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WEEK 22:
Molecular basis of cancer:
| Question | Answer |
|---|---|
| cancer cell | divides continuously and inappropriately becoming immortal where it no longer maintains original function and loses its differentiation with some being able to spread to other sites |
| features of cancer (5) | proliferation (grow independently of external signals), immortality (avoid senescence/ telomere shortening), avoiding cell death (apoptosis blocked), angiogenesis (sustain nutrients), and metastasis (move to other site) |
| driver mutations | mutations which affect regulation of apoptosis, proliferation and immortality leading to cancer |
| passenger mutations | all other mutations that do not promote cancer |
| sequential mutations | give clones of a cell a growth advantage |
| cancer is what disease | clonal and multihit-multistep-multibiological process disease |
| gain of function mutation (3) | occurs due to overexpression and amplification of gene which changes regulatory regions, or point mutations, or fusions |
| loss of function mutation (3) | occurs due to point mutations, deletion with frameshift, or loss of allele |
| ways to identify cancer (2) | whole genome analyses and finding genes commonly damaged in cancers |
| familial syndromes | rare but help identify important cancer genes eg in retinoblastoma, colon cancer, and breast cancer |
| retinoblastoma | rare childhood tumour which arises in precursors of photoreceptor cells and is treated by radiotherapy or surgery |
| difference between familial and sporadic cases of cancer | familial cases are bilateral and associated with other tumours (mainly osteosarcomas) whereas sporadic cases are unilateral |
| two hit hypothesis for retinoblastoma in familial and sporadic cancer cases | found familial is caused by single random somatic event and sporadic requires two random somatic events |
| which gene in two hit hypothesis is responsible for retinoblastoma | RB gene identified for retinoblastoma |
| retinoblastoma phenotype | dominant at level of whole organism |
| phenotype of mutant allele in retinoblastoma | recessive at cellular level (need both) |
| since is it highly unlikely for sporadic mutation to inactivate both copies by 2 successive mutational events in retinoblastoma, the second mutation can occur by | mitotic recombinization or associated with loss of heterozygosity (LOH) for region containing Rb gene |
| cell cycle control checkpoints (4) | restriction point, G1, G2, and M |
| restriction point of cell cycle | go-no-go signal, cell requires growth signals to pass this checkpoint where beyond this, cell divide |
| G1 of cell cycle control | DNA damage checkpoint, entrance to S blocked if DNA damaged |
| G2 of cell cycle control | checks if replication is complete |
| M of cell cycle control | checks if chromatids are properly assembled on spindle involving Rb and p53 |
| proteins eg p53 | can trigger cells to enter apoptosis if cell cycle/ DNA synthesis fails |
| role of TS genes | detect errors, mediate repair, inhibit replication or mediate entry to apoptosis (so if error repaired leads to proliferation but it error not repaired leads to apoptosis) to prevent cancer eg p53 |
| oncogenes | mutated/ occasionally viral forms of genes (eg EGFR) involved in secreted growth factors (eg PDGF-B), cell surface receptors (EGFR), signal transduction components (RAS), or transcription factors (eg myc) which help proliferation |
| TS genes and oncogenes in cancer | oncogenes = uncontrolled proliferation and TS genes damaged so cannot stop damaged cells from moving on in cell cycle |
| deletions or point mutations in EGFR result in | constitutively active receptor eg NSCLC |
| cytogenetics of oncogenes | |
| Bcr-Abl of oncogenes | |
| Burkitts lymphoma oncogenes | |
| relationship between familial cancer and oncogenes | rarely associated as in the germline their action would be dominant and mutations would disrupt normal embryonic development leading to miscarriage |
| sustained angiogenesis | provide nutrients and O2 from vasculature needed for cell function and survival |
| VEGF | many cancers express VEGF which induces angiogenesis (new vessel growth) and promotes endothelial precursor cell formation in bone marrow |
| appearance of vasculature due to cancer | disorganised due to imbalance of signals for growth v differentiation and leaky due to imperfect cell-cell junctions |
| metastasis and invasion of tissue mechanism | loss of adhesion (delamination eg E-cadherin loss), activation of endogenous metalloproteinases. Invasion of leaky blood vessels (or lymph system) and flows in blood where few survive due to immune surveillance (aka epithelial-mesenchymal-transition, EMT) |
| secondary tumours | cells move to part of body where environment is suitable or capillary beds where tumour cells are larger and tend to get stuck in capillary bed of next organ on in the circulatory system |
Created by:
kablooey
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