08 Lecture

08 Lecture - Avoid suicide by apoptosis Bypass limitations...

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10/23/08 Cancer Divide w/o restriction o Cell division usually very regulated -> cancer -> lose this regulation o Loss of contact inhibition (stop growing when touch other cells) Ability to invade and colonize foreign tissues o Achieved through genetic mutations o Proto-oncogenes – normally promote cell growth but is very regulated Mutated to oncogenes which promote cell growth w/o regulation “Gain a fxn” Ex: Abl o Tumor suppressors – Restrain growth Ex: Rb – retinoblastoma – loss of heterozygosity through random mutations Caretaker genes – protect genome by sensing DNA damage and initiating repair Loss of these genes will increase the rate of mutation in a cell “Loss of fxn” ex: p53 o Unstable Chromosomes Properties that make cells cancerous Disregard signals that prevent growth (tumor supressors) Generate own growth signals (oncogenes)
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Unformatted text preview: Avoid suicide by apoptosis Bypass limitations to proliferation (telomerase) Sustained angiogenesis (make new blood vessels) Able to invade other tissues (metastasize) Problems with treatments Cancer cell vs normal cell Drug delivery Several targets Multiple mutations Fast growing Need to kill all cells Actual Treatment? Angiogenesis Telomerase Surgically remove cells Block cell division Damage DNA Use ionizing radiation and drugs o Hope that: Normal cells will stop cell cycle to repair DNA Cancer cells wont stop replicating and wont repair and die from DNA damage Chronic Myelogenous Leukemia Philadelphia chromsome -> results in BCR-Abl fusion protein o This fusion protein will stimulate a number of cell cycle controlling proteins, speeding up cell cycle...
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This note was uploaded on 10/25/2008 for the course BIMM 100 taught by Professor Pasquinelli during the Fall '06 term at UCSD.

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08 Lecture - Avoid suicide by apoptosis Bypass limitations...

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