies or T-cells; and designing a vaccine to prevent cancer that would induce the memory of B or T cells for a specific cancer. Much hard work remains: identifying tumor associated antigens, most of which, says Chen, the body sees as -normal self proteins;" and then coming up with T or B cells specifically targeting these tumor associated antigens. About the Speaker(s): Jianzhu Chen is also an adjunct professor and co-director of the Center for Infection and Immunity, the Chinese Academy of Sciences. He received a Ph.D. in Genetics from Stanford University and was an instructor at Harvard Medical School before joining the faculty at MIT. The Chen lab is interested in understanding immune response and memory to respiratory virus infection at molecular, cellular, and organismal levels. The lab uses influenza virus infection in mice as a model system. Researchers follow immune cell responses to the virus during the entire course of infection, their subsequent development into memory lymphocytes, and the effect of specific gene mutation on the processes. Chen's lab is also using new molecular technologies to develop therapies that could be relevant for other infectious respiratory diseases such as SARS.Host(s): School of Science, School of Science

The RNAi Revolution

Thu, 08 Jun 2006 04:00:00 GMT

06/08/2006 10:30 AM 46-3002Phillip A. Sharp, HM, Institute Professor; Founding Director, McGovern Institute for Brain Research Description: When a Nobel Prize-winning pioneer of molecular biology embraces a new area of research as revolutionary, attention must be paid. Phillip A. Sharp's own discoveries involving gene expression opened up new territory in the search for the genetic causes of cancer and other diseases. He now has great hopes for similar breakthroughs with the process of gene silencing. This latest advance in understanding gene regulation is quite recent. In 1998, Andrew Fire and Craig Mello discovered the process of RNA interference in the worm C. elegans. When they introduced short, double strands of synthesized RNA into a cell, the RNA silenced a gene in the cell and turned off a specific protein. (Fire and Mello recently received Nobels for this work.) Previously, scientists had viewed RNA as simply -the slave molecule between DNA and protein," as Sharp puts it, or in spliced form, capable of generating a great number of diverse proteins. But revelation of the mechanism of interfering RNA has made the field -a lot more interesting," says Sharp. In just a few years, researchers have learned that small RNA -taps into a pathway that's present in every cell," says Sharp. -At minimum, one in four or one in five of our genes is controlled by small RNAs." Researchers also suspect RNA pathways may occupy a central role in establishing controls in the -human germ line" to prevent redundant pieces of DNA from being expressed in a destructive way. This offers researchers more than a powerful, new investigative tool. Says Sharp, -This is MIT. If you've got something in the lab that's new and you know people need it outside of the lab, you're under an obligation to try to translate it into therapy." One big question is whether small RNA can be used to treat cancers. There's evidence that small RNAs injected directly into the eyeball can potentially silence interconnecting genes responsible for cancers in the back of the eye. The same technique might also work for cancers in the brain and lung, says Sharp. One challenge involves getting the highly water soluble RNA across the cell membrane. Nanoparticle packaging may help prevent the RNAs from being absorbed before they're delivered to the target area. Sharp also mentions experiments that suggest misregulation of small RNAs can cause cancer. -We as a field are now struggling with the issue of just what role short RNAs play in general in control of our genes and our normal physiological processes. It's getting really interesting." About the Speaker(s): Phillip A. Sharp received the 1993 Nobel Prize in Physiology or Medicine. Much of Sharp's scientific work has been conducted at MIT's Center for Cancer Research, which he joined in 1974 and directed from 1985 to 1991. He subsequently led the Department of Biology from 1991 to 1999. Sharp is co-founder of Biogen, Inc and also co-founder of Alnylam Pharmaceuticals. He earned a B.A. from Union College, KY, and a Ph.D. in chemistry from the University of Illinois, Champaign-Urbana in 1969. Sharp has authored more than 300 scientific papers and is a member of the National Academy of Sciences, the Institute of Medicine, the American Academy of Arts and Sciences, and the American Philosophical Society. In 2006, he received the National Medal of Science. Host(s): School of Science, School of Science

