NEU 365D Lecture Notes - Lecture 23: Tumor Suppressor Gene, Oncogene, Myc
Document Summary
Covalent binding of ultimate carcinogen to dna (non-reversible) alters the coding of the dna at that site. If not detected & corrected before cell division error passed to daughter cells as a mutation. Single-strand breaks, mutations at one base pair (nt-excision repair enzymes), double-stranded breaks (more serious - no template) Chance for cell to repair mistakes that were found - stop mitosis until the enzymes have time to correct the defects. Individuals genetically deficient increased susceptibility to some (not all) cancers. Primary molecular target of carcinogens - oncogenes (cancer-causing genes) Proto-oncogenes = genes that code for proteins that normally have important or essential cellular functions (involved in cell division/growth) I. e. growth factors, growth factor receptors, transcription factors, etc. One mutation out of the two alleles is sufficient to produce cancer. Oncogenes drive abnormal cell division and cell differentiation (typically found in neoplastic growths (tumors) Tumor suppressor genes - break on cell division p53 - mutated in ~ all human cancers.
