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Robert Weinberg, PhD
RobertWeinbergPhD (Researcher (Verified) )| Communities: All Cancers | Answers: 8 |
| Member Since: Jun. 2012 |
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Professional Statement
Dr. 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). He is also the first Director of the Ludwig Cancer Center at MIT. He is an internationally recognized authority on the genetic basis of human cancer.
Dr. Weinberg and his colleagues isolated the first human cancer-causing gene, the ras oncogene, and the first known tumor suppressor gene, Rb, the retinoblastoma gene. The principal goal of his research program is to determine how oncogenes, their normal counterparts (proto-oncogenes), and tumor suppressor genes fit together in the complex circuitry that controls cell growth. More recently, his group has succeeded in creating the first genetically defined human cancer cells. He is particularly interested in applying this knowledge to improve the diagnosis and treatment of breast cancer.
His lab now primarily focuses on two areas: the interactions between epithelial and stromal cells (the two major types of cells found in mammalian tissue) that produce carcinomas and the processes by which cancer cells invade and metastasize.
Epithelial and stromal cells. Many mammalian tissues are formed from distinct epithelial and stromal cell layers. Often, a tumor that forms in an epithelial tissue layer must recruit stromal cells in order to become a carcinoma. Weinberg’s lab is exploring the molecular process by which this recruitment occurs. In addition, his lab has been investigating a signaling pathway operating within epithelial cells that enables them to release signals that stimulate blood vessel growth in nearby stromal cells.
Invasion and metastasis. Weinberg’s lab is focusing on a small group of transcription factors—proteins that control gene expression. These proteins, which are typically involved in embryogenesis, may contribute to cancer cells’ ability to disseminate to distant sites in the body where they may form metastases. Weinberg and his team are examining mechanisms by which tumors can reactivate the properties of these proteins that are active during embryonic development and exploit these transcription factors to execute various steps of the “invasion-metastasis” cascade—the sequence of steps that enables primary tumor cells to disseminate through the body and seed cancer cells. Additionally, the scientists are studying the role of cancer stem cells—the self-renewing, tumor-seeding cells that have been found in a number of solid tumors in the past few years. In 2008, Weinberg lab investigators reported a finding that brings together these two research themes: cancer cells induced to follow one of these embryonic pathways gain many of the properties of adult stem cells.
Dr. Weinberg and his colleagues isolated the first human cancer-causing gene, the ras oncogene, and the first known tumor suppressor gene, Rb, the retinoblastoma gene. The principal goal of his research program is to determine how oncogenes, their normal counterparts (proto-oncogenes), and tumor suppressor genes fit together in the complex circuitry that controls cell growth. More recently, his group has succeeded in creating the first genetically defined human cancer cells. He is particularly interested in applying this knowledge to improve the diagnosis and treatment of breast cancer.
His lab now primarily focuses on two areas: the interactions between epithelial and stromal cells (the two major types of cells found in mammalian tissue) that produce carcinomas and the processes by which cancer cells invade and metastasize.
Epithelial and stromal cells. Many mammalian tissues are formed from distinct epithelial and stromal cell layers. Often, a tumor that forms in an epithelial tissue layer must recruit stromal cells in order to become a carcinoma. Weinberg’s lab is exploring the molecular process by which this recruitment occurs. In addition, his lab has been investigating a signaling pathway operating within epithelial cells that enables them to release signals that stimulate blood vessel growth in nearby stromal cells.
Invasion and metastasis. Weinberg’s lab is focusing on a small group of transcription factors—proteins that control gene expression. These proteins, which are typically involved in embryogenesis, may contribute to cancer cells’ ability to disseminate to distant sites in the body where they may form metastases. Weinberg and his team are examining mechanisms by which tumors can reactivate the properties of these proteins that are active during embryonic development and exploit these transcription factors to execute various steps of the “invasion-metastasis” cascade—the sequence of steps that enables primary tumor cells to disseminate through the body and seed cancer cells. Additionally, the scientists are studying the role of cancer stem cells—the self-renewing, tumor-seeding cells that have been found in a number of solid tumors in the past few years. In 2008, Weinberg lab investigators reported a finding that brings together these two research themes: cancer cells induced to follow one of these embryonic pathways gain many of the properties of adult stem cells.