Animal Models of Cancer

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 11:00 AM 46-3002Jacqueline Lees, SM '86, PhD '90, Associate Director, Center for Cancer Research and Professor, Dept of BiologyDescription: Jacqueline Lees holds the lowly mouse in high regard. It is -beautifully developed" as a model system for cancer. Lees says that while researchers can learn much from cells in a Petri dish, they require living organisms to observe, for instance, the interplay of immune system and tumor cells, or how malignancies recruit new blood vessels to feed themselves. Because scientists now understand how to switch genes on and off to promote mutations in cells and specific cancers, Lees and other researchers can trigger the growth of malignancies in mice, to explore methodically the disease's progression from first mutation through metastasis. They also test new cancer detection methods and potential therapies. The point, says Lees, is to -always ask if our understanding can be applied to human disease." Lees discusses how researchers have learned to induce both hereditary-type cancers and sporadic (non-familial) cancers, through a range of procedures, including engineering an -inducing" agent that -flips a gene into being mutant;" and creating a gene that carries a mutation and inserting it into the mouse genome. Through various manipulations, researchers have created mouse equivalents for human cancers of the colon, breast and ovaries, as well some leukemias. Lees points in particular to MIT's success with modeling lung cancer. She presents dramatic 3-D images of lung cancer progression in a mouse over the course of several months, after scientists induce a mutation in its K-ras gene. By comparing mouse data with data on the human form of the disease, MIT researchers have strongly linked a mutation in the human K-ras gene to lung cancer. Lees and colleague Nancy Hopkins hope to make even more rapid advances in identifying the genetic bases for cancers, using the humble zebrafish. Since it fully develops in 72 hours, lives up to five years, and is transparent to boot, the zebrafish provides the opportunity for -large scale screens for novel cancer genes." About the Speaker(s): Jacqueline Lees research is focused on identifying the proteins and pathways that play a key role in tumorigenicity and establishing the mechanism of their action in both normal and tumor cells. Her lab uses a combination of molecular and cellular analyses, mutant mouse models and genetic screens in zebrafish. Lees received her Ph.D. in 1990 from the University of London.Host(s): School of Science, School of Science

Cancer Research in the Genomic Era

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 2:30 PM 46-3002Eric S. Lander, Professor of Biology ; Founding Director, Broad Institute of MIT and Harvard; Member, Whitehead InstituteDescription: Eric Lander likens the current age of biological discovery to the days of great ocean-going exploration. After the world was mapped, no one could imagine what it was like to live -before you knew what would happen if you sailed west." Following the current revolution in biology, we -won't be able to imagine what science was like..." This transformation, claims Lander, will be complete in the next decade or so. -MIT students in 2020 will look back with a mixture of amusement and horror at the late 20th century and say, 'Imagine, people spent years looking for the gene for something.'" Lander views biology as a vast library that will soon contain information not just about the DNA sequences of species, but 'volumes' on individuals, tissues, and cells. With great effort, researchers deciphered the secrets of chromosomes, the double helix, and more recently, the human genome and that of other species. But progress in such discoveries is now moving at a much faster clip due to high-speed computing and the Internet. MIT currently sequences _ million pieces of DNA per day, says Lander. He projects this pace will quicken by 20 fold in the next several years. Fortified by this progress, Lander has compiled an ambitious 'to-do list:' identifying -everything that matters" in the human genome, from proteins to the things that control genes; knowing all human genetic variation in the population; knowing how to recognize when a cell -is thinking of one thing or another" based on how genes are turned on or off; knowing all the mechanisms that cause cancer and how to modulate all the genes. Astonishingly, he says, -This is not the to-do list of the next century, but the next decade." Lander is confident that researchers will in the not-distant future generate a catalog of the unique genetic signatures associated with -different flavors" of a type of cancer. Scientists will find patterns in diseases, genes and drug responses, and eventually assemble a list of all the genetic variants in the human genome that put individuals at risk for different diseases. These various gene databases will serve -as foundational information for biology for centuries to come," concludes Lander. About the Speaker(s): Eric Lander was a world leader of the international Human Genome Project, the effort to map the blueprint for a human being. Today, Lander is using the knowledge of the human genome to tackle the fundamental issue of medicine: to find the causes of disease. Lander received his Ph.D. in mathematics from Oxford in 1981, as a Rhodes Scholar. He joined Whitehead Institute in 1986 and founded the Whitehead Institute/MIT Center for Genome Research in 1990. Lander became the founding director of the newly created Broad Institute in 2003. Lander is a member of the U.S. National Academy of Sciences, and U.S. Institute of Medicine. He was a MacArthur Fellow (1987-1992), and earned the Woodrow Wilson Prize from Princeton University(1998); the Baker Memorial Award for Undergraduate Teaching at MIT (1992); the City of Medicine Prize (2001); and the Gairdner International Prize (2002). Host(s): School of Science, School of Science

