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  1. 6 characteristics of cancer celss
    • evading apoptosis
    • self-sufficiency 
    • insensititvity to anti-growth signals
    • sustained angiogenesis
    • limitless replicative potential
    • tissue invasion and metastasis
  2. proto-oncogenes examples
    growth factors and their receptors: PDGF, FGF, EGF, CSF

    Signal transducer:  ras, src, abl

    Signal effectors: myc, fos, jun
  3. oncogene
    mutated proto-oncogene
  4. a G-protein that is normally involved in cellular proliferation (turn on and off for proliferation
  5. mutation of K-ras
    leads to constitutive activation in the absence of growth factor stimulation
  6. •Juxtaposes oncogene with constitutively active promoter: causes CML
    translocation of BCR-ABL

    BCR on all the time and ABL need signal for proliferation
  7. Imatinib - tx for CML
    BCR-ABL specifically inhibitor target --> reduce signals
  8. HER2/neu amplification tx
  9. Her2/neu vs BCR-ABL
    amplification vs constant activation
  10. tumor suppressors genes
    •Recessive loss of function

    Mutation in both copies required to have deleterious effect

    •Mutation in one allele can be inherited in germline, causing inherited predisposition towards developing cancer
  11. Mechanism of TSG Losses (2 hits)
    Mutation (genetic)

    Methylation (epigenetic)

    Deletion (loss of heterozygosity)
  12. Mutation in TSG
    • point mutation: missense and nonsense
    • Insertions: frameshifts
    • Microdeletions
  13. TSG - Gene Silencing by Hypermethylation
    •DNA methylation- addition of methyl group, no change in DNA sequence (Epigenetic)

    •Hypermethylation of CpG islands in gene promoters can lead to inactivation of the gene

    Occurs in nearly every type of neoplasm
  14. •Most common mechanism to lose second TSG allele
    chromosomal deletion
  15. •Leads to loss of heterozygosity (LOH) in TSG
    chromosomal deletion
  16. Loss of Heterozygosity

    • ØNormal
    • allele deleted (n=1)


    •Uniparental Disomy (UPD)

    ØNorma allele deleted

    ØMutated allele duplicated (n=2)
  17. Retinoblastoma (Rb) - TSG
    •Inhibits cell cycle progression until cell is ready to divide

    ØRb forms complex with E2F, preventing cell cycle progression from G1 to S

    ØPhosphorylated Rb cannot bind E2F, allowing cell cycle progression

    ØMutant Rb cannot bind E2F, allowing cell cycle progression
  18. p53 - TSG
    active p53 gene allow activation of cdk/cyclin complex 

    inactivated p53 lead to cancer because can't repair DNA, apoptosis etc
  19. Familial vs sporadic cancer
    familial just need loss of heterozygosity 

    sporadic cancer required mutation and LOH
  20. sustained angiogenesis
    for tumors to progress, they must stimulate angiogenesis
  21. limitless replicatie potential
    activation of telomerase 

    telomere gets shorter in normal cell --> cancer cell activate telomerase --> immortal cell
  22. true or false 

    cancer is a genetic disease
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