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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 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 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

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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OeRBITAL Project (Open educational Resources for Biologists Involved in Teaching And Learning)

Description

OeRBITAL is a discovery project co-ordinated by the UK Centre for Bioscience, working with a number of Discipline Consultants tasked to explore OER repositories to discover the most suitable resources for the attention of their discipline communities. Around 300 Open Educational Resources in areas relating to Bioscience disciplines have been identified by our experts, and evaluated for inclusion in a number of discipline-specific curated collections, as a means of highlighting these key resources for the benefit of the wider Bioscience academic community.

Subjects

ukoer | oer | biochemistry | oerbital | bioscience | biology | biomaths | pharmacology | neuroscience | physiology | cell biology | cancer biology | plant sciences | enzymology | ecology | marine biology | microbiology | molecular genetics | molecular biology | bioinformatics | ethics | Biological sciences | C000

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 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

Site sourced from

https://ocw.mit.edu/rss/all/mit-allarchivedcourses.xml

Attribution

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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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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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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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https://ocw.mit.edu/rss/all/mit-allcourses.xml

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