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Signaling Pathways in Cancer Symposium: David Sabatini
 
29:27
David Sabatini Whitehead Institute “Growth By The mTOR Pathway” https://ki.mit.edu/news/pathways/2012
Views: 4207 KochInstituteMIT
David Sabatini (Whitehead, MIT, HHMI) 1: Introduction to mTOR and the Regulation of Growth
 
34:06
www.iBiology.org David Sabatini outlines the critical role of mTOR in the regulation of growth. mTOR senses nutrient levels, growth factors and other signals and integrates a response to regulate cell growth. Growth can be defined as the increase in the size of a cell or organism, due to a gain in mass caused by nutrient uptake and assimilation. Surprisingly, how growth is regulated was not well understood until quite recently. In his first talk, David Sabatini describes how insight into this question came from an unusual direction. The small molecule drug rapamycin was known to have anti-growth effects, but its intracellular target was not known. Sabatini explains how he purified and cloned the target of rapamycin from rat brain and showed that it was a protein kinase. This protein was named mTOR in mammals and was shown to be homologous to the TOR proteins in yeast. Sabatini and others went on to show that mTOR is at the heart of two large protein complexes, mTORC1 and mTORC2, that sense upstream signals such as nutrient levels, hormones, and growth factors and direct downstream effectors to build or breakdown resources as needed for cell growth and proliferation. In his second talk, Sabatini explains that mTORC1 responds to many different upstream signals including a variety of growth factors, nutrients, and types of stress. How does mTORC1 sense all these different signals and integrate them to produce a response that regulates cell growth? Sabatini’s lab found that the first step in sensing nutrients such as amino acids is the movement of mTORC1 from a diffuse localization in the cytosol to the lysosomal surface. The lab then spent many years identifying the large number of proteins that regulate the movement of mTORC1 to the lysosome and allow it to sense nutrients and modulate the downstream processes that control cell growth. In particular, the lab identified several proteins that serve as direct sensors of metabolites or amino acids like leucine and arginine. Interestingly, mutations in several of the proteins in the nutrient sensing pathway upstream of mTORC1 are now known to cause human disease, including epilepsy. This suggests that modulation of mTOR, by inhibitors such as rapamycin, might provide a treatment for these conditions. In his final talk, Sabatini focuses on a lysosomal membrane protein that his lab had found to interact with mTORC1 and to sense arginine levels inside the lysosome. In some cell types, the amino acids needed to build new proteins are not taken up as free amino acids but instead come from the breakdown of proteins in the lysosome. This led the lab to ask which arginine-rich proteins are being degraded in the lysosome, which led to the realization that ribosomal proteins are amongst the most arginine-rich proteins in mammalian cells. After many more experiments, they showed that mTORC1 regulates a balance between the biogenesis of ribosomes, and the breakdown of ribosomes (known as ribophagy), dependent on the nutritional state of the cell. Ribophagy seems to be particularly important for supplying the cell with nucleosides during nutrient starvation. Speaker Biography: Dr. David M. Sabatini is a member of the Whitehead Institute for Biomedical Research, a professor of Biology at the Massachusetts Institute of Biology (MIT), an investigator of the Howard Hughes Medical Institute, a senior member of the Broad Institute of Harvard and MIT and a member of the Koch Institute for Integrative Cancer Research at MIT. His lab is interested in the regulation of growth and metabolism in mammals, with a focus on the critical mTOR pathway. Research from Sabatini’s lab has led to a better understanding of the role of the mTOR pathway in diseases such as cancer and diabetes, as well as in aging. Sabatini received his undergraduate degree in biology from Brown University. As a MD/PhD student at Johns Hopkins University School of Medicine, he did his first experiments on rapamycin and mTOR in the lab of Solomon H. Snyder. After completing his MD/PhD in 1997, Sabatini started his own lab as a Whitehead fellow at the Whitehead Institute. In 2002, he became a member of the Whitehead Institute and a faculty member at MIT. Sabatini’s groundbreaking work has been recognized with numerous awards and honors including the National Academy of Science Award in Molecular Biology (2014), the Dickson Prize in Medicine (2017), the Lurie Prize in Biomedical Sciences (2017), and the Switzer Prize (2018). Sabatini was elected to the National Academy of Sciences in 2016. Learn more about the research being done in Sabatini’s lab here: http://sabatinilab.wi.mit.edu and here: https://www.hhmi.org/scientists/david-m-sabatini
Views: 1143 iBiology
David Sabatini (Whitehead, MIT, HHMI) 2: Regulation of mTORC1 by Nutrients
 
