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7.341 Of Mice and Men: Humanized Mice in Cancer Research (MIT) 7.341 Of Mice and Men: Humanized Mice in Cancer Research (MIT)

Description

This course will act as an introduction to the latest developments in the fields of cancer biology and immunotherapy. Almost everyone knows someone whose life has been affected by cancer. Why is cancer such a difficult disease to treat? What is the best system to model the development of a human tumor? How can new treatment modalities, especially immune-based therapies that harness the natural ability of immune cells to kill target cells, be developed to treat cancer? These and other questions will be addressed in this course. We will explore the concepts of mouse models for human cancer, humanized cancer mice and cancer immunotherapy by reading recent and classic research articles. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These This course will act as an introduction to the latest developments in the fields of cancer biology and immunotherapy. Almost everyone knows someone whose life has been affected by cancer. Why is cancer such a difficult disease to treat? What is the best system to model the development of a human tumor? How can new treatment modalities, especially immune-based therapies that harness the natural ability of immune cells to kill target cells, be developed to treat cancer? These and other questions will be addressed in this course. We will explore the concepts of mouse models for human cancer, humanized cancer mice and cancer immunotherapy by reading recent and classic research articles. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These

Subjects

cancer | cancer | immunotherapy | immunotherapy | mouse models | mouse models | humanized cancer mice | humanized cancer mice | humice | humice | cancer biology | cancer biology | cancer therapy | cancer therapy | oncogenes | oncogenes | humanization | humanization | personalized mice | personalized mice

License

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7.27 Principles of Human Disease (MIT) 7.27 Principles of Human Disease (MIT)

Description

This course covers current understanding of, and modern approaches to human disease, emphasizing the molecular and cellular basis of both genetic disease and cancer. Topics include: The Genetics of Simple and Complex Traits; Karyotypic Analysis and Positional Cloning; Genetic Diagnosis; The Roles of Oncogenes and Tumor Suppressors in Tumor Initiation, Progression, and Treatment; The Interaction between Genetics and Environment; Animal Models of Human Disease; Cancer; and Conventional and Gene Therapy Treatment Strategies. This course covers current understanding of, and modern approaches to human disease, emphasizing the molecular and cellular basis of both genetic disease and cancer. Topics include: The Genetics of Simple and Complex Traits; Karyotypic Analysis and Positional Cloning; Genetic Diagnosis; The Roles of Oncogenes and Tumor Suppressors in Tumor Initiation, Progression, and Treatment; The Interaction between Genetics and Environment; Animal Models of Human Disease; Cancer; and Conventional and Gene Therapy Treatment Strategies.

Subjects

human disease | human disease | molecular basis of genetic disease | molecular basis of genetic disease | molecular basis of cancer | molecular basis of cancer | cellular basis of genetic disease | cellular basis of genetic disease | cellular basis of cancer | cellular basis of cancer | genetics of simple and complex traits | genetics of simple and complex traits | karyotypic analysis | karyotypic analysis | positional cloning | positional cloning | genetic diagnosis | genetic diagnosis | roles of oncogenes | roles of oncogenes | tumor suppressors | tumor suppressors | tumor initiation | tumor initiation | tumor progression | tumor progression | tumor treatment | tumor treatment | interaction between genetics and environment | interaction between genetics and environment | animal models of human disease | animal models of human disease | cancer | cancer | conventional treatment strategies | conventional treatment strategies | gene therapy treatment strategies | gene therapy treatment strategies

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.342 Cancer Biology: From Basic Research to the Clinic (MIT) 7.342 Cancer Biology: From Basic Research to the Clinic (MIT)

Description

This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana

Subjects

cancer | cancer | tumor | tumor | metastasis | metastasis | genetic analysis | genetic analysis | cancer biology | cancer biology | model organisms | model organisms | genetic pathways | genetic pathways | uncontrolled growth | uncontrolled growth | tumor suppressor genes | tumor suppressor genes | oncogenes | oncogenes | tumor initiation | tumor initiation | cell cycle | cell cycle | chromosomal aberration | chromosomal aberration | apoptosis | apoptosis | cell death | cell death | signal transduction pathways | signal transduction pathways | proto-oncogene | proto-oncogene | mutation | mutation | DNA mismatch repair | DNA mismatch repair | telomeres | telomeres | mouse models | mouse models | tissue specificity | tissue specificity | malignancy | malignancy | stem cells | stem cells | therapeutic resistance | therapeutic resistance | differentiation | differentiation | caner research | caner research | cancer therapeutics | cancer therapeutics | chemotherapy | chemotherapy

