BC #10-11 Cancer.txt
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What is the differnce b/t driver and passenger mutations?
- Driver: cancer grown
- Passenger: do not promote cancer growth
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)
Are both driver mutations needed for tumor growth?
- ***Tumor suppressors in quantity
- ***Proto-oncogenes work on the CDK4/6 complex
What are two tumor suppressor gene types and their functions?
- 1) Gatekeeper: halt cycle, DNA death
- 2) Caretaker: DNA repair
What are the four Gatekeeper genes?
What are the four groups of caretaker genes?
- 1) ATM
- 2) BRCA1/2
- 3) MSH2/MLH1
- 4) XP genes
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.
What kind of transmission and fashion does Rb depict?
- Transmission: AD
- Fashion: AR
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
What are the two main function of p53?
- 1) p21: give time for repair
- 2) Bax: apoptosis
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
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
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
Does p53 follow loss-of-function or gain-of-function? How does it occur?
- 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.
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
What are the four Ab's of Gardisil and what do they stop?
- HPV 16/18 = cervical cancer
- HPV 6/11 = genital warts
How does APC save the cell from tumor growth?
APC binds B-catenin which then inhibits B-catenin from entering the nucleus
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
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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