Professional Info
Credential: PhD
School / University: MIT Whitehead Institute
Awards and publications:
• Identified and characterized both the first oncogene and the first tumor suppressor gene
• Demonstrated how certain gene regulators, or transcription factors, contribute to cancer metastasis
• "Scientist of the Year" by Discover magazine (1982)
• Bristol-Myers Award for Distinguished Achievement in Cancer Research (1984)
• Member of the U.S. National Academy of Sciences
• National Medal of Science (1997)
• Wolf Prize in Medicine (2004)
• Landon-AACR Prize for Cancer Research (2006)
• Otto Warburg Medal (2007))
Personal Bio (My story)
Born in Pittsburgh in 1942, Dr. Weinberg received his B.S. (1964) and Ph.D. (1969) degrees in Biology from MIT. He did postdoctoral research at the Weizmann Institute and the Salk Institute in La Jolla, California, and then returned to MIT in 1972. In 1982, he was appointed Professor of Biology at MIT.
Dr. Weinberg is the author or editor of six books and more than 350 articles. He has written a comprehensive cancer textbook entitled "The Biology of Cancer". His other books, intended for a lay audience, are "One Renegade Cell," "Racing to the Beginning of the Road: The Search for the Origin of Cancer" and "Genes and the Biology of Cancer," co-authored with Dr. Harold E. Varmus, former Director of the National Institutes of Health. He is an elected Member of the U.S. National Academy of Sciences and Fellow of the American Academy of Arts and Sciences. He is a Member of the American Philosophical Society and the Institute of Medicine.
Dr. Weinberg is the author or editor of six books and more than 350 articles. He has written a comprehensive cancer textbook entitled "The Biology of Cancer". His other books, intended for a lay audience, are "One Renegade Cell," "Racing to the Beginning of the Road: The Search for the Origin of Cancer" and "Genes and the Biology of Cancer," co-authored with Dr. Harold E. Varmus, former Director of the National Institutes of Health. He is an elected Member of the U.S. National Academy of Sciences and Fellow of the American Academy of Arts and Sciences. He is a Member of the American Philosophical Society and the Institute of Medicine.
City: Cambridge
State: MA
Zip: 02142
RobertWeinbergPhD Activities
It is true that cancer cells often spread and generate metastases long before the primary tumor has been detected. So, even if one wipes out the primary tumor, there is always the danger that metastatic tumor colonies survive and begin to grow and threaten the survival of the person from whom a primary tumor has been removed. However, there is some hope: certain types of treatments that are in current use that succeed in eliminating primary tumors may also have effects on eliminating disseminated cancer cells, and thus eliminating metastases!
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Breast Cancer Tumor Detection, Metastatic Breast Cancer Treatment Process, Breast Tumor Detection New Developments, Treatments, Tumor Pathology, Treatment Process, Primary Tumor, Breast Cancer Tumor, Tumor Detection, Breast Cancer, Breast Tumor, Metastatic Breast Cancer, Breast Cancer Treatment, Breast Cancer Pathology, Metastatic Breast Cancer Pathology
1
Answer |
10 months ago
As mentioned in a previous answer (http://talkabouthealth.com/how-do-cancer-cells-grow-and-replicate-so-quickly-do-they-reproduce-from-themselves-or-somehow-change-normal-cells-to-cancer-cells), cancer cells arise from normal cells in which damaged genetic information accumulates that perturbs the behavior of these cells. For example, when a smoker inhales, the mutagenic chemicals in the cigarette smoke damage genes in lung cells, and these cells, which now carry damaged genes including oncogenes, now begin to proliferate uncontrollably, leading years later to a lung cancer.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Biology, Cancer Genetics, Tumor Biology, Cancer Biology, Cancer Pathology, Tumor Pathology, Cancer
1
Answer |
10 months ago
Cancer cells do not proliferate more rapidly than normal cells. The big difference is that normal cells, after they have created a normal tissue, stop multiplying because of signals that they receive that the tissue construction is now complete and that further cell proliferation is inappropriate. Cancer cells, in stark contrast, continue to proliferate even when such proliferation is inappropriate. Thus, they become "deaf" to the signals around them that would normally succeed in preventing them for continuing to proliferate. Cancer cells arise from normal cells when the genes and thus the DNA within these cells, which provides information and guidelines for normal cell behavior, becomes damage -- mutated. The resulting corrupted information includes, among other damaged genes, the oncogenes described above, which function to urge the cell to proliferate relentlessly rather than in measure amounts appropriate for the construction and maintenance of normal tissue.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Tumor Formation, Biology, Tumor Biology, Cancer Genetics, Gene Mutations, Cancer Pathology, Cancer Biology, Tumor Pathology, Cancer
1
Answer |
10 months ago