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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HST.525J Tumor Pathophysiology and Transport Phenomena (MIT) HST.525J Tumor Pathophysiology and Transport Phenomena (MIT)

Description

Tumor pathophysiology plays a central role in the growth, invasion, metastasis and treatment of solid tumors. This class applies principles of transport phenomena to develop a systems-level, quantitative understanding of angiogenesis, blood flow and microcirculation, metabolism and microenvironment, transport and binding of small and large molecules, movement of cancer and immune cells, metastatic process, and treatment response. Additional Faculty Dr. Pat D'Amore Dr. Dan Duda Dr. Robert Langer Prof. Robert Weinberg Dr. Marsha Moses Dr. Raghu Kalluri Dr. Lance Munn Tumor pathophysiology plays a central role in the growth, invasion, metastasis and treatment of solid tumors. This class applies principles of transport phenomena to develop a systems-level, quantitative understanding of angiogenesis, blood flow and microcirculation, metabolism and microenvironment, transport and binding of small and large molecules, movement of cancer and immune cells, metastatic process, and treatment response. Additional Faculty Dr. Pat D'Amore Dr. Dan Duda Dr. Robert Langer Prof. Robert Weinberg Dr. Marsha Moses Dr. Raghu Kalluri Dr. Lance Munn

Subjects

HST.525 | HST.525 | 10.548 | 10.548 | tumor | tumor | cancer | cancer | tumor vasculature | tumor vasculature | antiangiogenesis | antiangiogenesis | bone marrow-derived stem cells | bone marrow-derived stem cells | BMDC | BMDC | stem cell research | stem cell research | experimental cancer therapy | experimental cancer therapy | cancer research | cancer research | tumor-host interactions | tumor-host interactions | vascular normalization | vascular normalization | vascular transport | vascular transport | interstitial transport | interstitial transport | lymphatic transport | lymphatic transport | microcirculation | microcirculation | molecular therapeutics | molecular therapeutics | blood vessels | blood vessels | angiogenesis | angiogenesis | drug delivery | drug delivery | intravital microscopy | intravital microscopy

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT) 7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT)

Description

The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an

Subjects

DNA | DNA | damage checkpoints | damage checkpoints | cancer | cancer | cells | cells | human cells | human cells | exogenous | exogenous | endogenous | endogenous | checkpoints | checkpoints | gene | gene | signaling | signaling | cancer biology | cancer biology | cancer prevention | cancer prevention | primary sources | primary sources | discussion | discussion | DNA damage | DNA damage | molecular | molecular | enzyme | enzyme | cell cycle | cell cycle | extracellular cues | extracellular cues | growth factors | growth factors | Cdk regulation | Cdk regulation | cyclin-dependent kinase | cyclin-dependent kinase | p53 | p53 | tumor suppressor | tumor suppressor | apoptosis | apoptosis | MDC1 | MDC1 | H2AX | H2AX | Rad50 | Rad50 | Fluorescence activated cell sorter | Fluorescence activated cell sorter | Chk1 | Chk1 | mutant | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT) 7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT)

Description

Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching. Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

Subjects

DNA | DNA | damage checkpoints | damage checkpoints | cancer | cancer | cells | cells | human cells | human cells | exogenous | exogenous | endogenous | endogenous | checkpoints | checkpoints | gene | gene | signaling | signaling | cancer biology | cancer biology | cancer prevention | cancer prevention | primary sources | primary sources | discussion | discussion | DNA damage | DNA damage | molecular | molecular | enzyme | enzyme | cell cycle | cell cycle | extracellular cues | extracellular cues | growth factors | growth factors | Cdk regulation | Cdk regulation | cyclin-dependent kinase | cyclin-dependent kinase | p53 | p53 | tumor suppressor | tumor suppressor | apoptosis | apoptosis | MDC1 | MDC1 | H2AX | H2AX | Rad50 | Rad50 | Fluorescence activated cell sorter | Fluorescence activated cell sorter | Chk1 | Chk1 | mutant | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.342 Chronic Infection and Inflammation: What are the Consequences on Your Health? (MIT) 7.342 Chronic Infection and Inflammation: What are the Consequences on Your Health? (MIT)

