Imaging Zebrafish at MIT

Tue, 12 Feb 2013 15:31:20 GMT

MIT researchers have invented a new imaging system that allowed them to create this three-dimensional rendering of the cartilage that forms the skull of a five-day-old zebrafish larva.

DNA Fingerprinting Complete - no crime lab

Sat, 12 Jan 2013 08:06:02 GMT

Meet Guoping Feng - Investigator, McGovern Institute

Thu, 02 Aug 2012 07:05:45 GMT

Guoping Feng, an investigator at the McGovern Institute for Brain Research at MIT, studies the development and function of synapses and their disruption in brain disorders. He uses molecular genetics combined with behavioral and electrophysiological methods to study the molecular components of the synapse and to understand how disruptions in these components can lead to diseases like autims and OCD.

Learn more about Guoping Feng >>

BLOSSOMS - Tissue Specific Gene Expression

Wed, 01 Aug 2012 07:04:12 GMT

Teachers: Rabih Talhouk, PhD and Elia El-Habre, MSc. of the American University of Beirut in Lebanon

Summary: How is it that all cells in our body have the same genes, yet cells in different tissues express different genes? A basic notion in biology that most high school students fail to conceptualize is the fact that all cells in the animal or human body contain the same DNA, yet different cells in different tissues express, on the one hand, a set of common genes, and on the other, another set of genes that vary depending on the type of tissue and the stage of development. In this video lesson, the student will be reminded that genes in a cell/tissue are expressed when certain conditions in the nucleus are met.

How Does Cancer Learn to Spread?

Wed, 25 Jul 2012 20:30:09 GMT

This video profiles the Jacks Laboratory's work to understand the genetic pathways that enable the deadly spread of cancer. It is currently featured in the Koch Institute Public Galleries at MIT. See more educational exhibits from the Galleries at http://ki-galleries.mit.edu/.

Meet Robert Horvitz

Mon, 02 Jul 2012 19:24:37 GMT

MIT's Robert Horvitz has devoted much of his career to studying the nematode worm Caenorhabditis elegans.

11th Annual Koch Institute Symposium: Collaboration Between Transcriptional and Epigenetic Regulators

Sat, 30 Jun 2012 07:04:25 GMT

Richard Young, Whitehead Institute, MIT, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Dynamic and Coordinated Regulation of Developmental Transitions in the Cardiac Lineage

Sat, 30 Jun 2012 07:04:25 GMT

Laurie Boyer, MIT, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Introductory Remarks and Overview

Sat, 30 Jun 2012 07:04:25 GMT

Tyler Jacks and Jacqueline Lees of the Koch Institute deliver remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Role of Bmi I in Intestinal Development and Tumorigenesis

Sat, 30 Jun 2012 07:04:25 GMT

Jacqueline Lees, Kock Institute at MIT, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: The Cancer Epigenome and Therapeutic Implications

Sat, 30 Jun 2012 07:04:25 GMT

Stephen Baylin, John Hopkins University, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Closing Remarks

Sat, 30 Jun 2012 07:04:24 GMT

Tyler Jacks delivers closing remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Epigenetic Mechanisms and Leukemia Development

Sat, 30 Jun 2012 07:04:24 GMT

Scott Armstrong, Dana-Farber Cancer Institute, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

11th Annual Koch Institute Symposium: Stem Cells in Cancer: Do they Matter?

Sat, 30 Jun 2012 07:04:24 GMT

John Dick, Ontario Institute for Cancer Research, delivers remarks at the Koch Institute's 11th Annual Oncology Research Symposium

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.

Killian Lecture: Joanne Stubbe

Thu, 08 Mar 2012 08:03:37 GMT

Biology and chemistry professor presents the 40th Annual James R. Killian Jr. Faculty Achievement Award Lecture, titled "Radicals: Your Life Is In Their Hands."

DNA/RNA Kit Check

Thu, 08 Dec 2011 20:05:31 GMT

This video demonstrates how to do a kit check for the DNA/RNA kits. This video corresponds to DNA/RNA Booklet 1, page 2. NOTE: This video has no sound.

Decoding A Gene

Tue, 29 Nov 2011 16:56:29 GMT

This video demonstrates the decoding activity for the LEGO channel protein genes. The activity helps to clarify the triplet code prior to teaching transcription and translation. If transcription and translation are not appropriate for your group of students, this decoding of a gene can be the culminating activity. This video corresponds to DNA/RNA Booklet 1, pages 13-17. NOTE: This video has no sound.

Introduction to LEGO® Proteins - In-Class Demo

Tue, 29 Nov 2011 16:31:45 GMT

This video is an introduction to proteins using the LEGO DNA Learning Center Set. Teachers should perform this demonstration in front of the class. Students will learn that the proteins in our bodies are made from the protein we eat. Different proteins can be created by changing the order of the amino acids in the protein chain.

