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ch. 20

QuestionAnswer
tumor group of abnormally growing cells
benign tumor non-invasive tumor (stays in original place)
malignant/invasive tumor cancer
oncology study of tumors
transformation conversion of normal cell to cancer-like cell reuires multiple steps due to multiple changes in DNA
proto-oncogene normal gene that stimulates mitosis/growth
tumor supressor normal gene supresses mitosis/growth of loss of gene. increase tumor development
somatic mutation not passed to offspring. cancer initiation in one cell
uncontrolled proliferation decrease in dependence of growth factors, inhibitory factors. increase in abnormal autocrine signaling
failure to undergo apoptosis decrease in p53. ignore intrinsic and extrinsic death signals. loss of death factor receptor
VEGF vascular endothelial growth factor
binding of VEGF to RTK leads to increase in endothelium mitosis and growth, capillaries, metasatic risk (promotion of angiogenesis)
oncoagenes abnormal gene that increase cell cycling (genes from virus that increase cancer)
carcinogens radiation, chemicals, virues - all damage DNA and increae somatic mutations
tumor promoters molecules that increase mitosis
Human Papilloma Virus (HPV) non-enveloped dsDNA. mostly benign tumers
genetic predisposition associated with inherited genetic risk 5-10% of cancers
E7 promotes degradation of Rb to E2F free
E6 stimulates ubiquitination of p53
metastasis growing in a new location
contact inhibition contact between cells that stops mitosis and migration
cancer treatment chemotherapy, block receptors or signaling pathways, induce apopsotis, target Her2 receptor, induce differentation
irradation can be focused on one area
Created by: lutmanlucy21
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