30:54
www.iBiology.org David Sabatini outlines the critical role of mTOR in the regulation of growth. mTOR senses nutrient levels, growth factors and other signals and integrates a response to regulate cell growth. Growth can be defined as the increase in the size of a cell or organism, due to a gain in mass caused by nutrient uptake and assimilation. Surprisingly, how growth is regulated was not well understood until quite recently. In his first talk, David Sabatini describes how insight into this question came from an unusual direction. The small molecule drug rapamycin was known to have anti-growth effects, but its intracellular target was not known. Sabatini explains how he purified and cloned the target of rapamycin from rat brain and showed that it was a protein kinase. This protein was named mTOR in mammals and was shown to be homologous to the TOR proteins in yeast. Sabatini and others went on to show that mTOR is at the heart of two large protein complexes, mTORC1 and mTORC2, that sense upstream signals such as nutrient levels, hormones, and growth factors and direct downstream effectors to build or breakdown resources as needed for cell growth and proliferation. In his second talk, Sabatini explains that mTORC1 responds to many different upstream signals including a variety of growth factors, nutrients, and types of stress. How does mTORC1 sense all these different signals and integrate them to produce a response that regulates cell growth? Sabatini’s lab found that the first step in sensing nutrients such as amino acids is the movement of mTORC1 from a diffuse localization in the cytosol to the lysosomal surface. The lab then spent many years identifying the large number of proteins that regulate the movement of mTORC1 to the lysosome and allow it to sense nutrients and modulate the downstream processes that control cell growth. In particular, the lab identified several proteins that serve as direct sensors of metabolites or amino acids like leucine and arginine. Interestingly, mutations in several of the proteins in the nutrient sensing pathway upstream of mTORC1 are now known to cause human disease, including epilepsy. This suggests that modulation of mTOR, by inhibitors such as rapamycin, might provide a treatment for these conditions. In his final talk, Sabatini focuses on a lysosomal membrane protein that his lab had found to interact with mTORC1 and to sense arginine levels inside the lysosome. In some cell types, the amino acids needed to build new proteins are not taken up as free amino acids but instead come from the breakdown of proteins in the lysosome. This led the lab to ask which arginine-rich proteins are being degraded in the lysosome, which led to the realization that ribosomal proteins are amongst the most arginine-rich proteins in mammalian cells. After many more experiments, they showed that mTORC1 regulates a balance between the biogenesis of ribosomes, and the breakdown of ribosomes (known as ribophagy), dependent on the nutritional state of the cell. Ribophagy seems to be particularly important for supplying the cell with nucleosides during nutrient starvation. Speaker Biography: Dr. David M. Sabatini is a member of the Whitehead Institute for Biomedical Research, a professor of Biology at the Massachusetts Institute of Biology (MIT), an investigator of the Howard Hughes Medical Institute, a senior member of the Broad Institute of Harvard and MIT and a member of the Koch Institute for Integrative Cancer Research at MIT. His lab is interested in the regulation of growth and metabolism in mammals, with a focus on the critical mTOR pathway. Research from Sabatini’s lab has led to a better understanding of the role of the mTOR pathway in diseases such as cancer and diabetes, as well as in aging. Sabatini received his undergraduate degree in biology from Brown University. As a MD/PhD student at Johns Hopkins University School of Medicine, he did his first experiments on rapamycin and mTOR in the lab of Solomon H. Snyder. After completing his MD/PhD in 1997, Sabatini started his own lab as a Whitehead fellow at the Whitehead Institute. In 2002, he became a member of the Whitehead Institute and a faculty member at MIT. Sabatini’s groundbreaking work has been recognized with numerous awards and honors including the National Academy of Science Award in Molecular Biology (2014), the Dickson Prize in Medicine (2017), the Lurie Prize in Biomedical Sciences (2017), and the Switzer Prize (2018). Sabatini was elected to the National Academy of Sciences in 2016. Learn more about the research being done in Sabatini’s lab here: http://sabatinilab.wi.mit.edu and here: https://www.hhmi.org/scientists/david-m-sabatini
Views: 434 iBiology
2015 Whitehead Symposium :: Cancer: Treating the "Untreatable"
 