Professor Malone talk on: Mapping Genomes

Fri, 04 Nov 2011 15:09:01 GMT

Conquering Cancer: Opening Remarks Reflections on Major Milestones in Cancer Research and Technology Development

Wed, 16 Mar 2011 04:00:00 GMT

03/16/2011 8:30 AM KresgeDavid A. Mindell, PhD '96, Frances and David Dibner Associate Professor of the History of Engineering and Manufacturing; ; Dr. Susan Hockfield, President, MIT; Tyler Jacks, Director, David H. Koch Institute for Integrative Cancer Research and David H. Koch Professor, MITInvestigator, Howard Hughes Medical Institute; ; Nancy Hopkins, Amgen, Inc. Professor of Biology; Phillip A. Sharp, HM, Institute Professor; Founding Director, McGovern Institute for Brain Research ; Jacqueline Lees, SM '86, PhD '90, Associate Director, Center for Cancer Research and Professor, Dept of Biology; Robert S. Langer, Jr., ScD '74, Institute Professor, Kenneth J. Germeshausen Professor of Chemical and Biomedical Engineering, Department of Chemical Engineering and Harvard"MIT Division of Health Sciences and Technology ; Description: The breadth and depth of thinking represented in MIT's 150th anniversary symposia would do William Barton Rogers proud, believes David Mindell. MIT's founder and first president envisioned the university pursuing cutting edge work, and the "convergence of science and engineering 150 years later captures the essence, the special courage" that Rogers imagined, says Mindell. MIT's pursuit of a cure for cancer constitutes just this kind of convergence, states MIT president Susan Hockfield. While the Institute began significant research on the disease decades ago, work underway today promises major breakthroughs. "We've got the right place, the right people and this is the right time. We are riding the crest of a powerful wave in science," says Hockfield. And at MIT's new David H. Koch Institute for Integrative Cancer Research, states Tyler Jacks, partnerships between scientists and engineers are "already helping us treat the disease more sensitively, and one day will give us the tools to prevent it altogether." Jacks' colleagues from the Koch Institute describe past milestones in cancer research, and attest to the promise of science and engineering collaborations in current and future research. Nancy Hopkins starts with the Nixon Administration's declared "war on cancer" in 1971. Researchers could identify environmental factors, such as smoking, that caused cancers, and learned that early detection and treatment were critical in battling the disease. But these two avenues were not enough, and tackling cancer at the molecular level soon became essential. Energized by the revolution in molecular biology, MIT was "courageous or crazy enough" to take on this challenge, says Hopkins. She characterizes progress in understanding the cellular basis of cancer as "breathtaking," leading to the development of "smart drugs," some of which seriously extend the lifespan of cancer patients without the side effects of previous therapies. But while the number of cancer deaths this country avoids has grown enormously in the past decade, Hopkins believes "the true number being saved is not nearly as great as it should be," primarily because basic discoveries "are not exploited as effectively as they could be." There "are still major things about cancer we don't know," says Phillip Sharp, in spite of a raft of important discoveries from researchers at MIT. Salvador Luria, David Baltimore, Robert Horvitz, Susumu Tonegawa and Sharp himself pried apart such secrets as the function of genes in bacteria, genetic changes in the immune system, oncogenes, and programmed cell death. Sharp notes the long evolution of one of the first personalized cancer treatments, Gleevec (for chronic myelogenous leukemia), from MIT laboratories to actual drug. "To turn down the death rate due to cancer," says Sharp, "we must accelerate understanding and the ability to take fundamental discoveries and move them into therapy." Convergence of engineering and medicine will be critical to quickening the pace of drug discovery, says Sharp, and no better place than at MIT, which has brought together all the essential research elements. Cancer genes acquire mutations along a stepwise path that proves diabolically difficult to trace, as Jacqueline Lees describes. But the job of researchers has been elucidating this process of transformation from normal cell to metastatic cancer, and seeking opportunities to detect, disrupt, and destroy the disease at different points along the way. Lees points to several types of genes scientists have been targeting in their battle. Her lab has been exploring a tumor suppressor gene that plays a major role in retinoblastoma, a childhood cancer of the eyes, and that also predisposes some patients to other tumors. Researchers want to control this gene to inhibit mutations, and stop the cancer from marshaling resources from other cells. Lees advocates the use of mouse models, rather than "studying isolated cancer cells in cultures," in order to "analyze the progression of disease and most importantly, test chemotherapeutic agents in the context of a living organism." Robert Langer credits a series of lucky breaks for bringing him to the engineering side of medicine, including his entr_e to Judah Folkman's Boston lab, where he participated in pioneering work showing that tumors grow by recruiting new blood vessels (angiogenesis), and that targeting this process could thwart the spread of cancer. Langer tested hundreds of materials that could be released slowly in the body to block the growth of tumor"related blood vessels without harming healthy tissue. But he notes it took 28 years from the time this work was first published in 1976 to FDA approval of an angiogenesis inhibitor drug. The field is still young, says Langer, with new inhibitors emerging for different cancers, and bioengineering increasingly central to drug development. He is excited about Koch Institute work involving "nanoparticles decorated with different molecules" that attack tumor cells. The interface of engineering and biology also promises minute sensors, cancer vaccines, and ways of measuring changes in cells at "1 one"millionth the weight of a nanogram-the most sensitive scale in the world." Says Langer, "I hope these will change our future." 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, 1999 election to the Institute of Medicine and 2004 election to the National Academy of Sciences. 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 President, MIT150 Inventional Wisdom

