BC #10-11 Cancer.txt

  1. What is the differnce b/t driver and passenger mutations?
    • Driver: cancer grown
    • Passenger: do not promote cancer growth
  2. What are the two driver genes and their mutations? What do they do
    • Tumor suppressor (Repair/kill):Inactive tumore suppressor
    • Proto-oncogenes(normal cell growth):oncogenes (tumor cell growth)
  3. Are both driver mutations needed for tumor growth?
    • Yes
    • ***Tumor suppressors in quantity
    • ***Proto-oncogenes work on the CDK4/6 complex
  4. What are two tumor suppressor gene types and their functions?
    • 1) Gatekeeper: halt cycle, DNA death
    • 2) Caretaker: DNA repair
  5. What are the four Gatekeeper genes?
    • 1) Rb
    • 2) APC
    • 3) p53
    • 4) NF1
  6. What are the four groups of caretaker genes?
    • 1) ATM
    • 2) BRCA1/2
    • 3) MSH2/MLH1
    • 4) XP genes
  7. What is the loss-of-function theory of tumor suppressors?
    Generally start homozygous for the suppressor, and then lose one at a time until homozygous for the mutant.
  8. What kind of transmission and fashion does Rb depict?
    • Transmission: AD
    • Fashion: AR
  9. What is the diff. b/t familial Rb and Sporadic Rb?
    • Familial Rb: passed on to 50% of offspring, bilateral
    • Sporadic Rb: randomly appearl, unilateral
  10. What are the two main function of p53?
    • 1) p21: give time for repair
    • 2) Bax: apoptosis
  11. How does phospho. relate to the p53 system?
    No Phospho. = lack of ATM kinase and degradation of p53 by MDM2 ubiquitination

    Phospho. = ATM kinase and dissociation of p53 from MDM2 = DNA halting and repair by by p21
  12. How does apoptosis by p53 and Bax function? What is the functioning capsase?
    • Bax opens Cytochrome C channels in Mitochondria
    • Cytochrome C binds Apaf-1 which binds Capsase 9 = Apoptosome
    • ***Cells disintegrate into membrane-bound particles to stop infection
  13. What is the function of Bcl'2?
    • Stop release of Cytochrome C after Bax initiation from p53
    • *** it is an oncogene b/c it allows tumor cell to continue growing
  14. Does p53 follow loss-of-function or gain-of-function? How does it occur?
    • GOF
    • As it is mutated, there are four tetramers with binding domains. Sometimes, a few of the four can be mutated and bind to healthy p53 systems and stop their activity.
  15. How does HPV interfere with p53 tumor suppression?
    • two genes, E6, E7
    • E6: destroys p53 = no apoptosis
    • E7: binds to Rb and releases EF2 so cell cannot halt at restriction point
  16. What are the four Ab's of Gardisil and what do they stop?
    • HPV 16/18 = cervical cancer
    • HPV 6/11 = genital warts
  17. How does APC save the cell from tumor growth?
    APC binds B-catenin which then inhibits B-catenin from entering the nucleus
  18. What are two was that APC can be inhibited and what is the result?
    • 1) WNT: binds to G-protein = dissociation of APC from B-catenin = B-catenin in nucleus = TCF + B-catenin = tumor
    • 2) APC mutation: even w/o WNT, B-catenin is not bound and degraded so it enters the nucleus to bind TCF and produce a tumor
  19. How do polyps form from the FAP disease due to APC mutation?
    • -Generally WNT is in stromal cells causing them to divide until they reach the midline and then stop growth until outside of the crypt to be sloughed off
    • -When APC is mutated, the cells that pass the stromal cells don't stop dividing and overcome the sloughing off
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BC #10-11 Cancer.txt
BC #10-11 Cancer