Introduction and Overview

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 8:00 AM 46-3002Susan Hockfield, President, MIT; ; Tyler Jacks, Director, David H. Koch Institute for Integrative Cancer Research and David H. Koch Professor, MITInvestigator, Howard Hughes Medical Institute; Description: This inaugural address lays the groundwork for an 11-part series on MIT's efforts in cancer research. Susan Hockfield views MIT's Center for Cancer Research as a central example of how -life sciences are coming into conversation with engineering in a powerful way." Robert Silbey provides historical background on the notion of faculty 'short courses', and positions the Center as -the jewel in the crown of MIT, a spawning ground for scientific discovery and rewards." Tyler Jacks introduces the key research areas and scientists who will speak in the succeeding sessions. He offers a thumbnail sketch of cancer as a molecular genetic progression involving sequential alterations in, and the proliferation of, abnormal cells. -Think of a cancer cell like an integrated circuit: the same kinds of complexities in electronic networks also exist within cells," notes Jacks. Because of work on the human genome, and advances in scientists' ability to untangle these complex molecular interactions, -We now have the first generation of anti-cancer drugs targeted against molecular alterations in cancer," says Jacks. Two highly successful drugs have already been derived from MIT research. In addition, says Jacks, collaboration among biologists, engineers and mathematicians are yielding -a tremendous collection of tools and technologies." These include tiny probes that enable diagnosis of cancers at earlier stages, nanoparticles that deliver a therapeutic payload directly to cancer cells, and devices that can be implanted in the body.About the Speaker(s): Tyler Jacks received his A.B. in biology from Harvard College and his Ph.D. in Biochemistry and Biophysics from the University of California, San Francisco. His graduate work with Harold Varmus involved the mechanism of ribosomal frameshifting in retroviral gene expression. As a postdoctoral fellow with Robert Weinberg at the Whitehead Institute at MIT, Jacks initiated his studies on tumor-suppressor gene function, using gene targeting in the mouse. Jacks was named the 2005 Simon M. Shubitz Lecturer and Award recipient, and shared the 2005 Paul Marks Prize for Cancer Research awarded by Memorial Sloan-Kettering Cancer Center.Host(s): School of Science, School of Science

Introduction to Cancer Genetics

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 8:30 AM 46-3002Robert A. Weinberg, '64, PhD '69, Daniel K. Ludwig and American Cancer Society Professor for Cancer Research Department of BiologyDescription: During the human lifetime, there are 10 million billion cell divisions and each division represents, as Robert Weinberg puts it, -an opportunity for disaster, for chaos to occur." The longer-lived the organism, the more likely it is that one cell eventually -will lose the ability to collaborate with its neighbors" in maintaining structure and function, and just start multiplying uncontrollably. Weinberg and other researchers are delving at the molecular and genetic level to understand why and how this single cell begins to proliferate, leading over years and through different stages, to cancer. Weinberg offers a primer on the process of cancer formation, which he likens to Darwinian evolution but within the microcosm of human tissue. Healthy organisms carry tumor suppressor genes, and proto-oncogenes. If these genes become corrupted somehow or prevented from functioning, the result may be cell proliferation. There are, unfortunately, lots of ways these genes become damaged: via a virus, or chromosomes changing places, or by chemical carcinogens, for instance. Weinberg describes how high rates of liver cancer in China were traced to a DNA-mutating mold found in damp rice, grain and fruit. Given the number of ways genetic alternations can come about, it's a relief that as many as five changes are required to convert a normal human cell into a malignant one. -If single mutations sufficed, we would all be covered by tumors by age three. Our cells are wired to be highly resistant," says Weinberg. The latest cancer therapies attempt to capitalize on advancing knowledge of genetic and cellular networks. Weinberg points to two drugs that shut down growth stimulatory signals: Herceptin, which has proven very successful in a specific class of breast cancers, and Gleevec, for chronic myelogenous leukemia. About the Speaker(s): Robert A. Weinberg has earned some of the top honors in his field. Most recently, he won the 2006 Landon-AACR Prize for Basic and Translational Cancer Research. He is also a 1997 National Medal of Science awardee. Weinberg's laboratory discovered the first human oncogene and the first tumor suppressor gene. Today, much of his research focuses on new models of breast cancer development including the stages of tumor invasiveness and metastasis. He earned his Ph.D. in biology from MIT in 1969, and was one of the Founding Members of the MIT Center for Cancer Research in 1973. He was appointed a professor at MIT in 1982, the same year he joined the Whitehead Institute. Weinberg was named American Cancer Society Research Professor in 1985 and received the Daniel K. Ludwig Professorship for Cancer Research in 1997. He is a member of the National Academy of Sciences and the Institute of Medicine.Host(s): School of Science, School of Science