Inside the Lab: Michael Hemann, Ph.D.

Tue, 01 Mar 2011 22:23:21 GMT

Learn more about the Hemann lab's work in system biology and how they use high throughput genetics in model systems to screen for mechanisms of drug resistance.

The Human Genome and Cancer

Tue, 22 Jun 2010 17:14:52 GMT

Eric Lander - Broad Institute

Dendrite Morphogenesis and Channel Regulation: Implications for Mental Health and Neurological Disorders

Fri, 28 May 2010 04:00:00 GMT

05/28/2010 4:00 PM 46"3002Lily Jan, University of California, San Francisco; Yuh"Nung Jan, University of California, San FranciscoDescription: Lily and Yuh"Nung Jan have been pioneers in the field of molecular neurobiology for more than 30 years, and their genetic studies of fruit flies and mice have provided major insights into many different aspects of brain function and development. In this joint lecture, they summarize their recent work on the genetic control of neuronal shape and of electrical properties, including many implications for human brain disorders. The brain's extraordinary wiring complexity is largely due to dendrites, the elaborate branched structures through which neurons receive incoming signals. In the first part of their joint lecture, Yuh"Nung Jan summarizes the genetic mechanisms that control the shapes of these elaborate structures. Jan describes how dendrites recognize and avoid other dendrites of the same neuron, while ignoring dendrites from adjacent neurons. The key to this self/non"self discrimination ability is a remarkable gene called dsCAM, which encodes some 38,000 different splice variants. Each neuron is believed to express a different subset of these variants, giving it a unique molecular identity. Genetic studies are also starting to reveal how dendritic arbor size is regulated. Like a well" pruned tree, dendritic arbors are dynamic structures in which new growth and branch removal are kept in precise balance. Jan estimates that around 100 genes are involved in this process, and he argues that mutations in these genes could contribute significantly to many human brain disorders. Studies of dendritic structure are providing insights into neurodegenerative diseases such as Huntington's disease. Jan shows that over"expression of the human mutant protein in fruit fly neurons causes systematic changes to their dendrites, making these flies an ideal system in which to study the disease mechanism and identify new therapeutic strategies. The Jans have been pioneers in the study of potassium channels (K channels), the most abundant class of ion channels in the brain. In the second part of their joint presentation, Lily Jan examines the complex regulatory mechanisms by which K channels regulate brain's activity. To function properly, K channels must be targeted to the correct part of the neuron. Jan describes how this is accomplished for a prototypical mouse K channel known as Kv1, with the help of two associated proteins that are responsible for transporting the channel molecules along axons. Kv1 is also present in dendrites but it gets there via a different mechanism. Rather than transporting the protein, as happens in axons, the RNA encoding the channel is localized to dendrites, where its translation is controlled locally by electrical activity at synaptic sites. Jan describes the pathway by which this happens, which appears to constitute a positive feedback loop _ synaptic activity suppresses the synthesis of Kv1.1, thus increasing activity levels still further. She then shows how disruptions to this feedback pathway could contribute to autism and pervasive developmental disorder. In the final part of the talk, Jan describes the regulation of another class of K channels known as GIRKs. Unlike the voltage"gated Kv channels, which open and close rapidly in response to electrical activity, the GIRK channels open more slowly (seconds rather than milliseconds) in response to chemical signals between neurons. GIRK channels were recently found to be concentrated at excitatory synapses within the brain, and Jan presents evidence that GIRK channels may play a fundamental role in controlling synaptic plasticity and learning. About the Speaker(s): Lily Jan, PhD Jack and DeLoris Lange Professor of Physiology and Biophysics at the University of California, San Francisco Howard Hughes Medical Institute Investigator Lily Jan studies the function and regulation of potassium channels and calcium"activated chloride channels in the brain. Jan earned her B.Sc. in Physics from National Taiwan University in 1968 and her M.Sc. in Physics from the California Institute of Technology in 1970. Lily married Yuh Nung Jan in 1971, when they were graduate students at CalTech, and have shared a laboratory since 1979. After beginning their PhD studies at Caltech set on careers in theoretical physics, they both chose to switch careers and follow their interest in biology. Their first significant discovery was to prove the existence of peptide neurotransmitters. Since then, the Jans have been pioneers in the study of potassium channels, which are central to understanding the brain's electrical properties, and they have become leaders in the field of developmental neuroscience. http://www.hhmi.org/research/investigators/janly_bio.html http://physio.ucsf.edu/jan/ Yuh"Nung Jan, PhD Jack and DeLoris Lange Professor of Molecular Physiology at the University of California, San Francisco Howard Hughes Medical Institute Investigator Yuh"Nung Jan is interested in the basic mechanisms that control diversity of neuronal morphology, dendrite development, and neuronal circuitry formation. Using the relatively simple nervous system of Drosophila as a model, Yuh Nung hopes to discover the genetic program that controls its development and uncover evolutionarily conserved core programs that control neural development in animals. Jan earned his B.Sc. in Physics from National Taiwan University in 1967 and went on to earn his M.Sc. in Physics from California Institute of Technology in 1970. Yuh"Nung married Lily Jan in 1971, when they were graduate students at CalTech, and have shared a laboratory since 1979. After beginning their PhD studies at Caltech set on careers in theoretical physics, they both chose to switch careers and follow their interest in biology. Their first significant discovery was to prove the existence of peptide neurotransmitters. Since then, the Jans have been pioneers in the study of potassium channels, which are central to understanding the brain's electrical properties, and they have become leaders in the field of developmental neuroscience. http://physio.ucsf.edu/jan/ http://www.hhmi.org/research/investigators/janyn_bio.html Host(s): School of Science, McGovern Institute for Brain Research at MIT

