Cancer note - Cancer (Lodish Chapter 25) I. Cancer is a...

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Cancer (Lodish Chapter 25) I. Cancer is a leading cause of mortality A. Responsible for 20% of all deaths in the US 1. Many different types B. Caused by genetic alterations 1. Environmental (carcinogens causing somatic mutations) 2. Genetic background (germ-line mutations) C. Two general classes of cancer causing genes 1. Oncogenes: promote cancer 2. Tumor-suppressor genes: inhibit cancer II. Cancer cells are different from normal cells A. Cancer types 1. Carcinomas: from epithelial cells 2. Sarcomas: from connective tissues or muscle cells 3. Leukemia: from blood cells B. Six major differences (Lodish Fig. 25-1) 1. Self-sufficiency in growth signals: activation of proto-oncogenes 2. Insensitivity to antigrowth signals: reduced checkpoint control and tumor suppressor genes. 3. Evasion of apoptosis: inhibition of apoptosis and increased cell survival 4. Limitless replicative potential: Telomerase activity increases 5. Tissue invasion and metastasis: cell adhesion breakdown (Lodish Fig. 25-2) 6. Sustained angiogenesis III. Cancer development-- Cancer is a multi-step process A. Most cancers derive from a single abnormal cell. 1. Primary tumor: A tumor that is at the original site where it first arose. 2. Secondary tumor: A tumor has spread from the original site where it first arose. B. Cancer result from somatic mutation 1. Cancer cells have abnormality in their DNA sequence. 2. Carcinogens that cause DNA mutagenesis also cause carcinogenesis. 3. The susceptibility to cancer can be family related and inherited. C. A single mutation is not enough to cause cancer-- Cancer is a multi-step process 1. An estimated 10 16 cell divisions take place in a normal human body. 2. DNA mutation rate is about 10 -6 . 3. This means each of us have 10 10 separate occasions of DNA mutations. D. Cancer development requires mutations in many genes (Lodish Fig. 25-7, Alberts Fig. 25-7) 1. Frequency of cancers increases with age (Lodish Fig. 25-7). The incidence of cancer rises steeply as a function of age (Alberts Fig. 23-7) 2. This can be accumulated in many years with more than 10 genes. 3. Tumor appearance is enhanced by more than one oncogene. Co-expression of Myc and activated Ras in mice cause animal death more than each individual gene (Lodish Fig. 25- 8) 1
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4. Similar experiment in cell culture: Activated Ras can transform “immortalized” cell lines, but not primary cell cultures. Co-transfection of Src and activated Ras can cause primary cells to adopt a transformed phenotype. 5. Study of tumor development in colorectal cancer provides excellent support for the multi- hit model (Lodish Fig. 25-9). E. Tumor progression (Alberts Figs. 25-11) 1. A tumor begins as a single abnormal cell with multiple mutations or genetic changes 2. Growth is mitogen independent 3. Unlimited replicative potential 4. Invasive 5. Metastasize to other tissues 6. Lacks responses to antigrowth signals or apoptotic/death signals 7. Loss of DNA repair mechanisms: Cannot repair DNA damage due to DNA polymerase
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Cancer note - Cancer (Lodish Chapter 25) I. Cancer is a...

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