Metastasis

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 1:45 PM 46-3002Richard O. Hynes, PhD '71, Daniel K. Ludwig Professor for Cancer Research, Department of Biology; Investigator, Howard Hughes Medical InstituteDescription: No diagnosis of cancer is welcome, but some scenarios are more dreaded than others. Richard Hynes discusses what happens -when cells in the primary tumor lose their sense of address and wander off to places they're not supposed to go." His talk lays out the process of invasion, by which the cancer spreads into tissues adjacent to the tumor, and that of metastasis, where the cancer disseminates to distant sites. Hynes describes the transitions a cancer undergoes as it spreads. He explains how tissue in our bodies is made of sheets of epithelial cells that are carefully arranged on a -basement membrane" by a series of adhesion receptors. These receptors, if functioning properly, don't usually allow the cells to go anywhere. When a cell becomes tumorigenic, it loses some adhesion, and then if it becomes more damaged -wanders off into the underlying tissue." This is called invasion. Hynes and other researchers are looking at the molecules responsible for cells' adhesive qualities, and at the mutations in genes that trigger a loss of adhesion. Some of these processes are part of normal development, but occasionally, a -switch gets thrown in cells that should have stayed epithelial" and they become migratory instead. Once on the move, cancer cells -need plumbing to grow," says Hynes. Tumors recruit blood vessels to feed them and remove waste, and they can also exploit the body's white blood cells and platelets to promote their own growth. Hynes describes -cross talk between tumor cells and cells in bone," where the -two cells get together in evil combination to damage the bone and enhance the growth of metastases." Scientists have discovered -a lot of different mechanisms by which metastatic cells learn new tricks and suborn the mechanism of the host to get them where they're going." Hynes finds such insidious workings an -appealing thing, since these alterations offer opportunities for therapies." Researchers can tinker with circuits between cells, restore growth suppression and interfere with blood vessel recruitment. It's -a complex problem," says Hynes, but there are -lots of ways to get at this." About the Speaker(s): Richard Hynes received his B.A. in biochemistry from the University of Cambridge, U.K., and his Ph.D. in biology from MIT. After postdoctoral work at the Imperial Cancer Research Fund in London, where he initiated his work on cell adhesion, he returned to MIT as a faculty member. Hynes is a fellow of the Royal Society of London, the American Academy of Arts and Sciences, and the American Association for the Advancement of Science, and a member of the National Academy of Sciences and the Institute of Medicine. He has received the Gairdner Foundation International Award for achievement in medical science and recently served as president of the American Society for Cell Biology.Host(s): School of Science, School of Science