Mouse Genetic Models of Schizophrenia

Fri, 07 May 2010 04:00:00 GMT

05/07/2010 3:30 PM 46"3002Maria Karayiorgou, Columbia UniversityDescription: Schizophrenia is a devastating psychiatric disorder that affects around 1% of the world's population. Maria Karayiorgou discusses the genetic origins of schizophrenia and describes progress in modeling the disorder in animals in order to understand its root cause. Schizophrenia, like other psychiatric disorders, is defined by its clinical symptoms. These include positive symptoms (hallucinations, delusions, thought disorders) and negative symptoms (blunted emotion, lack of volition, poverty of speech and social interactions). People with schizophrenia also show deficits in cognitive functions such as working memory, which although not used as formal diagnostic criteria, are nevertheless characteristic features of the condition. The biological basis of schizophrenia remains largely unknown, but risk of developing the disorder is strongly influenced by heredity. Many genes are involved, including common alleles with weak effects and rarer alleles with stronger effects. The relative contributions of each type are still debated, but Karayiorgou argues that regardless of their overall contribution to the population risk, the genes with the strongest effects are most likely to give insights into biological mechanism. One such mutation, identified previously by Karayiorgou and her colleagues, is a chromosomal deletion known as 22q11, which involves the loss of up to 3 million bases of DNA and some 27 genes. About 30% of people carrying this deletion develop schizophrenia, making it one of the strongest known genetic risk factors for the disorder. In order to understand how this deletion could lead to disease symptoms, Karayiorgou and her colleagues have made a genetically engineered mouse strain with an equivalent deletion. She describes their efforts to characterize the behavioral deficits in these mice, and to explain them in terms of underlying alterations of brain function. Mice with two copies of the deletion die before birth, but mice with a single copy (like humans) are viable and normal in appearance. The mice do however show a number of behavioral deficits, including altered sensorimotor gating and poor performance on tests of working memory, both of which are also seen in human schizophrenia. The mutant mice also show altered electrical activity within the brain _ specifically, a deficit in the synchronization of activity between hippocampus and prefrontal cortex that is linked to working memory. Again, similar disruptions of activity are seen in human patients, suggesting that these mice do indeed represent a useful model for understanding the underlying disease mechanisms. In a search for molecular clues, Karayiorgou then examined how gene expression was altered in the affected brain regions of the mutant mice, using DNA microarrays to measure RNA levels. Not surprisingly, these mice show reduced expression of the genes that are encompassed by the chromosomal deletion (now present in only one copy instead of the normal two), but a number of other transcripts were also affected. Intriguingly, among these are numerous microRNAs (miRNAs); these are small non"coding transcripts that are thought to regulate the expression of many other genes. One of the genes in the deleted region, dgcr8 (also known as Pasha), is known to be involved in the biosynthesis of miRNAs, which could explain why so many miRNA's are affected. Karayairgou then knocked out the dgcr8 gene to see if loss of this gene alone was sufficient to explain the effects on brain function. Mice lacking one copy of dgcr8 showed at least some of the schizophrenia"like features that are also present in the larger deletion. Thus, altered expression of dgcr8, and by extension the many microRNAs that it helps to produce, are likely important contributors in the mouse phenotype, and perhaps also to human schizophrenia. Host(s): School of Science, McGovern Institute for Brain Research at MIT

