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

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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 won’t stop replicating and won’t 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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08 Lecture - Avoid suicide by apoptosis • Bypass...

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