The Cell Cycle and Cancer

Wed, 07 Jun 2006 04:00:00 GMT

06/07/2006 1:00 PM 46-3002Angelika Amon, Associate Professor of Biology, MIT;; Investigator, Howard Hughes Medical InstituteDescription: We all start out as a single fertilized cell, and wind up, as fully formed humans, with 10 to the 13th cells. -The name of the game," says Angelika Amon, is to replicate the genetic information in those cells accurately. -Only if that happens all the time and with high fidelity will you end up with a healthy individual." Amon shows a beautiful video of dance-like cell division in the African blood lily, which demonstrates the migration of chromosomes to opposite ends of the cell -- prelude to a single cell becoming two daughter cells. It's -like a curtain opening," Amon says in wonder. This process of cell division, she continues, is -highly conserved" among organisms. For instance, if a yeast cell contains a defect that prevents it from dividing correctly, plugging in the human equivalent of a protein to correct the defect will enable the yeast to begin dividing again. Amon describes how cells contain special proteins called growth factors that work together to inhibit or initiate cell division. -The cell puts in place layers and layers of controls, like an onion," says Amon. If someone inherits a mutation that affects one of these growth factors, then cells may proliferate uncontrollably. Another route to cancer is if a cell's internal mechanisms for detecting DNA damage malfunctions, perhaps due to exposure to X-rays or UV rays. When these checkpoints break down, instead of putting the brakes on cell division, the cell will proceed unchecked through division with broken chromosomes, or extra chromosomes. Pieces of DNA lie around, information gets lost or amplified and -a mess ensues." Researchers have identified several key chromosomes in which defects lead to malfunctioning growth factors or checkpoints. And they've begun to design new drugs that target the specific proteins involved in these errant cell growth pathways. About the Speaker(s): Angelika Amon has been a faculty member of the Center for Cancer Research since 1999. Previously, she was a Whitehead Institute fellow. She was born in Austria in 1967, and earned her bachelor's and doctoral degrees at the University of Vienna. She first came to the U.S. in 1994 for postdoctoral studies. Amon has analyzed the yeast cell cycle as the first step in an effort to unravel the controls that govern cell-cycle progression. In 2003, she received the National Science Foundation's $500,000 Alan T. Waterman Award, NSF's highest honor for young scientists and engineers.Host(s): School of Science, School of Science

Human Genetics: Our Past and Our Future

Tue, 15 Nov 2005 05:00:00 GMT

11/15/2005 6:00 PM MuseumDavid Altshuler, '86, Founding Member, and Director of the Program in Medical and Population Genetics, Broad Institute; Associate Professor, Genetics and Medicine, Harvard Medical SchoolDescription: Will genomics vanquish our most common diseases, or create a society based on vile eugenics _ or both? David Altshuler outlines these possibilities in his informal talk and conversation at the MIT Museum. Altshuler is a self-described optimist, and sees promise in current genetic research that attempts to pinpoint why some people develop diseases like adult-onset diabetes or schizophrenia. If we can identify the precise mechanisms inside cells that go haywire in individuals with an inherited predisposition to a certain disease, then it may be possible to design drugs much more accurately. "We're searching for a culprit who committed a crime, where the culprit is a mutation in a DNA sequence that made somebody get sick '. And scientists are the detectives -- CGI: Crime Gene Investigators," says Altshuler. Scientists have a very powerful tool in the human genome sequence, and they are quickly mapping out genes that cause diseases. But the very tools that permit insight into illness may also permit researchers to isolate genes for other human traits. And this has Altshuler musing: "How about hair loss, intelligence, criminality, athletic ability '.Should society regulate the use of genetic information in reproductive choices?" What if insurance companies gain access to individuals' genetic predictors, and use this to determine risk, and rates? "There's no federal legislation to prevent someone from shaking your hand, scraping off DNA, doing a genetic test and not hiring you or refusing to give you insurance," Altshuler points out. Ultimately, he says, it will be in the hands of the public to strike a balance between restricting the use of genetic information, and permitting its application to cure disease. About the Speaker(s): Clinical endocrinologist and human geneticist David Altshuler is one of the world's leading scientists in the study of human genetic variation and its application to disease, using tools and information from the Human Genome Project. He is a lead investigator in The SNP Consortium and the International HapMap Project, public-private partnerships that have created public maps of human genome sequence variation as a foundation for disease research. Among his discoveries is the finding of a common genetic variant that increases the risk of contracting type 2 diabetes. He received his B.S. in 1986 from MIT; a Ph.D. in 1993 from Harvard University, and an M.D. in 1994 from Harvard Medical School; he completed his internship, residency and clinical fellowship training at Massachusetts General Hospital.Host(s): Office of the Provost, MIT MuseumTape #: T20603