Sex Battles in the Brain

Fri, 07 May 2010 04:00:00 GMT

05/07/2010 10:30 AM 46"3002Catherine Dulac, Harvard UniversityDescription: The expression of certain genes depends on whether they were inherited from the mother or the father, a phenomenon known as imprinting. Catherine Dulac of Harvard University has discovered that a surprisingly large number of brain genes are imprinted, often in complex ways. Her findings have broad implications for understanding the inheritance of behavioral traits and disease susceptibility. Diploid species such as mammals inherit two copies (alleles) of each gene, one from the mother and one from the father. For most genes, the maternal and paternal alleles are expressed at equal levels. But for imprinted genes, only one allele is expressed while the other is silenced. Twenty years ago, David Haig proposed an evolutionary explanation for imprinting based on genetic conflict between the parents. For species such as mammals, in which the mother contributes more resources (through pregnancy and lactation) than the father, he proposed that genes from the father maximize their fitness by inducing the offspring to consume more maternal resources, whereas genes from mother benefit by sharing resources with their siblings. This idea was supported by findings that paternally expressed genes tend to promote embryonic growth and maternally expressed genes tend to restrict growth. But sibling competition does not end at birth. It continues after birth, through competition for food, parental attention and so on -- and these behaviors are controlled by the brain. For this reason, Dulac and colleagues sought to identify imprinted genes within the mouse brain. Using high throughput sequencing technology, they were able to study gene expression patterns in the cortex and hypothalamus of adult mice, and also in the embryonic brain. These mice were derived by crossing two strains of mice that diverge enough to have at least one difference at every gene, allowing the researchers to identify the parental origin of every transcript. Remarkably, Dulac and colleagues have identified some 1300 imprinted genes _ more than ten times the number that were previously known. The expression patterns of these new genes are surprisingly complex. A given gene can be imprinted in the cortex but not in the hypothalamus or vice versa. Or it can be imprinted in the embryo but not in the adult. In some cases, the same gene can give rise to different transcripts with different patterns of imprinting. There is also an intriguing bias to the pattern of imprinting. In the cortex, the majority of imprinted genes are maternally expressed, whereas in the hypothalamus the majority are paternally expressed. This is consistent with Haig's model, in which paternally derived genes are expected to promote competitive behaviors whereas maternally derived genes will tend to promote cooperation and sharing with siblings. Dulac's team also examined the imprinting of the X"chromosome, which carries a disproportionate number of genes expressed in the brain. Females inherit two copies of the X chromosome, and it is well established that one copy is silenced in every cell, a phenomenon known as X"inactivation. In general, the maternal and paternal X are thought to be silenced with equal probability, but Dulac found that in the cortex, there is a 20% bias toward expression of the maternal X and silencing of the paternal copy. Finally, Dulac describes how some imprinted genes show different patterns of expression in male and female offspring. For example, an allele inherited from the father can be silenced in male but not female offspring, or vice versa. The significance of this finding is not yet fully clear, but one implication is that it provides a potential explanation for sex"specific disease susceptibility. About the Speaker(s): Catherine Dulac is investigating the molecular biology of olfactory signaling and is interested in the developmental processes that ensure appropriate connections between the olfactory sensory neurons and the brain. After completing a Ph.D. in developmental biology at the University of Paris, Dulac joined the laboratory of neuroscientist and HHMI investigator Richard Axel at Columbia University in New York City in 1993. As a postdoc in Axel's lab, Dulac developed a new technology for generating libraries of complementary DNA in individual neurons and, using that technology, identified the first family of pheromone receptors. In 1996, Dulac joined the faculty of Harvard University and was named a Howard Hughes Medical Institute Investigator one year later. She has published more than 50 papers and continues to accumulate honors, including her 2004 election to the American Academy of Arts and Sciences. Host(s): School of Science, McGovern Institute for Brain Research at MIT

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."

Global Pandemics

Tue, 17 Nov 2009 05:00:00 GMT

In his role as a biochemist, Hidde Ploegh explains the "essential features of the lifestyle of the flu virus."

