Cancer.ppt - MCDB428 Final Exam When: Wednesday, April 23rb...

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MCDB428 Final Exam When: Wednesday, April 23rb from 4 - 6 p.m. Where: Nat. Sci. Aud We will have a review section on Wednesday, April 16th from 9-10 a.m. in this lecture room. I will be happy to answer your questions during this time. I. Intro to cancer II. The genetic basis of cancer III.Targeted anti-cancer therapeutics Cancer
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I. Intro to cancer What is Cancer? A mass of cells (e.g. a tumor) that 1) proliferate in defiance of the normal restraints on cell division; 2) invade and colonize territories reserved for other cells. Cancer is the #1 cause of death (~20%). Process of cancer formation = Tumorigenesis (Formation or production of tumors); = Carcinogenesis (the creation of cancer); = Oncogenesis (a tumor forming process) Carcinomas Cancer derived from epithelial cells. Sarcomas Cancer arisen from connective tissue or muscle cells. Leukemia Cancer derived from hemopoietic (blood) cells. Types of cancer Acute myelogenous leukemia Melanoma tumor
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Six fundamental cellular properties are altered during tumorigenesis Telomerase VEGF Lodish Fig. 25-1, Hanahan D & Weinberg R (2000) Cell 100: 57 1 2 3 5 4 6 Apoptosis Cell survival Checkpoint control Tumor suppressor genes Oncogenes Metastasis Liver Cancer (from lung) Cell adhesion Cancer development: a multi-step process Most cancers derive from a single abnormal cell Primary tumor: A tumor that is at the original site where it first arose. Secondary tumor: A tumor has spread from the original site where it first arose. Cancer result from somatic mutation Cancer cells have abnormality in their DNA sequence. Carcinogens that cause DNA mutagenesis also cause carcinogenesis. The susceptibility to cancer can be family related and inherited. A single mutation is not enough to cause cancer--Cancer is a multi-step process An estimated 10 16 cell divisions take place in a normal human body. DNA mutation rate is about 10 -6 . This means each of us have 10 10 separate occasions of DNA mutations. Cancer incidence is age dependent The incidence of cancer rises steeply as a function of age. Cancer development requires mutations in many genes This can be accumulated in many years with more than 10 genes.
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Incidence of human cancer increases as a function of age Lodish Fig. 25-7 All kinds of cancer Survival of mice carrying mutations in Ras, myc or both Cancer development requires mutations in many genes
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Focus formation assay in NIH-3T3s: Assays ability of cells to lose contact dependence Vector Control Oncogene: v-Src v-Fos Activated-Ras The genetic basis of colorectal cancer development Lodish Fig. 25-9 APC: adenomatous polyposis coli DCC: Deleted in Colon Carcinoma
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Tumor progression • A tumor begins as a single abnormal cell with multiple mutations or genetic changes • Growth is mitogen independent • Unlimited replicative potential • Invasive • Metastasize to other tissues • Lacks responses to antigrowth signals or apoptotic/death signals • Loss of DNA repair mechanisms: Cannot repair DNA damage due to DNA polymerase copy error or mutations Possible origins of cancer stem cells
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Possible origins of cancer stem cells (2) Possible origins of cancer stem cells
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Possible origins of cancer stem cells Possible origins of cancer stem cells
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This note was uploaded on 09/03/2009 for the course MCDB 428 taught by Professor Wang during the Winter '08 term at University of Michigan.

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Cancer.ppt - MCDB428 Final Exam When: Wednesday, April 23rb...

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