Academic Perspectives/Panel Discussion

Fri, 09 Jan 2004 05:00:00 GMT

01/09/2004 3:15 PM Wong AuditoriumDouglas A. Lauffenburger, Ford Professor and Head of the Department of Biological Engineering, MIT; James Cassatt, Director, Division of Cell Biology and Biophysics ; National Institute of General Medical Sciences; Acting Director, Center for Bioinformatics and Computational BiologyNational Institute of General Medical Sciences, National Institutes of Health; Leroy Hood, President, Institute for Systems Biology; H. Steven Wiley, Director, Biomolecular Systems ; Pacific Northwest Labs; Huntington Willard, Director, Institute for Genome Sciences and Policy Duke University; Marc W. Kirschner, Professor of Systems Biology; Harvard Medical School; George Poste, Director, Arizona Biodesign Institute; Arizona State University ; ; Peter Sorger, Director, Computational and Systems Biology Initiative (CSBi),MIT ; ; David Botstein, Director and Anthony B. Evnin Professor of Genomics Lewis-Sigler Institute of Integrative Genomics, Princeton University Description: In this wide-ranging discussion, panelists seized on redesigning science education as a way of ensuring the success of systems biology. The first challenge lies in improving instruction in the earliest years. David Botstein said, "K-12 education has never been that great '(kids) don't need to know everything in excruciating detail '.Anything they find out by themselves is worth 10 or 20 of anything you tell them to do." Mark Kirschner remarked, "What's left out is appropriate kinds of inquiry, and at the appropriate age." Leroy Hood spoke with master teachers and "understood that the worst way to teach was lecture." Another obstacle lies with the culture of higher education, where scientists are rewarded for focusing on a single specialty and for research, not teaching. George Poste pointed to "rampant egotism that's destructive," preventing collaboration. Peter Sorger commented, "Autonomy is given to faculty members in classroom. We need expectations. Students will gravitate to those courses that are taught well." A major hurdle for budding systems biologists involves embracing a larger biology. Matt Scott spoke of building "excitement about things beautiful and mysterious." Other panelists expressed hope that the diversity of living things would generate a passion not only to understand the fundamental interdependence among all living things but to preserve species as well. Host(s): School of Science, Computational and Systems Biology

An Introductory Science Curriculum for 21st Century Biologists

Fri, 09 Jan 2004 05:00:00 GMT

01/09/2004 1:00 PM Wong AuditoriumDavid Botstein, Director and Anthony B. Evnin Professor of Genomics Lewis-Sigler Institute of Integrative Genomics, Princeton University Description: How will biology move beyond the Human Genome Project and the task of reducing living things to their genetic sequences? According to David Botstein, the answer lies in "educating the biologist of the 21st century" someone who will be conversant not just with molecular biology, but with computer science, physics and chemistry. At Princeton's new Lewis-Sigler Institute, Botstein is spearheading an innovative effort at interdisciplinary undergraduate education. Students will take advantage of state of the art laboratories and computers capable of crunching vast amounts of data generated by actual research. Professors will "provide essential fundamental concepts as required, using the just-in-time-principle"-- no more of the "learn this now, it will be good for you later" approach, which Botstein likens to hazing. Botstein says there is "lots of overhead in teaching historical and traditional origins" so his students will learn instead "with ideas and technologies of today." He wants to create a new basic language that will enable his biology students to make sense of the fundamental issues of other disciplines. About the Speaker(s): Botstein was educated at Harvard (A.B. 1963) and the University of Michigan (Ph.D. 1967). He joined the faculty of MIT in 1967 and developed an innovative series of undergraduate courses called "project labs," which emphasized current research questions and cutting-edge techniques. In 1987 he moved to Genentech, Inc. as Vice President _ Science, and in 1990 he joined Stanford University's School of Medicine, where he was Chairman of the Department of Genetics. In 2003 he became Director of the Lewis-Sigler Institute of Integrative Genomics at Princeton University. Dr. Botstein's research has centered on genetics, especially the use of genetic methods to understand biological functions. In 1980, Botstein and three colleagues proposed a method for mapping genes that laid the groundwork for the Human Genome Project. Dr. Botstein was elected to the U.S. National Academy of Sciences in 1981 and to the Institute of Medicine in 1993. He has served on many policy-making and peer-review committees, including the NAS/NRC study on the Human Genome Project (1987-88), the NIH Program Advisory Panel on the Human Genome (1989-90) and the Advisory Council of the National Center for Human Genome Research (1990-1995). Host(s): School of Science, Computational and Systems Biology