StarGenetics

Wed, 04 Nov 2009 13:05:03 GMT

The Power of Basic Science Applied to Medical Progress: Past Examples and Hope for Schizophrenia and Bipolar Illness

Thu, 22 Oct 2009 04:00:00 GMT

10/22/2009 4:00 PM 26"100Ed Scolnick, Director, Psychiatric Disease Program and the Stanley Center for Psychiatric Research, Broad InstituteDescription: An exemplar of the purpose"driven life in medical science, Ed Scolnick details research milestones from a remarkably varied career, revealing how scientific insight and collaborative effort translate into life"saving solutions for millions. This physician turned biochemist has held distinguished positions at the National Institutes of Health, Merck, and now at MIT, but common themes unite his pursuits: "I'm always excited by the inherent beauty of molecular and biochemical insights into how biology works. Making scientific discoveries for me is tremendously emotionally satisfying and in fact addicting." In his talk, Scolnick touches on such research breakthroughs as identifying virus oncogenes, and developing treatments for cardiovascular disease, Hepatitis B, and osteoporosis, among others. He emphasizes that teasing out the biochemistry of diseases is "the key to success in drug discovery." In Marfan syndrome, for example, investigators learned that a mutant gene leads to a malfunctioning aorta. Finding a cure flowed from understanding the underlying pathological processes. Scolnick proudly describes research on a gene involved with cholesterol buildup and an elevated risk for cardiovascular disease. This led to the development of statins, which has helped dramatically reduce the death rate in people with heart disease. Scolnick offers a dramatic chronology of his pioneering work at Merck starting in 1981 to find an effective AIDS treatment, an effort leading to the protease inhibitor Crixivan. His timeline covers more than a decade of scientific collaboration to block the mechanism of HIV, and involves false starts, the death of a key scientist in the Lockerbie bombing, pressure from AIDS activists and corporate overseers, a "miracle" AIDS patient, breakthroughs in measuring viral protein, and more than one "twist of fate." In 2004, Scolnick turned in a new direction: toward mental illness, a field stalled for decades due to ignorance "about the underlying biochemistry and physiology of the disease." Today, with the help of genomics and computative technologies, researchers are beginning to reveal the basic genetic architecture of schizophrenia and bipolar illness, says Scolnick. The "outline of their biochemistry" is starting to come clear for the first time, leading to the real possibility of novel therapeutics. While the challenges are formidable, he believes, consolidating MIT's "first rate neuroscience, human genetics, chemistry (creates) a unique opportunity to do something in a field that desperately needs the kind of approach and change we were able to bring to the AIDS field." NOTE: Audio levels for Kastner and Horvitz are very low, but improve when Scolnick begins his talk. We apologize for the inferior audio. 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, School of Science

MITES: Genomics Enrichment Course at the Broad

Thu, 29 Jan 2009 15:16:33 GMT

This summer in Genomics, sixteen MITES students were transformed into research scientists. In groups of four, students researched monogenic disorders such as Early Onset Breast Cancer and sequenced the DNA of several individuals to discover novel human genetic variation. Under the guidance of Broad researchers, the students sequenced the genes of diseased and healthy individuals, found mutations in the diseased genomes and studied their effects. In addition to the genomics lab research project, students also participated in a lecture series. Lecture topics included DNA technologies, an overview of genomics research, drug design, and the ethical and social implications of genomics research. Needless to say, the students truly had a blast!

Environmental Health Sciences: Bridging the Gap Between Genetics and Environment

Mon, 17 Dec 2007 19:10:43 GMT

Researchers at MIT's Center for Environmental Health Sciences probe the relationship between genetics and environment in the development of illnesses such as lung cancer. A video produced by AMPS/MIT Libraries for the MIT Museum's classroom/exhibit, "Learning Lab: The Cell."