Description

In this course we will explore the new emerging field of pathogen-induced chronic diseases. Work in this field has redefined the causes of some major disorders, such as ulcers. By reading the primary research literature we will learn about the molecular mechanisms through which pathogens cause disease. The diseases that we cover will be introduced with a short patient case study. We will discuss the bacterium Helicobacter pylori and gastric disease, HPV and cervical cancer, hepatitis C virus and liver disease, Epstein-Barr virus and lymphoma, Cytomegalovirus and atherosclerosis, as well as diabetes and multiple sclerosis. We will study technical advances in the fight against microbes and explore future directions for new treatment strategies of chronic infections and inflammation. This cou In this course we will explore the new emerging field of pathogen-induced chronic diseases. Work in this field has redefined the causes of some major disorders, such as ulcers. By reading the primary research literature we will learn about the molecular mechanisms through which pathogens cause disease. The diseases that we cover will be introduced with a short patient case study. We will discuss the bacterium Helicobacter pylori and gastric disease, HPV and cervical cancer, hepatitis C virus and liver disease, Epstein-Barr virus and lymphoma, Cytomegalovirus and atherosclerosis, as well as diabetes and multiple sclerosis. We will study technical advances in the fight against microbes and explore future directions for new treatment strategies of chronic infections and inflammation. This cou

Subjects

Seminar | Seminar | literature review | literature review | cancer | cancer | vaccine | vaccine | antibiotic | antibiotic | chronic | chronic | atherosclerosis | atherosclerosis | diabetes | diabetes | human papilloma virus | human papilloma virus | HPV | HPV | helicobacter pylori | helicobacter pylori | epstein-barr | epstein-barr | treatment strategies | treatment strategies | laboratory techniques | laboratory techniques | lab | lab | herpes | herpes | microbes | microbes | infection | infection | health | health | Epstein-Barr | Epstein-Barr | cervical cancer | cervical cancer | cirrhosis | cirrhosis | multiple sclerosis | multiple sclerosis | hepatitis | hepatitis | hepatocellular carcinoma | hepatocellular carcinoma | gastric | gastric

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.341 Of Mice and Men: Humanized Mice in Cancer Research (MIT)

Description

This course will act as an introduction to the latest developments in the fields of cancer biology and immunotherapy. Almost everyone knows someone whose life has been affected by cancer. Why is cancer such a difficult disease to treat? What is the best system to model the development of a human tumor? How can new treatment modalities, especially immune-based therapies that harness the natural ability of immune cells to kill target cells, be developed to treat cancer? These and other questions will be addressed in this course. We will explore the concepts of mouse models for human cancer, humanized cancer mice and cancer immunotherapy by reading recent and classic research articles. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These

Subjects

cancer | immunotherapy | mouse models | humanized cancer mice | humice | cancer biology | cancer therapy | oncogenes | humanization | personalized mice

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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Breast Cancer: Causes and Prevention

Description

Dr Valerie Beral talks about her research into the causes of breast cancer, looking into the history of the cancer as well as offering ways of reducing the risk of contracting breast cancer. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

breast cancer | alumni | cancer | breast cancer | alumni | cancer | 2009-09-26

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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Breast Cancer: Causes and Prevention

Description

Dr Valerie Beral talks about her research into the causes of breast cancer, looking into the history of the cancer as well as offering ways of reducing the risk of contracting breast cancer. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

breast cancer | alumni | cancer | breast cancer | alumni | cancer | 2009-09-26

License

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Breast Cancer: Causes and Prevention

Description

Dr Valerie Beral talks about her research into the causes of breast cancer, looking into the history of the cancer as well as offering ways of reducing the risk of contracting breast cancer.

