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| cytoskeleton collapses; chromatin condense and localizes to edge of nucleus; chromosomes digested into ~200bp; phagocytes recognize cell surface signals |
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| Extrinsic pathway I; cell-surface ligand; |
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| insulin-like growth factor; extrinsic pathway II |
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| inhibitds cytochrome c from leaving the mitochondria |
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| binds to cytochrome c to have pC9 --> C9 |
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| activate other caspases; dgrade proteins, lamins, MAPs, etc; activate DNase |
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| function in normal cells to prevent cancer; mutations promote oncogenesis |
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| function in normal cells to promote growth and survival; mutations hyperactivate expression to promote oncogeesis |
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| maintaining genetic stability; regulated cell proliferation; apoptosis of damaged cell and senescence of high proliferating cells; cell localization in body |
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| repaire DNA polymerase mutation |
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| TSG; genetic stability example |
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| not nomal balance of chromosomes |
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| proto-oncogene; causes multiple centrosomes, mutiple spindles and aneuploidy |
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| proto-oncogene; cell proliferation unregulated (always ON) |
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| proto-oncogene; cell proliferation unregulated; autophorphorylates and activates proliferation regardless of EGF |
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| proto-oncogene; cell proliferation unregulated; cant hydrolyze GTP |
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| proto-oncogene; never binds to E2F so proliferation no longer needs CdkLcyclin G1 |
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| TSG; cell proliferation unregulated; Cdi inhibitor |
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| restrains apoptosis regardless of damage |
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| re-activated, so proliferation continues; promotes oncogenesis |
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| TSG; cells reorganize actin cytoskelton allowing it to move to a new location |
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| proto-oncogenes; expression of thesse specific for a different tissue allows tumor to colonize these tissues |
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| cancer stem cell hypothesis |
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| small subpopulation that gives rise to the different tumor cell types |
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| role of cells around tumor |
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| angiogenesis- new vessels are made to the tumore in order to stimulate growth and metastasis |
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