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15 Cards in this Set
- Front
- Back
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Hallmarks of Cancer |
- Sustaining proliferative signalling - Evading growth suppressors - Activating invasion and metastases - Enabling replicative immortality - Inducing angiogenesis - Resisting cell death |
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Tumour suppressor genes |
p53 - Blocks cell cycle following cell damage - Induces apoptosis when DNA damage irreparable - Transcription factor - Binds to target promoters to regulate transcription - > changes in general expression - Upregulates tumour suppressors, downregulates protooncogenes - Commonly mutated gene
RB1 (Retinoblastoma 1) - Binds and inhibits E2F transcription factors - Inhibits genes needed for cell cycle progression - Inhibited by phosphorylation (cyclin D-CDK4) -> changes in gene expression |
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Proto-oncogenes |
MYC - Transcription factor - Promotes cell growth - > changes in gene expression
RAS - G protein - GDP (inactive) GTP (active) - Activated by growth factors - Activates downstream signalling pathways - > changes in gene expression - Codon 12,13 + 61 mutations > constitutively active RAS |
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Intrinsic Apoptosis Pathway |
- Apototic stimuli > cytochrome C release from mitochondria - Activation of Apaf1 - dATP>dADP - Exposure of CARD - Assembly of apoptosome - dADP>dATP - Recruitment and activation of procaspase-9 - Caspase-9 cleaves and activates executioner procaspases- Caspase cascade > apoptosis procaspases - Caspase cascade > apoptosis |
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Extrinsic Apoptosis Pathway |
- Killer lymphocyte + Fas ligand > Fas death receptor - FADD adaptor protein binding + Procaspase-8/10 - Assembly of Death Inducing Signalling Complex - Activation and cleavage of Procaspase 8/10 > executioner procaspases |
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Warburg Effect |
- Tumour aerobic glycolysis preferred even in oxygen - Maximise availability of raw materials for proliferation - Precursors of fatty acids, amino acids and nucleotides limited - Glucose = carbon - Wasted in CO² if oxidative phosphorylation |
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EGFR |
- Epidermal Growth Factor Receptor - EGF bind > conformational change > dimer - RAS > RAF > MEK > ERK > Cell division - PI3K > AKT > Cell proliferation - EGFRvIII lacks most extracellular domain + constitutively active |
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EGFR Drugs |
- Cetuximab = block EGF-EGFR - Erlotinib + Gefitinib = block EGFR activation (ATP mimetic) |
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Estrogen Receptor |
- Estradiol into cell - Binds to receptor, displacing associated chaperone proteins HSP90 - Dimerises > into nucleus - Coactivators or corepressors to modify transcription |
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Estrogen receptor drugs |
Tamoxifen - Prodrug by CYP2D6 - less active protein = less active drug - Greater affinity - Agonist in AF1 (allows dimerisation) - Antagonist in AF2 - Selective ER modifier (SERM)
Fulvestrant - Anti-estrogen - Prevents dimerisation - Increases degradation - Selective ER downregulator (SERD) |
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MicroRNAs (miRs) |
- Short RNA molecules - Bind to (almost) complementary sequences in 3' UTRs of target mRNAs - Inhibition of translation - mRNa degradation - Inhibit tumour suppressors = oncomirs - Inhibit oncogenes = tumour suppressor miRs - Mutation in miRs or binding sites can prevent regulation |
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INK4 |
- Inhibit cyclin dependent kinases (cyclin D-CDK4) - Prevent RB1 phosphorylation - Frequently deleted in cancers |
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MDM2 |
- Regulate p53 - Ubiquitinates p53 > targeted for degradation |
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BCR/ABL |
- BCR = serine threonine kinase and GTPase - ABL = signalling tyrosine kinase - Reciprocal translocation of chromosome 9+22 fuses BCR + ABL = Philadelphia chromosome - TK activity but no longer regulated |
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Genetic Information + testing |
1. Predictive of genetic predispositions 2. Impact on family members 3. Significance may not be apparent at time of collection 4. May have cultural significance 5. Constant throughout life 6. Obtained from any cell 7. Of value to research 8. Abuse potential |