The intercommunication of cancer cells with surrounding normal cells -- the latter typically called the tumor "stroma" -- is achieved via the exchange of a complex array of biochemical signals. When a carcinoma first forms, the abnormal cancer cells recruit normal stromal cells from surrounding normal host tissue, doing so in order to procure various types of support from these recruited stromal cells; included among this support is that conveyed by new blood vessels that are recruited into the tumor stroma and supply the tumor as a whole with fresh nutrients and oxygen. Once the stroma of a tumor has existed for a considerable period of time, the cells within the recruit stroma release biochemical signals that impinge on the cancer cells that previously recruited them. These stroma-to-carcinoma signals often affect the behavior of the cancerous carcinoma cells, sometimes inducing them to acquire novel traits, including traits associated with high-grade malignancy. One of these changes in the carcinoma cells is described by the epithelial-mesenchymal transition (EMT) which I described in a previous question (http://talkabouthealth.com/would-you-explain-the-epithelial-mesenchymal-transition-emt-and-how-this-is-involved-in-cancer-metastasis), and which carcinoma cells will often activate in response to signals that they receive from nearby normal stromal cells within the tumor.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Metastatic Cancer Research, Tumor Formation, Tumor Biology, Cancer Biology, Cancer Pathology, Carcinoma Formation, Tumor Pathology, Cancer, Tumor Microenvironment, Biology, Cancer Research, Carcinomas, Research
1
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10 months ago
The invasion-metastasis cascade is simply a sequence of steps that describes how cancer cells from the midst of a primary tumor are able to form distant metastases. In particular, it involves the following steps: local invasion within the tumor, invasion into blood vessels (termed intravasation), transportation via the blood to distant sites in the body, lodging in small vessels in those tissues, invasion through the wall of the vessels out of the circulation and into the tissues themselves (extravasation), the founding of a tiny colony of cancer cells, often termed a micrometastasis, and finally the outgrowth of that colony into a colony of macroscopic size, the last step sometimes being termed "colonization".
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Metastastasis Cascade, Tumor, Tumor Formation, Tumor Biology, Colonization, Cancer Pathology, Cancer Biology, Extravastion, Invasion-Metastasis Cascade, Metastatic Cancer, Tumor Pathology, Intravastation, Biology, Micrometastases, Metastatic Cancer Pathology
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10 months ago
The EMT is a cell-biological behavioral program that operates during the development of normal embryos and is responsible for interconverting one type of cell to another type of cell, more specifically a cell with epithelial properties to one with mesenchymal properties. An epithelial cell typically sits still and surrounds itself with other epithelial neighbors; without this surrounding company, a typical epithelial cell will quickly die. Epithelial cells line the cavities of all of our organs, including the mouth, lungs, stomach, GI tract, liver, pancreas, prostate, breast milk ducts and so forth. Mesenchymal cells are, in contrast, typically mobile cells that do not establish stable long-term relationships with their neighbors and are quite resistant to cell death. When a cell passes through an EMT, typically a carcinoma cell that arises from a normal epithelial tissue will acquire mesenchymal traits that confer on it the ability to invade and even to metastasize to distant sites in the body. Hence by resurrecting a normal cell-biological program, carcinoma cells can acquire an entire suite of traits and ability that make them truly malignant and life-threatening.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Tumor, Biology, Epithelial-Mesenchymal Transition (EMT), Cancer Pathology, Cancer Biology, Metastatic Breast Cancer Pathology, Metastatic Cancer, Tumor Pathology, Carcinoma, Cancer
1
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10 months ago
An oncogene is a cancer-causing gene. We have about 20 thousand genes in each of our cells, some of which are involved in fostering or promoting cell proliferation. When one of the proliferation-promoting gene suffers damage, it begins to urge the cell to proliferate uncontrollably rather than to do so in carefully measured amounts. Such a damaged growth-promoting gene is an oncogene. Indeed, within the genomes -- the collection of genes -- in virtually all human cancer cell types one can find oncogenes that have undergone damage -- mutation -- and are responsible for driving the uncontrolled proliferation of the cancer cells. Such oncogenes are something likened to accelerator pedals that are stuck to the floor of a car.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Genetics, Oncology, Cancer Genetics, Causes, Oncogene, Cancer Biology, Cancer Pathology, Cancer Causes, Cancer
1
Answer |
10 months ago
We knew that cancer-causing agents -- carcinogens -- also function as mutagens -- DNA-damaging agents. Hence, we speculated that within the DNA of cancer cells there must lie damaged sequences -- corrupted genetic information -- that somehow instructs the cell to grow abnormally. With that speculation in mind, we proceed to take the DNA from cancer cells, including human cancer cells, and introduce this DNA (and the associated cellular genes) into normal cells. When the normal cells that had taken up the cancer-cell DNA became themselves converted into cancer cells, we knew that we had found cancer-causing information in the DNA, that is, a damaged gene that instructs the cell around it to multiply uncontrollably.
New answer by RobertWeinbergPhD (Researcher (Verified)) in topic(s) Genetics, Cancer Genetics, Tumor Biology, Oncogene, Cancer Pathology, Cancer Biology, Cancer
1
Answer |
10 months ago
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