23:59
David Sabatini, Member, Whitehead Institute "Cancer: Treating the "Untreatable" Part II"
David Sabatini (Whitehead, MIT, HHMI) 3: Ribophagy and Nucleotide Recycling
 
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www.iBiology.org David Sabatini outlines the critical role of mTOR in the regulation of growth. mTOR senses nutrient levels, growth factors and other signals and integrates a response to regulate cell growth. Growth can be defined as the increase in the size of a cell or organism, due to a gain in mass caused by nutrient uptake and assimilation. Surprisingly, how growth is regulated was not well understood until quite recently. In his first talk, David Sabatini describes how insight into this question came from an unusual direction. The small molecule drug rapamycin was known to have anti-growth effects, but its intracellular target was not known. Sabatini explains how he purified and cloned the target of rapamycin from rat brain and showed that it was a protein kinase. This protein was named mTOR in mammals and was shown to be homologous to the TOR proteins in yeast. Sabatini and others went on to show that mTOR is at the heart of two large protein complexes, mTORC1 and mTORC2, that sense upstream signals such as nutrient levels, hormones, and growth factors and direct downstream effectors to build or breakdown resources as needed for cell growth and proliferation. In his second talk, Sabatini explains that mTORC1 responds to many different upstream signals including a variety of growth factors, nutrients, and types of stress. How does mTORC1 sense all these different signals and integrate them to produce a response that regulates cell growth? Sabatini’s lab found that the first step in sensing nutrients such as amino acids is the movement of mTORC1 from a diffuse localization in the cytosol to the lysosomal surface. The lab then spent many years identifying the large number of proteins that regulate the movement of mTORC1 to the lysosome and allow it to sense nutrients and modulate the downstream processes that control cell growth. In particular, the lab identified several proteins that serve as direct sensors of metabolites or amino acids like leucine and arginine. Interestingly, mutations in several of the proteins in the nutrient sensing pathway upstream of mTORC1 are now known to cause human disease, including epilepsy. This suggests that modulation of mTOR, by inhibitors such as rapamycin, might provide a treatment for these conditions. In his final talk, Sabatini focuses on a lysosomal membrane protein that his lab had found to interact with mTORC1 and to sense arginine levels inside the lysosome. In some cell types, the amino acids needed to build new proteins are not taken up as free amino acids but instead come from the breakdown of proteins in the lysosome. This led the lab to ask which arginine-rich proteins are being degraded in the lysosome, which led to the realization that ribosomal proteins are amongst the most arginine-rich proteins in mammalian cells. After many more experiments, they showed that mTORC1 regulates a balance between the biogenesis of ribosomes, and the breakdown of ribosomes (known as ribophagy), dependent on the nutritional state of the cell. Ribophagy seems to be particularly important for supplying the cell with nucleosides during nutrient starvation. Speaker Biography: Dr. David M. Sabatini is a member of the Whitehead Institute for Biomedical Research, a professor of Biology at the Massachusetts Institute of Biology (MIT), an investigator of the Howard Hughes Medical Institute, a senior member of the Broad Institute of Harvard and MIT and a member of the Koch Institute for Integrative Cancer Research at MIT. His lab is interested in the regulation of growth and metabolism in mammals, with a focus on the critical mTOR pathway. Research from Sabatini’s lab has led to a better understanding of the role of the mTOR pathway in diseases such as cancer and diabetes, as well as in aging. Sabatini received his undergraduate degree in biology from Brown University. As a MD/PhD student at Johns Hopkins University School of Medicine, he did his first experiments on rapamycin and mTOR in the lab of Solomon H. Snyder. After completing his MD/PhD in 1997, Sabatini started his own lab as a Whitehead fellow at the Whitehead Institute. In 2002, he became a member of the Whitehead Institute and a faculty member at MIT. Sabatini’s groundbreaking work has been recognized with numerous awards and honors including the National Academy of Science Award in Molecular Biology (2014), the Dickson Prize in Medicine (2017), the Lurie Prize in Biomedical Sciences (2017), and the Switzer Prize (2018). Sabatini was elected to the National Academy of Sciences in 2016. Learn more about the research being done in Sabatini’s lab here: http://sabatinilab.wi.mit.edu and here: https://www.hhmi.org/scientists/david-m-sabatini
Views: 257 iBiology
3rd de Duve Lecture - D. Sabatini: mTOR and lysosomes in growth control
 
