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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

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7.345 Non-coding RNAs: Junk or Critical Regulators in Health and Disease? (MIT) 7.345 Non-coding RNAs: Junk or Critical Regulators in Health and Disease? (MIT)

Description

Every time we scientists think that we have dissected the precise biological nature of a process, an incidental finding, a brilliantly designed experiment, or an unexpected result can turn our world upside down. Until recently thought by many to be cellular "junk" because they do not encode proteins, non-coding RNAs are gaining a growing recognition for their roles in the regulation of a wide scope of processes, ranging from embryogenesis and development to cancer and degenerative disorders. The aim of this class is to introduce the diversity of the RNA world, inhabited by microRNAs, lincRNAs, piRNAs, and many others. 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 us Every time we scientists think that we have dissected the precise biological nature of a process, an incidental finding, a brilliantly designed experiment, or an unexpected result can turn our world upside down. Until recently thought by many to be cellular "junk" because they do not encode proteins, non-coding RNAs are gaining a growing recognition for their roles in the regulation of a wide scope of processes, ranging from embryogenesis and development to cancer and degenerative disorders. The aim of this class is to introduce the diversity of the RNA world, inhabited by microRNAs, lincRNAs, piRNAs, and many others. 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 us

Subjects

Non-coding RNAs | Non-coding RNAs | microRNAs | microRNAs | lincRNAs | lincRNAs | piRNAs | piRNAs | RNA interference | RNA interference | miRNA | miRNA | tumor suppressors and oncogenes | tumor suppressors and oncogenes | RNAi therapeutics | RNAi therapeutics

License

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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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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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7.27 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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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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7.345 Non-coding RNAs: Junk or Critical Regulators in Health and Disease? (MIT)

Description

Every time we scientists think that we have dissected the precise biological nature of a process, an incidental finding, a brilliantly designed experiment, or an unexpected result can turn our world upside down. Until recently thought by many to be cellular "junk" because they do not encode proteins, non-coding RNAs are gaining a growing recognition for their roles in the regulation of a wide scope of processes, ranging from embryogenesis and development to cancer and degenerative disorders. The aim of this class is to introduce the diversity of the RNA world, inhabited by microRNAs, lincRNAs, piRNAs, and many others. 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 us

Subjects

Non-coding RNAs | microRNAs | lincRNAs | piRNAs | RNA interference | miRNA | tumor suppressors and oncogenes | RNAi therapeutics

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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7.344 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

Subjects

tumor suppressor gene | p53 | p53 protein | cancer | cell-growth signals | cell cycle regulation | DNA damage | DNA repair | programmed cell death | apoptosis | genome integrity | oncogenes | p53 mutations | mouse cancer models | Mdm2 | 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 https://ocw.mit.edu/terms/index.htm

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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

Site sourced from

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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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