BC #10-11 Cancer.txt
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BC #10-11 Cancer.txt
BC #10-11 Cancer
What is the differnce b/t driver and passenger mutations?
: cancer grown
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?
halt cycle, DNA death
What are the four Gatekeeper genes?
What are the four groups of caretaker genes?
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?
What is the diff. b/t
passed on to 50% of offspring, bilateral
randomly appearl, unilateral
What are the two main function of p53?
: give time for repair
How does phospho. relate to the p53 system?
= lack of
and degradation of
and dissociation of
= DNA halting and repair by by
How does apoptosis by p53 and Bax function? What is the functioning capsase?
opens Cytochrome C channels in Mitochondria
***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
destroys p53 = no apoptosis
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?
which then inhibits B-catenin from entering the nucleus
What are two was that APC can be inhibited and what is the result?
binds to G-protein = dissociation of APC from B-catenin = B-catenin in nucleus = TCF + B-catenin = tumor
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