01:01:09
given by Prof. David Sabatini (Cambridge, MA, USA) on March 1, 2018
Views: 1048 de Duve Institute
30. Cancer 2
 
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MIT 7.013 Introductory Biology, Spring 2011 View the complete course: http://ocw.mit.edu/7-013S11 Instructor: Tyler Jacks In this lecture, Professor Jacks discusses the genes and mutations involved in the development of cancer, how to find them, and why they are important. License: Creative Commons BY-NC-SA More information at http://ocw.mit.edu/terms More courses at http://ocw.mit.edu
Views: 14200 MIT OpenCourseWare
2011 Summer Symposium: David Sabatini
 
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mTOR signaling and cancer metabolism David Sabatini, Whitehead Institute https://ki.mit.edu/news/symposium/2011
Views: 234 KochInstituteMIT
Signaling Pathways in Cancer Symposium: Rudolf Jaenisch
 
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Rudolf Jaenisch Whitehead Institute “Stem Cells, Pluripotency and Nuclear Reprogramming” https://ki.mit.edu/news/pathways/2012
Views: 96 KochInstituteMIT
David Sabatini, Ph D , M D , Growth By The mTOR Pathway
 
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David Sabatini, Ph.D., M.D. of the Whitehead Institute at MIT discussed his work defining the role of mTOR in the amino acid sensing pathway.
Signaling Pathways in Cancer Symposium: Michael Yaffe
 
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Michael Yaffe David H. Koch Institute for Integrative Cancer Research at MIT “Harnessing Cross-Talk Between Signaling Pathways to Improve Cancer Treatment” https://ki.mit.edu/news/pathways/2012
Views: 358 KochInstituteMIT
Dr. David Sabatini's Research on the mTOR Pathway
 
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The FNIH selected David M. Sabatini, M.D., Ph.D., as the recipient of the 5th annual Lurie Prize in Biomedical Sciences for discovery of the mTOR (mechanistic target of rapamycin) cellular pathway as a key regulator of growth and metabolism in response to nutrients. Learn about Dr. Sabatini's work on nutrient sensing and the impact of caloric restriction on health and lifespan. Dr. Sabatini is a Member of the Whitehead Institute for Biomedical Research, a Professor of Biology at the Massachusetts Institute of Technology and an Investigator of the Howard Hughes Medical Institute.
Views: 2626 FNIH
2015 Whitehead Symposium :: Cancer: Treating the "Untreatable"
 
24:12
Lyerka Miller introduces Whitehead Director David C. Page
2015 Whitehead Symposium :: Cancer: Treating the "Untreatable"
 
18:13
Hazel Sive, Member, Whitehead Institute "An Introduction to the Importance of Basic Research"
2011 KI Symposium: David Sabatini (Part 2 of 2)
 
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Part 2 of David Sabatini's talk, "mTOR Signaling and Cancer Metabolism," presented at the 2011 Koch Institute Summer Symposium.
Views: 1962 KochInstituteMIT
2011 KI Symposium: David Sabatini (Part 1 of 2)
 
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Part 1 of David Sabatini's talk, "mTOR Signaling and Cancer Metabolism," presented at the 2011 Koch Institute Summer Symposium.
Views: 5154 KochInstituteMIT
ROBERT A. WEINBERG, PhD - EMT, Cancer Stem Cells and the Mechanisms of Malignant Progression
 