Subjects

breast cancer | alumni | cancer | breast cancer | alumni | cancer | 2009-09-26

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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INDOX Cancer Research Network

Description

Dr Raghib Ali talks about INDOX, the cancer research network in India. Dr Raghib Ali is the Director of INDOX Cancer Research Network. His main interest is in colorectal (bowel) cancer and other chronic, non-communicable diseases. Incidence of colorectal cancer in India has been relatively low historically; understanding why may help us establish risk factors and also lead to new treatments. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

Epidemiology | colorectal cancer | cancer | clinical trials | Epidemiology | colorectal cancer | cancer | clinical trials

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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Cancer Metabolism

Description

Dr Patrick Pollard tells us about his research on cancer metabolism. Cancer cells produce energy predominately by a high rate of glycolysis. It has been suggested that this change in metabolism is a fundamental cause of cancer. Dr Patrick Pollard aims to elucidate the alternative metabolic strategies used by cancer cells to proliferate, even under conditions of stress. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

renal cancer | hypoxia | fumarate hydratase | kidney | cancer metabolism | renal cancer | hypoxia | fumarate hydratase | kidney | cancer metabolism

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.343 Network Medicine: Using Systems Biology and Signaling Networks to Create Novel Cancer Therapeutics (MIT) 7.343 Network Medicine: Using Systems Biology and Signaling Networks to Create Novel Cancer Therapeutics (MIT)

Description

In this course, we will survey the primary systems biology literature, particularly as it pertains to understanding and treating various forms of cancer. We will consider various computational and experimental techniques being used in the field of systems biology, focusing on how systems principles have helped advance biological understanding. We will also discuss the application of the principles of systems biology and network biology to drug development, an emerging discipline called "network medicine." This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive sett In this course, we will survey the primary systems biology literature, particularly as it pertains to understanding and treating various forms of cancer. We will consider various computational and experimental techniques being used in the field of systems biology, focusing on how systems principles have helped advance biological understanding. We will also discuss the application of the principles of systems biology and network biology to drug development, an emerging discipline called "network medicine." This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive sett

Subjects

systems biology | systems biology | network medicine | network medicine | cancer | cancer | cancer therapeutics | cancer therapeutics | quantitative high-throughput data acquisition | quantitative high-throughput data acquisition | genomic analysis | genomic analysis | signaling network biology | signaling network biology | statistical/computational modeling | statistical/computational modeling | network biology | network biology | drug development | drug development

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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INDOX Cancer Research Network

Description

Dr Raghib Ali talks about INDOX, the cancer research network in India. Dr Raghib Ali is the Director of INDOX Cancer Research Network. His main interest is in colorectal (bowel) cancer and other chronic, non-communicable diseases. Incidence of colorectal cancer in India has been relatively low historically; understanding why may help us establish risk factors and also lead to new treatments. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

Epidemiology | colorectal cancer | cancer | clinical trials | Epidemiology | colorectal cancer | cancer | clinical trials

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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Cancer Metabolism

Description

Dr Patrick Pollard tells us about his research on cancer metabolism. Cancer cells produce energy predominately by a high rate of glycolysis. It has been suggested that this change in metabolism is a fundamental cause of cancer. Dr Patrick Pollard aims to elucidate the alternative metabolic strategies used by cancer cells to proliferate, even under conditions of stress. Wales; http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

Subjects

renal cancer | hypoxia | fumarate hydratase | kidney | cancer metabolism | renal cancer | hypoxia | fumarate hydratase | kidney | cancer metabolism

License

http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.344 Tumor Suppressor Gene p53: How the Guardian of our Genome Prevents Cancer (MIT) 7.344 Tumor Suppressor Gene p53: How the Guardian of our Genome Prevents Cancer (MIT)

Description

Cancer is a leading cause of death worldwide. Cancer involves uncontrolled cell growth, resistance to cell death, failure to differentiate into a particular cell type, and increased cellular motility. A family of gate-keeper genes, known as tumor suppressor genes, plays important roles in preventing the initiation and progression of cancer. Among these, p53 is the most famous. Because of its essential role in maintaining genomic integrity, p53 is often called the guardian of the genome. During this course, we will study how p53 serves as a pivotal tumor suppressor gene in preventing cancer.This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to disc Cancer is a leading cause of death worldwide. Cancer involves uncontrolled cell growth, resistance to cell death, failure to differentiate into a particular cell type, and increased cellular motility. A family of gate-keeper genes, known as tumor suppressor genes, plays important roles in preventing the initiation and progression of cancer. Among these, p53 is the most famous. Because of its essential role in maintaining genomic integrity, p53 is often called the guardian of the genome. During this course, we will study how p53 serves as a pivotal tumor suppressor gene in preventing cancer.This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to disc

