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Lecture 29

BIOLOGY 172 Lecture 29: Cancer

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University of Michigan - Ann Arbor
Stephen Clark

Biology 172: Lecture 29 Dr. Clark- Winter 2017 CANCER Cancer is cell proliferation that is uncontrolled, but also lots of other characteristics o Increased cell growth o Decrease in apoptosis, cell death o Loss of contact inhibition o Gain ability to migrate and colonize new locations o Escape immune system o Up-regulation of telomerase activity o Up-regulation of metabolism Cancer is a disease of individual cells and the genetic changes that happen within those cells Changes within an individual cell lineage Normal v. benign v. malignant Cancer is not a bimodal state: not just “normal” or “cancerous” Accumulation of defect and mutations over time have variable combinations that can lead to cancers; huge gradient  many phenotypes CANCER TARGETS o Cancer is lack of control of various processes which are normally controlled by genes and their proteins o Tumor Suppressor normally BLOCKS cancerous phenotype; i.e.) limits cell growth and promotes cell death (LOF) o INACTIVATED IN CANCER CELLS o Proto-oncogenes are genes that hyper-activate mutations; normally they function to promote cancer phenotype but in a REGULATED way (GOF) o PROMOTE CANCER WHEN MUTATED, mutations make them constitutively expressed Genetic changes leading to cancer o Point mutations o DNA deletions o Duplications o Change in patterns of methylation o Retroviral or retrotransposon insertion o Genetic instability Retinoblastoma (RB) is a tumor suppressor  blocks cell cycle progression from G1 to S by holding transcription factors in an inactive state  G1/S cyclin phosphorylates RB to inactive state so that the cell cycle can proceed What kind of mutation in RB would lead to cancer? LOSS OF FUNCTION “Knock out” are the most common type of mutation o Only needs one copy of RB to work, and it is unlikely to knock out the second copy right away o Eventually, both copies are knocked out and the cell cycle can proceed constitutively because the tumor suppressor cannot function in its normal role o NEED TO INACTIVATE BOTH ALLELE IN THE SAME CELL Ras signaling pathway  most components are proto-oncogenes, they promote growth in a regulated fashion  Can turn into an oncogene if one allele
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