01:04:53
Winner of the Salk Institute Medal for Research Excellence An internationally recognized authority on the genetic basis of human cancer, Robert A. Weinberg is a founding member of the Whitehead Institute for Biomedical Research and the Daniel K. Ludwig Professor for Cancer Research at the Massachusetts Institute of Technology (MIT). In 1992, he earned the Gairdner Foundation International Award for Achievements in Medical Science. He is also a recipient of the National Medal of Science, the Wolf Prize and the Breakthrough Prize in Life Sciences. He is the first Director of the Ludwig Cancer Center at MIT. Over the past three decades, Weinberg has made breakthrough discoveries in the molecular and genetic roots of cancers. His lab discovered the first oncogene in 1982 and the first tumor suppressor gene in 1986. Most recently, Weinberg and his colleagues were the first to define the genetic hallmarks that a normal human cell must acquire to be transformed into a human cancer cell.
Views: 10307 Salk Institute
Big Ideas for Busy People 2013 - David Sabatini
 
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"Caloric Restriction: How Beneficial Is It?" David Sabatini | Professor of Biology, MIT; Whitehead Institute for Biomedical Research; Broad Institute Big Ideas for Busy People (April 12, 2013) House rules: 5 minutes per speaker, 5 minutes for audience questions, 10 total Big Ideas throughout the night.
Regulation of growth by the mTOR pathway
 
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Regulation of growth by the mTOR pathway Air date: Wednesday, March 20, 2013, 3:00:00 PM Wednesday Afternoon Lecture Series The mammalian target of rapamycin (mTOR), the target of the immunosuppressive drug rapamycin, is the central component of a nutrient- and hormone-sensitive signaling pathway that regulates cell growth and proliferation. This pathway becomes deregulated in many human cancers and plays an important role in the control of metabolism and aging. Sabatini's lab has identified two distinct mTOR-containing proteins complexes, one of which regulates growth through S6K and another that regulates cell survival through Akt. These complexes, mTORC1 and mTORC2, define both rapamycin-sensitive and insensitive branches of the mTOR pathway. New results on the regulation and functions of the mTORC1 and mTORC2 pathways will be discussed. Author: David M. Sabatini, M.D., Ph.D., MIT Runtime: 00:59:04 Permanent link: http://videocast.nih.gov/launch.asp?17962
Views: 45940 nihvcast
2015 Whitehead Symposium :: Cancer: Treating the "Untreatable"
 
23:55
Richard Young, Member, Whitehead Institute "Cancer: Treating the "Untreatable" Part I"
Whitehead Institute: How to boost the efficacy of the chemotherapy drug methotrexate
 
03:19
Naama Kanarek, a postdoctoral researcher in the lab of Whitehead Member David Sabatini, explains how new genetic tools are allowing insights into the sensitivity of cancer cells to methotrexate.
2015 Summer Symposium:  Jacks
 
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Engineering the Cancer Genome Tyler Jacks, PhD Director David H. Koch Professor of Biology Koch Institute at MIT https://ki.mit.edu/news/symposium/2015
Views: 146 KochInstituteMIT
Dr. David Sabatini - Conferencia IDIBELL 2012, Barcelona.
 
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El Dr. David Sabatini habla con ecancer en la Conferencia de IDIBELL en Medicina Personalizada. Explica el uso de la rapimicina y su implicación en el sistema de "MTor Pathway". Para mayor información visite http://www.ecancerlatinoamerica.org
2010 KI Symposium: David Tuveson (Part 1 of 3)
 
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Part 1 of David Tuveson's talk, "Oncogenic Kras: Models and Medicines," presented at the 2010 Koch Institute Summer Symposium. http://ki.mit.edu
Views: 680 KochInstituteMIT
Promise, Progress and Politics of Cancer Research - Harold Varmus
 
01:17:47
Nobel Laureate Harold Varmus delivered his lecture 'Promise, Progress and Politics of Cancer Research' at Institut Curie in Paris. Dr Varmus visited Paris in May 2016 as part of the Nobel Prize Inspiration Initiative. Through the Initiative, Nobel Laureates give career advice for young scientists, explain their discoveries and give insights into life after the Nobel Prize. To hear more insights from Nobel Laureates please subscribe to our YouTube channel or visit www.nobelprizeii.org.
Views: 606 NobelPrizeII
2016 Killian Lecture: Tyler Jacks, "Unlocking the Secrets of Cancer"
 