Computational and Systems Biology at MIT

Fri, 09 Jan 2004 05:00:00 GMT

01/09/2004 2:45PM Wong AuditoriumPeter Sorger, Director, Computational and Systems Biology Initiative (CSBi),MIT ; Description: Once the young field of systems biology really picks up steam, there will be reams of difficult new data to sort through, warns Peter Sorger. As scientists move away from the heavily structured information of gene-protein sequencing to analyzing the dizzyingly complex links among systems in living organisms, they'll need better tools. Bigger and faster computers alone will not make sense of these intricate networks. "The barrier is going to be crossed by more creativity, not by more CPUs," Sorger says. "As you go from a single molecule to the full genomic complement, as you go to ever more components, you know less and less about each component." Sorger calls for new methods in modeling the dense connections within a cell or a piece of tissue. While researchers might wish for the logical layout of circuit boards, what they actually find may more resemble an engineer's nightmare: a huge interconnected mass of wires. Sorger hopes that interdisciplinary efforts at MIT and beyond will help link experimentation to varied but systematic modeling approaches.About the Speaker(s): n addition to his position at CSBi, Peter Sorger also holds associate appointments at the MIT Center for Cancer Research and the Broad Institute. Sorger received his A.B. in Molecular Biology from Harvard in 1984, and his Ph.D. from Trinity College, Cambridge University, in 1993. He trained as a postdoctoral fellow with Harold Varmus and Andrew Murray at the University of California, San Francisco. Sorger's lab -- 19 graduate students, postdoctoral fellows and staff scientists -- is attempting to identify the molecular lesions that cause genomic instability, to determine their frequency in normal and cancerous cells and to develop improved means to kill selectively diseased tissues Host(s): School of Science, Computational and Systems Biology

Keynote Presentation: Academic Perspectives

Fri, 09 Jan 2004 05:00:00 GMT

01/09/2004 10:15 AM Wong AuditoriumLeroy Hood, President, Institute for Systems BiologyDescription: Very simply stated, systems biology attempts to "capture the dynamic nature of living systems." To accomplish this, says Hood, you "have to bring together the flavors of biology, chemistry, computer science, engineering and physics," among others. It's a vast area to tackle. But with tools like the internet and digital DNA and protein sequencers on hand, it's now possible to perform research aimed at unraveling the complex interaction of genes and environment in simple organisms. Hood describes knocking out yeast cell genes, and turning off the machinery that metabolizes simple sugars. This sort of microscopic tampering allows scientists to build models of increasing complexity. A blueprint of gene regulation in sea urchins helped one scientist figure out a way to redesign the organism with two guts. But the ultimate prize is a deep understanding of human biology. Hood foresees a database built with the help of nanotechnology that categorizes and quantifies all proteins in the human genome. Scientists will be able to predict disease by detecting defective genes in blood samples, and then manipulate the genes to prevent the disease. "The integration of biology and medicine," says Hood, "is where the rubber meets the road."About the Speaker(s): Dr. Hood has published more than 500 peer-reviewed papers, received 12 patents, and co-authored textbooks in biochemistry, immunology, molecular biology, and genetics, and is a member of the National Academy of Sciences, the American Philosophical Society and the American Association of Arts and Sciences. He earned an M.D. from Johns Hopkins University in 1964 and a Ph.D. in biochemistry from the California Institute of Technology in 1968. His professional career began at Caltech where he and his colleagues pioneered four instruments--the DNA gene sequence and synthesizer, and the protein synthesizer and sequencer--which comprise the technological foundation for contemporary molecular biology. Dr. Hood was also one of the key players in the Human Genome Project. In 1992, Dr. Hood moved to the University of Washington to create the cross-disciplinary Department of Molecular Biotechnology. In his role as the William Gates III Professor of Biomedical Science, Dr. Hood applied his laboratory expertise in DNA sequencing to the analysis of human and mouse immune receptors and initiated studies in prostate cancer, autoimmunity, and hematopoietic stem cell development. In 2000, Dr. Hood co-founded the Institute for Systems Biology in Seattle. Host(s): School of Science, Computational and Systems Biology

