1362-SU09-Lecture-6-_40773 - Cancer &division...

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Cancer Cancerous diseases result from cells that do not respond to the normal l l f h ll l gene regulatory controls of the cell cycle. Mutations in such genes disrupt normal growth & division In complex multicellular types like mammals such mutations can have De differentiation : cells revert to an embry i t t l ki l t t l In complex multicellular types, like mammals, such mutations can have significant effects: Normal cells onic state, lacking regulatory controls – Characterized by uncontrolled growth & formation of tumors (a tissue mass of many mutated cells) Cancer cell Benign tumors : cells remain in a single mass, Malignant tumors : cells invade & disrupt surrounding tissues; are cancerous . not generally life threatening. Metastasis : cells break off malignant tumor & spread to other bodily locations.
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Two Classes of Genes Show Altered Activity in Cancer Cells Class I: proto oncogenes ; encode various proteins in cells that stimulate normal growth & cell division; cancer causing forms are oncogenes . Oncogenes 1 st discovered in viruses Proto oncogene Æ oncogene? Due to genetic change leading to: Proto oncogene (a) increase in amount of proto oncogene’s protein or (b) increase in activity of protein Proto oncogene Chromosomal Translocation: gene moved to new, active l l Mutation in coding sequence of gene. Gene amplification; increase in the control element Mutation in promoter &/or enhancer of gene. number gene copies Normal growth stimulating protein in excess altered protein that is abnormally Normal growth stimulating protein in excess active Certain viruses may introduce oncogenes to chromosomal regions where expression of the gene disrupts cell cycle control.
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Class II: tumor suppressor genes ; encode proteins that inhibit cell division; prevent uncontrolled growth. Functions in: DNA repair; cell adhesion/anchorage; cell signal pathways TP53: gene codes for p53, a transcriptional activator for several genes; has a major role in the management & control of cellular repair mechanisms. The TP53 gene is mutant in half of all cancers; as a result, p53 does not function correctly. Healthy, dividing cell Cellular damage; i.e., to DNA, membranes, proteins. p53 functions here Damage control: Stop cell division Damage assessment Cellular repair Successful Repair Failed Repair Extensive Damage Return to Cell Cycle Damage accumulation Cancer Apoptosis & Cell Death
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• Cancer develops from an accumulation of mutations to proto Common Features of Cancer Cells Cancer develops from an accumulation of mutations to proto oncogenes & tumor supressor genes. • As a result, all cancers generally exhibit the features described: Self Sufficiency in Growth Signals – Overactive growth factor (GF) receptor systems, ll mutant GF receptors, mutant CDK’s: all serve to over stimulate cells Insensitive to growth inhibitory signals – Example: defective in cell anchorage Evasion of apoptosis Unlimited growth potential
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