01:10:55
Lecture title: "Unlocking the Secrets of Cancer" Tyler Jacks, the David H. Koch professor of biology and director of the Koch Institute for Integrative Cancer Research, was MIT’s James R. Killian Jr. Faculty Achievement Award winner for 2015–2016. A pioneering cancer biologist, Professor Jacks was recognized by the committee for his influence on the field of cancer research and for his leadership of MIT’s multidisciplinary cancer research community. Thursday, February 11, 2016 4 pm Huntington Hall (10-250)
Views: 1677 MIT Institute Events
Killing cancer cells by targeting glucose metabolism
 
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Cristina Muñoz Pinedo. Cell Death Regulation Group IDIBELL (Institut d'Investigació Biomèdica de Bellvitge) Oncogenic transformation promotes metabolic changes which makes tumors "addicted" to certain metabolites. For this reason, inhibition of tumor metabolism is a promising new therapeutic approach. However, little is known about how metabolic stress triggers tumor cell death. Glucose depletion has been shown to kill cells either by necrosis (non-apoptotic, pro-inflamatory cell death) or by the mitochondrial pathway of apoptosis. Our studies indicate that several tumor cell lines of different origins die in a non-apoptotic manner when deprived of glucose. However, we have recently described an atypical apoptotic pathway engaged in cells from solid tumors. Surprisingly, apoptosis induced by glucose deprivation is independent of the Bcl-2-regulated mitochondrial pathway. We will describe this apoptotic pathway mediated by caspase-8, which is the initiator caspase engaged by death receptors of the TNF family. 2-deoxyglucose is a non-metabolizable glucose analog which competes with glucose and has shown anti-tumor effects in animals. Moreover, this compound is been tested in clinical trials. We are currently studying sensitivity of tumor cells, especially sarcoma cell lines, to 2-deoxyglucose. Interestingly, 2-deoxyglucose promoted apoptosis in cell lines in which glucose deprivation promoted necrosis, suggesting different death mechanisms. 2-deoxyglucose activates the mitochondrial apoptotic pathway and regulates several apoptotic proteins in p53-deficient cells. We found death under normoxia to be associated to endoplasmic reticulum stress rather than lack of ATP. We will discuss the signaling pathways involved in responses to nutritional stress and how to improve sensitivity of tumor cells to metabolic targeting.
Conquering Cancer: Personalized Cancer Care
 
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Session Chair: Michael B. Yaffe, David H. Koch Institute for Integrative Cancer Research at MIT; Professor, Departments of Biology and Biological Engineering, MIT; Senior Associate, Broad Institute Panel: Daniel A. Haber SB '77 SM '77, Director, Massachusetts General Hospital Cancer Center; Isselbacher/Schwartz Professor, Harvard Medical School; Investigator, Howard Hughes Medical Institute Michael T. Hemann, David H. Koch Institute for Integrative Cancer Research at MIT; Latham Family Career Development Assistant Professor of Biology, MIT David M. Livingston, Emil Frei Professor of Genetics and Medicine, Harvard Medical School; Deputy Director, Dana-Farber/Harvard Cancer Center; Chief, Charles A. Dana Division of Human Cancer Genetics Corbin Elizabeth Meacham, G, David H. Koch Institute for Integrative Cancer Research at MIT; Department of Biology, MIT
2010 KI Symposium: David Raulet (Part 1 of 3)
 
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Part 1 of David Raulet's talk, "Recognition of Cancer Cells by Natural Killer Cells," presented at the 2010 Koch Institute Summer Symposium. http://ki.mit.edu
Views: 400 KochInstituteMIT
Signaling Pathways in Cancer Symposium:  William Kaelin
 
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William Kaelin Dana Farber Cancer Institute “The VHL Tumor Suppressor Protein: Insights into Oxygen Sensing and Cancer Metabolism” https://ki.mit.edu/news/pathways/2012
Views: 701 KochInstituteMIT
2012 Koch Institute Symposium: Introductory Remarks
 
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Introductory remarks by Director Tyler Jacks at the 2012 Summer Symposium on Epigenetics, Plasticity and Cancer at the Koch Institute for Integrative Cancer Research at MIT. http://ki.mit.edu/news/symposium
Views: 150 KochInstituteMIT
What Can Fat Cells Teach Us About Cancer?
 