Subjects

tumor suppressor gene | tumor suppressor gene | p53 | p53 | p53 protein | p53 protein | cancer | cancer | cell-growth signals | cell-growth signals | cell cycle regulation | cell cycle regulation | DNA damage | DNA damage | DNA repair | DNA repair | programmed cell death | programmed cell death | apoptosis | apoptosis | genome integrity | genome integrity | oncogenes | oncogenes | p53 mutations | p53 mutations | mouse cancer models | mouse cancer models | Mdm2 | Mdm2 | microRNA | microRNA

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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HST.525J Tumor Pathophysiology and Transport Phenomena (MIT)

Description

Tumor pathophysiology plays a central role in the growth, invasion, metastasis and treatment of solid tumors. This class applies principles of transport phenomena to develop a systems-level, quantitative understanding of angiogenesis, blood flow and microcirculation, metabolism and microenvironment, transport and binding of small and large molecules, movement of cancer and immune cells, metastatic process, and treatment response. Additional Faculty Dr. Pat D'Amore Dr. Dan Duda Dr. Robert Langer Prof. Robert Weinberg Dr. Marsha Moses Dr. Raghu Kalluri Dr. Lance Munn

Subjects

HST.525 | 10.548 | tumor | cancer | tumor vasculature | antiangiogenesis | bone marrow-derived stem cells | BMDC | stem cell research | experimental cancer therapy | cancer research | tumor-host interactions | vascular normalization | vascular transport | interstitial transport | lymphatic transport | microcirculation | molecular therapeutics | blood vessels | angiogenesis | drug delivery | intravital microscopy

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT)

Description

The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an

Subjects

DNA | damage checkpoints | cancer | cells | human cells | exogenous | endogenous | checkpoints | gene | signaling | cancer biology | cancer prevention | primary sources | discussion | DNA damage | molecular | enzyme | cell cycle | extracellular cues | growth factors | Cdk regulation | cyclin-dependent kinase | p53 | tumor suppressor | apoptosis | MDC1 | H2AX | Rad50 | Fluorescence activated cell sorter | Chk1 | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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Cancer advice : colon and rectal cancer resource stub

Description

A resource stub for the "Cancer advice: colon and rectal cancer" webpage. It discusses incidence, screening, causes, symptoms, treatment, outcomes, and current issues.

Subjects

colonic neoplasms | colon neoplasms | colon cancer | colonic cancer | rectal cancer | Technology | Diseases | SAFETY | Medicine and Dentistry | UK EL04 = SCQF 4 | Foundational Level | NICAT 1 | CQFW 1 | Foundation | GCSE D-G | NVQ 1 | Intermediate 1 | | UK EL05 = SCQF 5 | Intermediate level | Intermediate | NICAT 2 | CQFW 2 | Intermediate | GSCE A-C | NVQ 2 | | UK EL06 = SCQF 6 | Advanced courses | | NICAT 3 | CQFW 3 | Advanced | A/AS Level | NVQ 3 | Higher | SVQ 3 | UK EL07 = SCQF 7 | Higher Certificate | NICAT 4 | CQFW 4 | NVQ 4 | Advanced Higher | SVQ 4 | HN Certificate | Learning | Teaching | Students | dentistry | A000 | EDUCATION / TRAINING / TEACHING | HEALTH CARE / MEDICINE / HEALTH and SAFETY | INFORMATION TECHNOLOGY and INFORMATION | G | P | C

License

Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales http://creativecommons.org/licenses/by-nc-sa/2.0/uk/ http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT)

Description

Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

Subjects

DNA | damage checkpoints | cancer | cells | human cells | exogenous | endogenous | checkpoints | gene | signaling | cancer biology | cancer prevention | primary sources | discussion | DNA damage | molecular | enzyme | cell cycle | extracellular cues | growth factors | Cdk regulation | cyclin-dependent kinase | p53 | tumor suppressor | apoptosis | MDC1 | H2AX | Rad50 | Fluorescence activated cell sorter | Chk1 | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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Everyman : action against male cancer resource stub

Description

A resource stub for the Everyman: action against male cancer website. It provides facts about prostate and testicular cancer.

