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7.340 Avoiding Genomic Instability: DNA Replication, the Cell Cycle, and Cancer (MIT) 7.340 Avoiding Genomic Instability: DNA Replication, the Cell Cycle, and Cancer (MIT)

Description

In this class we will learn about how the process of DNA replication is regulated throughout the cell cycle and what happens when DNA replication goes awry. How does the cell know when and where to begin replicating its DNA? How does a cell prevent its DNA from being replicated more than once? How does damaged DNA cause the cell to arrest DNA replication until that damage has been repaired? And how is the duplication of the genome coordinated with other essential processes? We will examine both classical and current papers from the scientific literature to provide answers to these questions and to gain insights into how biologists have approached such problems. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored f In this class we will learn about how the process of DNA replication is regulated throughout the cell cycle and what happens when DNA replication goes awry. How does the cell know when and where to begin replicating its DNA? How does a cell prevent its DNA from being replicated more than once? How does damaged DNA cause the cell to arrest DNA replication until that damage has been repaired? And how is the duplication of the genome coordinated with other essential processes? We will examine both classical and current papers from the scientific literature to provide answers to these questions and to gain insights into how biologists have approached such problems. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored f

Subjects

cell | cell | genetic material | genetic material | cell death | cell death | tumorigenesis | tumorigenesis | mutations | mutations | genes | genes | DNA replication | DNA replication | cell cycle | cell cycle | damaged DNA | damaged DNA | genome | genome | tumor formation | tumor formation | anti-cancer drugs | anti-cancer drugs | viruses | viruses | cellular controls | cellular controls

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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7.340 Ubiquitination: The Proteasome and Human Disease (MIT) 7.340 Ubiquitination: The Proteasome and Human Disease (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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe 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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitination | ubiquitin | ubiquitin | proteasome | proteasome | post-translational mechanisms | post-translational mechanisms | ubiquitin-conjugation system | ubiquitin-conjugation system | neurodegenerative diseases | neurodegenerative diseases | immune response | immune response | cell cycle regulation | cell cycle regulation | apoptosis | apoptosis | signal transduction pathways | signal transduction pathways | tumorigenesis | tumorigenesis | protein degradation | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | Endoplasmic Reticulum Associated Degradation Pathway | ligases | ligases | translocated proteins | translocated proteins | misfolded proteins | misfolded proteins | trafficking membranes | trafficking membranes | cell cycle control | cell cycle control | programmed cell death | programmed cell death | Huntington's Disease | Huntington's Disease | Von Hippel-Lindau Disease | Von Hippel-Lindau Disease

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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7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT) 7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT)

Description

During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res

Subjects

cancer | cancer | embryogenesis | embryogenesis | sonic hedgehog | sonic hedgehog | tumor | tumor | signaling | signaling | proto-oncogene | proto-oncogene | Kras | Kras | apoptosis | apoptosis | self-renewal | self-renewal | regeneration | regeneration | angiogenesis | angiogenesis | VEGF | VEGF | tumorigenesis | tumorigenesis | metastasis | metastasis | 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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7.340 Ubiquitination: The Proteasome and Human Disease (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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitin | proteasome | post-translational mechanisms | ubiquitin-conjugation system | neurodegenerative diseases | immune response | cell cycle regulation | apoptosis | signal transduction pathways | tumorigenesis | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | ligases | translocated proteins | misfolded proteins | trafficking membranes | cell cycle control | programmed cell death | Huntington's Disease | Von Hippel-Lindau Disease

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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7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT)

Description

During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res

Subjects

cancer | embryogenesis | sonic hedgehog | tumor | signaling | proto-oncogene | Kras | apoptosis | self-renewal | regeneration | angiogenesis | VEGF | tumorigenesis | metastasis | 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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Attribution

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7.340 Avoiding Genomic Instability: DNA Replication, the Cell Cycle, and Cancer (MIT)

Description

In this class we will learn about how the process of DNA replication is regulated throughout the cell cycle and what happens when DNA replication goes awry. How does the cell know when and where to begin replicating its DNA? How does a cell prevent its DNA from being replicated more than once? How does damaged DNA cause the cell to arrest DNA replication until that damage has been repaired? And how is the duplication of the genome coordinated with other essential processes? We will examine both classical and current papers from the scientific literature to provide answers to these questions and to gain insights into how biologists have approached such problems. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored f

Subjects

cell | genetic material | cell death | tumorigenesis | mutations | genes | DNA replication | cell cycle | damaged DNA | genome | tumor formation | anti-cancer drugs | viruses | cellular controls

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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7.340 Ubiquitination: The Proteasome and Human Disease (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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitin | proteasome | post-translational mechanisms | ubiquitin-conjugation system | neurodegenerative diseases | immune response | cell cycle regulation | apoptosis | signal transduction pathways | tumorigenesis | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | ligases | translocated proteins | misfolded proteins | trafficking membranes | cell cycle control | programmed cell death | Huntington's Disease | Von Hippel-Lindau Disease

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-allcourses.xml

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