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Dana-Farber Cancer Institute's Bruce Spiegelman, PhD, explains the importance of fat cell differentiation, energy metabolism and the potential implications of his research for the treatment of cancer.
Whitehead Institute: Reducing the toxicity of the chemotherapy drug methotrexate
 
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Naama Kanarek, a postdoctoral researcher in the lab of Whitehead Member David Sabatini, discusses some of the challenges of methotrexate chemotherapy treatment and how research might help address these challenges.
Clevers H (2015): Wnt signaling, Lgr5 stem cells, organoids and cancer
 
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Walter and Eliza Hall Institute Centenary Scientific Symposium 31 July 2015 Session 9: Cancer Professor Hans Clevers Hubrecht Institute, Netherlands
Views: 17964 WalterandElizaHall
Koch Institute Public Galleries: Cutting off Cancer's Food Supply
 
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How can cancer medicine take advantage of cancer's peculiar eating habits? This video traces the work of the KI's Vander Heiden lab to understand why cancer burns sugar differently from other human cells, and how this could lead to better cancer therapies. The video currently appears in the interactive exhibits of the KI Public Galleries. Learn more at http://ki.mit.edu/galleries.
Views: 585 KochInstituteMIT
The PI3K / AKT / mTOR Pathway Part 1
 
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In this video we discuss the PI3K / AKT / mTOR pathway and its involvement in cancer.
Views: 9185 Ben1994
The Edge of Medicine and Ageing - David Sinclair
 
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Before the 1990’s, old age was seen as an unavoidable fact of life; like an old car, we just wear out. Since then we’ve addressed ageing like a set of fixable parts. When an organ breaks down, we medicate it or replace it. When cancer appears we seek to eradicate it. David Sinclair doesn’t want you to think that way. Speaking at Amplify, David described ageing as something we can prevent, and in doing so, avoid the diseases that we become more vulnerable to. According to David, when we successfully eradicate cancer, we only extend someone’s lifespan by 2.3 years, because in an ageing body, another organ is nearing expiry. AMP’s Amplify innovation and ideas program is Australia’s leading business and innovation platform for exploring technology, thought leadership and customer experience with some of the world’s boldest thinkers. For more information on this talk, head to https://www.amp.com.au/amplify/amplify-insights/david-sinclair-the-edge-of-medicine-and-ageing
Views: 23817 AMPAMPLIFY
Prof David Kwiatkowski discusses recent developments in understanding kidney cancer genetics
 
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At the Thirteenth International Kidney Cancer Symposium, Prof David Kwiatkowski (Brigham and Women's Hospital, MA) discusses targeting the mTOR pathway in kidney cancer treatment. It may be clinically necessary to target different proteins, mTOR, TSC1 and TSC2, of the mTOR pathway. Mutations in genes encoding for these proteins correlate with therapeutic response, and this may influence clinical trial design and provide the basis for personalised medicine in kidney cancer.
2011 KI Symposium: Benjamin Cravatt (Part 2 of 2)
 
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Part 2 of Benjamin Cravatt's talk, "Mapping Dysregulated Metabolic Pathways in Cancer by Activity-Based Proteomics," presented at the 2011 Koch Institute Summer Symposium.
Views: 1258 KochInstituteMIT
SOLUTIONS with/in/sight: Matthew Vander Heiden
 
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KI member Matthew Vander Heiden, Eisen and Chang Career Development Professor and associate professor of biology at MIT, discusses the recent discovery of cancer-associated mutations in a family of enzymes known as IDH and his own work in translating this discovery into new tools for cancer detection. Presented as part of the Koch Institute's with/in/sight public lecture series: http://ki.mit.edu/news/events/withinsight
Views: 1579 KochInstituteMIT
Founding of the Whitehead Institute
 