Subjects

prostatic neoplasms | prevention and control | diagnosis | radiotherapy | prostatic cancer | genetics | prostate neoplasms | prostate cancer | testicular cancer | testicular neoplasms | Technology | Diseases | SAFETY | Subjects allied to Medicine | UK EL04 = SCQF 4 | Foundational Level | NICAT 1 | CQFW 1 | Foundation | GCSE D-G | NVQ 1 | Intermediate 1 | | UK EL05 = SCQF 5 | Intermediate level | Intermediate | NICAT 2 | CQFW 2 | Intermediate | GSCE A-C | NVQ 2 | | UK EL06 = SCQF 6 | Advanced courses | | NICAT 3 | CQFW 3 | Advanced | A/AS Level | NVQ 3 | Higher | SVQ 3 | UK EL07 = SCQF 7 | Higher Certificate | NICAT 4 | CQFW 4 | NVQ 4 | Advanced Higher | SVQ 4 | HN Certificate | Learning | Students | Subjects allied to medicine | B000 | HEALTH CARE / MEDICINE / HEALTH and SAFETY | INFORMATION TECHNOLOGY and INFORMATION | P | C

License

Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales http://creativecommons.org/licenses/by-nc-sa/2.0/uk/ http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.27 Principles of Human Disease (MIT)

Description

This course covers current understanding of, and modern approaches to human disease, emphasizing the molecular and cellular basis of both genetic disease and cancer. Topics include: The Genetics of Simple and Complex Traits; Karyotypic Analysis and Positional Cloning; Genetic Diagnosis; The Roles of Oncogenes and Tumor Suppressors in Tumor Initiation, Progression, and Treatment; The Interaction between Genetics and Environment; Animal Models of Human Disease; Cancer; and Conventional and Gene Therapy Treatment Strategies.

Subjects

human disease | molecular basis of genetic disease | molecular basis of cancer | cellular basis of genetic disease | cellular basis of cancer | genetics of simple and complex traits | karyotypic analysis | positional cloning | genetic diagnosis | roles of oncogenes | tumor suppressors | tumor initiation | tumor progression | tumor treatment | interaction between genetics and environment | animal models of human disease | cancer | conventional treatment strategies | gene therapy treatment strategies

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.342 Cancer Biology: From Basic Research to the Clinic (MIT)

Description

This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana

Subjects

cancer | tumor | metastasis | genetic analysis | cancer biology | model organisms | genetic pathways | uncontrolled growth | tumor suppressor genes | oncogenes | tumor initiation | cell cycle | chromosomal aberration | apoptosis | cell death | signal transduction pathways | proto-oncogene | mutation | DNA mismatch repair | telomeres | mouse models | tissue specificity | malignancy | stem cells | therapeutic resistance | differentiation | caner research | cancer therapeutics | chemotherapy

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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ASCRS : colorectal cancer resource stub

Description

A resource stub for the "ASCRS: colorectal cancer" webpage. It explains who is at risk, symptoms, treatment and prevention.

Subjects

colonic neoplasms | colonic cancer | colon cancer | colon neoplasms | rectal cancer | rectal neloplams | Technology | Diseases | SAFETY | Medicine and Dentistry | UK EL04 = SCQF 4 | Foundational Level | NICAT 1 | CQFW 1 | Foundation | GCSE D-G | NVQ 1 | Intermediate 1 | | UK EL05 = SCQF 5 | Intermediate level | Intermediate | NICAT 2 | CQFW 2 | Intermediate | GSCE A-C | NVQ 2 | | UK EL06 = SCQF 6 | Advanced courses | | NICAT 3 | CQFW 3 | Advanced | A/AS Level | NVQ 3 | Higher | SVQ 3 | UK EL07 = SCQF 7 | Higher Certificate | NICAT 4 | CQFW 4 | NVQ 4 | Advanced Higher | SVQ 4 | HN Certificate | Learning | Teaching | Students | dentistry | A000 | EDUCATION / TRAINING / TEACHING | HEALTH CARE / MEDICINE / HEALTH and SAFETY | INFORMATION TECHNOLOGY and INFORMATION | G | P | C

License

Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales http://creativecommons.org/licenses/by-nc-sa/2.0/uk/ http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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