The Evolution of Sex: Rethinking the Rotting Y Chromosome

Mon, 08 Dec 2003 05:00:00 GMT

12/08/2003 4:00 PM McGovern AuditoriumDavid C. Page, Associate Director of Science, Whitehead Institute; Professor of Biology, MITDescription: According to David Page, "the Y chromosome is the Rodney Dangerfield of the human genome." Regarded for 50 years as a genetic wasteland, the Y chromosome just doesn't get any respectEURuntil now. Page's lab has made some startling discoveries that reverse the prevailing view. Recall from basic biology that pairs of chromosomes exchange genetic material through a process of crossing over. This leads to genetic variation in offspring, and can weed out dangerous mutations. Although there's limited gene swapping between the sex-determining X and Y chromosomes, the popular belief has been that a large portion of the Y could not recombine, and therefore will sooner or later self destruct. The long-term outlook for the Y chromosome was bleak. But now there is hope and renewed respect for the Y. Page has found vast sequences of DNA on the Y that appear like palindromes (words like "mom" that read the same backwards and forwards). Page believes the two halves of the palindrome engage in a kind of crossing over. This can lead to repairing mutations, just as in ordinary chromosomes. Through this unique method, the Y chromosome not only endures but prevails. About the Speaker(s): David C. Page studies the Y chromosome the chromosome that distinguishes males from females. In 1992, his laboratory mapped and cloned the entire Y chromosome. Today, he uses the map and other tools to trace the genetic causes of male infertility, the history of the Y chromosome and human populations, and the origins of common genetic diseases. He is also chair of the Whitehead Task Force on Genetics and Public Policy. Page received his MD degree with a concentration in genetics in 1984 from Harvard Medical School and the Harvard-MIT Health Sciences and Technology Program, and was immediately appointed a Whitehead Fellow. He joined the faculty of the Whitehead Institute and MIT in 1988. His honors include a MacArthur Foundation Prize Fellowship in 1986, a Searle Scholar's Award in 1989, and the Amory Prize for advances in reproductive biology from the American Academy of Arts and Sciences in 1997.Host(s): School of Science, Whitehead Institute for Biomedical ResearchTape #: T18064

Evolution: From the Fossil Record to Genomic Revolution Probing the Origin of the Planets from Spacecraft

Sat, 09 Jun 2001 04:00:00 GMT

06/09/2001 KresgeCharles Marshall, Professor of Geology and Biology; Curator, Invertebrate Paleontology, Museum of Comparative Zoology, Harvard University; Dr. Maria T. Zuber, E.A. Griswold Professor of Geophysics, Head of the Department of Earth, Atmospheric and Planetary Sciences, MIT ; Host(s): Alumni Association, Alumni Association

The Origin of the Universe The Human Genome and Beyond

Sat, 09 Jun 2001 04:00:00 GMT

06/09/2001 KresgeClaude Canizares, VP for Research, Associate Provost; Eric S. Lander, Professor of Biology ; Founding Director, Broad Institute of MIT and Harvard; Member, Whitehead InstituteHost(s): Alumni Association, Alumni Association

The Human Genome Project

Fri, 16 Feb 2001 05:00:00 GMT

02/16/2001 10"250Eric S. Lander, Professor of Biology ; Founding Director, Broad Institute of MIT and Harvard; Member, Whitehead InstituteDescription: Dr. Lander is a geneticist, molecular biologist and a mathematician, with research interests in human genetics, mouse genetics, population genetics and computational and mathematical methods in biology. He and his research group have developed many of the tools of modern genome research including genomic maps of the human, mouse and rat genomes in connection with the Human Genome Project and techniques for genetic analyses of complex, multigenic traits. He has applied these techniques to the understanding of cancer, diabetes, hypertension, renal failure and dwarfism. About the Speaker(s): Eric Lander was a world leader of the international Human Genome Project, the effort to map the blueprint for a human being. Today, Lander is using the knowledge of the human genome to tackle the fundamental issue of medicine: to find the causes of disease. Lander received his Ph.D. in mathematics from Oxford in 1981, as a Rhodes Scholar. He joined Whitehead Institute in 1986 and founded the Whitehead Institute/MIT Center for Genome Research in 1990. Lander became the founding director of the newly created Broad Institute in 2003. Lander is a member of the U.S. National Academy of Sciences, and U.S. Institute of Medicine. He was a MacArthur Fellow (1987"1992), and earned the Woodrow Wilson Prize from Princeton University(1998); the Baker Memorial Award for Undergraduate Teaching at MIT (1992); the City of Medicine Prize (2001); and the Gairdner International Prize (2002). Host(s): School of Science, Department of Biology

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