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Whitehead Institute provides scientists with the resources and freedom to follow their scientific instincts, form novel collaborations and conduct high-risk research. This retrospective video includes comments from founder Jack Whitehead, founding Director David Baltimore, and founding Faculty.
Views: 380 ngiese
"The regulation of cell metabolism and proliferation by mTOR complex 2" Estela Jacinto, PhD
 
03:31
Estela Jacinto, PhD, discusses her ongoing research around a protein called mTOR, the role it plays in cancer cell metabolism and why it is one of the keys to controlling cancer. Dr. Jacinto also discusses the personal connection that drives the work that both she and her husband do, as they seek to discover new therapeutic targets for cancer, diabetes, obesity and autoimmunity. Dr. Jacinto represented the medical school in the Association of American Medical Colleges, "AAMC Basic Research Snapshot to Highlight Basic Biomedical Research" competition. Nominated by Gary Brewer, PhD, interim chair, Biochemistry and Molecular Biology. Dr. Jacinto's submission included this video describing the exciting research supported by her NIH grant: "The regulation of cell metabolism and proliferation by mTOR complex 2." Sponsored by AAMC's Group on Research Advancement and Development, the competition seeks to raise the profile of promising new research at member institutions and to communicate to the public the human face of discovery at medical schools and teaching hospitals.
2010 KI Symposium: James Collins (Part 1 of 3)
 
10:47
Part 1 of James Collins' talk, "A Network Biology Approach to Cancer," presented at the 2010 Koch Institute Summer Symposium. http://ki.mit.edu
Views: 237 KochInstituteMIT
81st Symposium - Targeting Cancer - David Tuveson
 
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2016 Cold Spring Harbor Laboratory Symposium on Quantitative Biology Targeting Cancer Interview with David Tuveson Cold Spring Harbor Laboratory, NY Interviewer: Gemma Alderton Nature Reviews Cancer, London, UK Attend a CSHL meeting: http://bit.ly/cshlmtg Train at a CSHL course: http://bit.ly/cshlcourses Subscribe to receive new video notifications: http://bit.ly/2aVrXaM CONNECT WITH US Blog: http://bit.ly/cshlcxblog Twitter: http://bit.ly/cshlmctwitter Instagram: http://bit.ly/cshlmcinsta Facebook: http://bit.ly/cshlmcfb Website: http://bit.ly/cshlmtgcrs
Views: 1081 CSHL Leading Strand
Black Cat by D. Sabatini at Sister Wicked Open Mic, Sept 2017
 
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Black Cat, an original by David Sabatini performed at Sister Wicked Open Mic, Sept 30, 2017
Dispelling Cancer Myths Panel - Living with Cancer Symposium 2018
 
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Dr. Donald W. Northfelt, Mayo Clinic, is joined by a panel of experts to dispell common cancer myths. This patient and caregiver symposium provides comprehensive, patient-friendly information on the diagnosis and treatment of cancer. This annual symposium is the first of its kind and provides a unique opportunity for supportive and beneficial dialog between patients, their family members and national thought leaders. Learn more: https://www.Mayoclinic.org/ArizonaCancerSymposium
Views: 276 Mayo Clinic
The Human Genome: Collaboration is the New Competition | Dr. David Haussler | TEDxSantaCruz
 
15:56
Dr. David Haussler shares the compelling story about the race between private and public entities to complete the first DNA sequencing of the human genome. What is the significance of providing the world with the first open source sequenced genome and the accompanying Genome Browser tool? Only the opportunity for scientists and medical professionals around the globe to collaborate in ways that are producing gene therapies previously thought impossible... and more. David Haussler is scientific director of the UC Santa Cruz Genomics Institute and director of the Center for Biomolecular Science and Engineering. His work has spawned a cancer research project, a project to map the genome of 10,000 animal species, and programs in computer science, mathematics, microbiology, and medical research. He has a private firm, Five3 Genomics, and is a leader in a global alliance of 70 organizations to fight disease via sharing of genomics and clinical data. This talk was given at a TEDx event using the TED conference format but independently organized by a local community. Learn more at http://ted.com/tedx
Views: 14979 TEDx Talks