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ch. 20
Question | Answer |
---|---|
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 |