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

Worms, Life and Death: Cell Suicide in Development and Disease

Tue, 24 Apr 2007 04:00:00 GMT

04/24/2007 4:30 PM 32-123H. Robert Horvitz, '68, David H. Koch Professor of Biology, MITDescription: A microscopic roundworm has come to play a dominant role in some of the most pivotal medical research of our time. In the labs of Robert Horvitz and his colleagues, C. elegans has helped reveal cell death as a normal part of biological development. In this talk, Horvitz painstakingly delineates the series of discoveries based on C. elegans that identified the genetics behind programmed cell death (apoptosis), the disorders that emerge if this normal process stalls, and human counterparts to these disorders, which suggest potential targets for therapy. Because the mature roundworm consists of just 959 cells, it was possible for scientists to track the organism's entire lineage of cell divisions, and to characterize what genetic accidents created mutant worms. Scientists figured out genetic pathways that were essential to normal development in the worm, and which, if disrupted, led to harmful mutations. For instance, the immature roundworm contains 131 cells that are not found in the adult, because they are genetically programmed to die. Every animal, Horwitz says, undergoes apoptosis as a -normal aspect of development." Tadpoles lose their tails to become frogs; lots of animals have webbing -sculpted out by the process of programmed cell death." Over years, Horvitz and his colleagues determined the precise genes responsible for programmed cell death in C. elegans, as well as the genes that protect cells from dying, and the way these genes interact. Horvitz's teams also found likely human equivalents to these critical genes and pathways. If these genes go awry, says Horvitz, -then something is going to lead to disease." Cancer, autoimmune diseases and viral infections result from too little programmed cell death. That's because cell division goes unchecked. There are also human diseases that occur because cells die when they should not: neurodegenerative disorders, retinal degeneration, liver disease, and heart attacks. As a result of Horvitz's work, many new targets have emerged for these diseases, some of which Horvitz himself is pursuing. Horvitz is now aiming his sights at different genetic regulators that tell certain types of cells to live or die, leading to novel therapies for some of our most formidable diseases. About the Speaker(s): H. Robert Horvitz won the 2002 Nobel Prize in Physiology or Medicine (with Sydney Brenner and John Sulston), for his work on programmed cell death (apoptosis), and for his studies concerning organ development in C. elegans. His apoptosis studies may also improve the understanding of neurological disorders such as amyotrophic lateral sclerosis (ALS), a disease that killed Horvitz's father in 1989. In collaboration with others, Horvitz identified a gene involved in the inherited form of ALS, and he is also pursuing other genes involved in the disease. "My hope is that my discoveries will one day lead to advances in medicine that alleviate human suffering and contribute to the world in ways that will benefit mankind," Horvitz has said. He is also an investigator for the Howard Hughes Medical Institute and a member of the McGovern Institute for Brain Research at MIT, and a member of the MIT Center for Cancer Research. He holds appointments at the Massachusetts General Hospital in neurology and in medicine. Horvitz received bachelor's degrees in mathematics and economics from MIT (1968) and an M.A. and Ph.D. (1974) in biology from Harvard University. He was a postdoctoral researcher at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England. He joined the faculty of MIT in 1978 and became professor of biology in 1986 and an investigator of the Howard Hughes Medical Institute in 1988. Host(s): Office of the President, Killian Lecture

Computational and Systems Approaches to Cancer

Thu, 08 Jun 2006 04:00:00 GMT

06/08/2006 8:00 AM 46-3002Michael Yaffe, Professor of Biology, MITDescription: Early on in his lecture, Michael Yaffe serves up an amazing fact: If the distance between each DNA base pair were one foot apart, then each time a cell divided, it would have to copy 568 thousand miles of DNA. This, says Yaffe, is enough to go around the circumference of the earth more than 22 times. What's more, the cell has to copy its DNA with no errors. -I don't know (if) civil engineers ... could make 10 miles of road without making single error," says Yaffe. In the 12 hours a cell takes to copy its DNA to create two daughter cells, -it goes to great pains to make sure everything is done correctly. It initiates checkpoints, like border crossings." Because everyday life exposes DNA to all kinds of damage, cells have evolved -an elaborate surveillance mechanism" to -blow the whistle, signal repair, and recruit repair machinery," or if damage is too great, essentially commit suicide. If something goes wrong with this mechanism at crucial times during cell division, cancer frequently results. Yaffe's in the business of exploring and mathematically mapping the elaborate signal pathways inside cells that sense broken DNA and coordinate damage response. While studying one such process, cell death in the colon, Yaffe found that the traditional biochemistry approach -- picking one molecule, one stimulus and one readout-- doesn't work. -It's like the blind man feeling the elephant's tail, and saying it's a long, thin animal." Yaffe learned that one signal may activate a series of proteins, triggering an amplification loop. A slight change might yield a -whopping response." Just as engineers test integrated circuits at a variety of points, Yaffe came up with a method of testing cell signaling with a variety of proteins. His team came up with 7,000 signaling measurements in 760 dimensions, and 1,400 signal responses. But this data-heavy model for predicting which molecules lead to cell death didn't satisfy Yaffe. With additional mathematical sleight of hand, Yaffe's group boiled down the cell signaling measurements to what Yaffe calls two -canonical super axes": -a global measure of cell stress and death, and another of survival signaling." He hopes to use this slimmed-down model to think about drugs targeting cancer and inflammation. About the Speaker(s): Michael Yaffe received his Ph.D. in Biophysical Chemistry in 1987, and an M.D. in 1989, both from Case Western Reserve University. Before MIT, he served as a surgeon in teaching hospitals in Cleveland and the Boston area, including the Harvard Medical School. He received multiple teaching awards from University Hospitals of Cleveland, and earned the 1998 Howard Hughes Physician Scientist Award, and the 1999 Burroughs Wellcome Career Development Award.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

Innovation Everywhere How the Acceleration of "GNR" (genetics, nanotechnology, robotics) Will Create a Flat and Equitable World

Thu, 29 Sep 2005 04:00:00 GMT

09/29/2005 3:30 PM Ray Kurzweil, '70, Chairman and CEO, Kurzweil Technologies, IncDescription: Ray Kurzweil may be the closest thing we have to a crystal ball. And if anyone has the right to some credibility in the prognostication arena, this overachieving inventor can. With crackling speed, Kurzweil powerpoints through charts illustrating the growth of various technologies over the centuries. His main points: technology evolves exponentially; the rate of technical progress itself is accelerating, so expect to "see 20,000 years of progress in the 21st century, about 1000 times greater than the 20th century." Before you can say, "Hold your horses," Kurzweil is off and running. Say goodbye to cancer and heart disease within 15 years, and hello to living way past 80. And try to survive until the year 2029, which according to Kurzweil's mathematical models, represents "25 turns of the screw in terms of doubling the power of information technology in every aspect of our lives." We'll see reverse engineering of the human brain, and computers that "will combine the subtlety and pattern recognition of human intelligence with the speed, memory and knowledge sharing of machine intelligence." The marriage of nanotechnology and AI will bring us "a killer app"-- nanobots that can keep us healthy from the inside. These will also enable "full immersion virtual reality from within nervous systems" and expand human intelligence, facilitating "brain to brain communication. As for human conflict, Kurzweil sees an end to starvation and energy concerns, but doesn't quite complete his utopia. New technologies may be used in anti-social ways, say, by a bioterrorist. "I'm less optimistic we can avoid all painful issues; we certainly did not do that in the 20th century," concludes Kurzweil.About the Speaker(s): Ray Kurzweil was the principal developer of the first omni-font optical character recognition (OCR), the first print-to-speech reading machine for the blind, the first CCD flat-bed scanner, the first text-to-speech synthesizer, the first music synthesizer capable of recreating the grand piano and other orchestral instruments, and the first commercially marketed, large-vocabulary speech recognition. Ray Kurzweil received the $500,000 Lemelson-MIT Prize, the nation's largest award in invention and innovation, and was inducted in 2002 into the National Inventor Hall of Fame. He won the Winston Gordon medal from the Canadian National Institute for the Blind for his pioneering work using technology for the benefit of blind people. He also received the 1999 National Medal of Technology, the nation's highest honor in technology, from President Clinton in a White House ceremony. He has received 12 honorary Doctorates and honors from three U.S. presidents. Kurzweil has written five books and hundreds of articles. His most recent work,The Singularity is Near, When Humans Transcend Biology (Viking), was published in Spring 2005.Host(s): Office of the Provost, Technology Review

How Cancer Begins

Mon, 22 Sep 2003 04:00:00 GMT

09/22/2003 McGovern AuditoriumRobert A. Weinberg, '64, PhD '69, Daniel K. Ludwig and American Cancer Society Professor for Cancer Research Department of BiologyDescription: If you're worried about getting cancer, do yourself a favor: steer clear of red meat and rich foods, and avoid cigarettes. In this lecture, Robert Weinberg provides the scientific basis for this commonplace advice, as well as a layman's look at the genetic, biochemical and environmental factors that make good cells go bad. Normal cells are civic-minded, lining up together in a precise architecture that gives structure to body tissue. When the cell's genes are damaged, they send out faulty instructions, turning orderly structure into a chaotic mess. This kind of injury to cells likely comes from the outside _ as many as 90% of human cancers are due to bad diets and smoking. Weinberg wants to understand the specific pathways by which the cells' enemies invade and do their damage, in hopes of then being able to halt the process and freeze a cancer's growth. But, cautions Weinberg, better to count on prevention than a cure in the fight against cancer.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, Whitehead Institute for Biomedical ResearchTape #: T17277

Transforming the Next Century

Fri, 23 May 2003 04:00:00 GMT

05/23/2003 3:45 PM KresgeRafael Reif, Provost, and Professor of Electrical Engineering & Computer Science; Tomas Lozano- Perez, '73, SM '77, PhD '80, TIBCO Founders Professor of Computer Science and Engineering ; Jeffrey H. Shapiro, '67, SM '68, EE '69, PhD '70, Julius A. Stratton Professor of Electrical Engineering Description: This panel serves as a fitting finale to the 100th anniversary celebration of EECS, focusing as it does on a fundamental shift in electrical engineering and computing toward biology, and toward a physics of the nearly unimaginable. Tomas Lozano-Perez describes how the designs of nature serve as both models and modeling clay for engineers. Researchers have learned to extract pieces of DNA and paste them onto "chips" to determine what type of proteins are expressed from particular segments of genetic code. They are pursuing a "wiring diagram" of the extremely complex and wireless workings of human cells. And the ultimate prize is a bioengineered drug, fashioned from molecules that can bind precisely with a protein to disable the reproductive machinery of a virus like HIV. Jeffrey Shapiro is working at the intersection of quantum mechanics and engineering. He is developing ways to manipulate photons to achieve not only more secure communications (quantum cryptography), but to attain the far more futuristic goal of quantum computing. Of course, once you have quantum computers, you're going to network them and so you'll need a quantum Internet _ and for that, the only hope is quantum teleportation. That may sound like Star Trek squared, but Shapiro expects to see laboratory demonstrations of qubit teleportation within five years. Host(s): School of Engineering, Electrical Engineering and Computer Science

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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