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BMS 2 > Cancer > Flashcards

Cancer Flashcards

1
Q

neoplasm

A

tumor-any abnnormal new grwoth of cell

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2
Q

genetic basis of cancer

A

most cancer-causing mutatons are somatic

mutagens are mostly environmental

Need mutliple mutations in many pathways
-major target is cell diviosn

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3
Q

Clonallyrelated cancer cells

A

all tumors begin with single cell-increase in size as population of tumor cells grow

accumulate aditional mutations-increase malignancy
-hetergenicty of cells

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4
Q

Contact inhibition

A

cells lose thjier abilty to respond to ECM and neighboring cell signals

-sto cells from prolifeating and migrating

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5
Q

how loss of contact inhibition

A

loss of cadherins-break link to other cells

metallopretases0degrade ECM and facilitate tissue invaision

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6
Q

g1/s transition

A

any pathwa that messes with this may cause cancer

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7
Q

tumor supressor genes meaning and 2 typse

A

prevent tumor dev

  • caretakeer-protein prevents damage or repairs DNA damage
  • gatekeeper-induce apop or restain cell diviosn
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8
Q

ocnogene

A

prteins promote cell growth and division

gain of funciton mutation leads to cancer-release of control

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9
Q

tumor represor mutations

A

receissive-need to lose both copies
-loss of heterozygostiy

need loss of function to iactivate protein

appear domoinant in pedigrees

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10
Q

exmaples of caretakes (3) and gat keeper (2)

A

MLH, BRCA, ERCC1

Rb and p53

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11
Q

rb/p53 fucntions

A

rb-controls g1/s transition

-53 halts cell di]viosn/initatse apoptosis in response to DNA stress

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12
Q

repair patway of MLH, ERCC1, BRCA1/2

A

MMR

NER-XP

DSBR-breast cancer

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13
Q

two rb disease

A

sporadic-single tumors in one eye of one person

familial-usually bilateral tumors (possibly multiple in one young). younger age, multiple family members affected

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14
Q

Two hit hypothesis

A

unilateral tumor-expected if two events needed for tumorto start forming
-loss of heterozygosity

bilateral-one even is required

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15
Q

how to get loss of hetero

A

chrom loss, duplicaton, mitotic recomb, gene conversion, deletion, epigentic, etc

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16
Q

p53 and cancer cells

A

loss of p53 renders cancercells immun toapop

stimulate trx of factors that block cell cycle (CDK inhibs/pro apoptotic proteins)

Converence point for many pathways

17
Q

how to stimulate p53

A

DNA damage-protein kinases

growth factors-arf protin synthesis

18
Q

arf protein

A

alternative reading frames-transcribed from DNA that encodes CDK inhibitor

pro apoptotic

19
Q

MDM2

A

binds to ARF-destbilizes p53 since ARF cant stabilize

MDM2 is antiapoptotic

20
Q

p53 structure

A

p53 is intriniscally unstable-stablized by DNA damage

  • no inherent tertiary structure
  • oncgogenic mutations can block DNA binding domain
  • drugs are used to stablize p53
21
Q

proto-oncogene

A

normal gene that can trn into an oncogene as result of mutations or increased expression

22
Q

two tyes of oncogene

A

viral-v-src-get DNA from cell, mutate it, put into another cell

cellulr oncogene-leads to continuous activity of protin GOF (dominant)-or LOF (recessive)

23
Q

cell cycle control pathway GF to end

A 
growth facotors
GFR-TK
ras
protein kinase cascade
TF's
cyclin and cdk-inhibits RB
Rb-inhibits nex step-
E2F/G1/S

all of ones where not inhiibited-stimulate next step

all of these except RB and G1/S are oncogenes

obviously many places for mutaions

24
Q

cell cycle control pathway tumor spupressor genes

A

NF1 (ras GAP)-supreses ras

TGfbeta-TGFbeta receptors-TF-CDK inhibtor
-inhbits CDK

25
Q

mTOR pathway, what are oncogenes or tumor sups

A

pip2-pip3-pkb-tsc-mTOR-protein synthesis/growth
pip2 to 3-P13K
pip3 t2-PTEN

oncogenes-PKB, mTOR, P13K
tumor sup-TSC, PTEN

26
Q

activaton of c-myc, c-abl, c-ras

A

myc-overproduction

abl-self activation-no need for normal reg stim

ras-prevent inactivation

27
Q

c-myc what it does and how mutation occurs that leads to problem

A

stimulate cell cycle
-amplified in many tumor

number of copies can be increased (gene amplification) and chromasmal translocation can occur-put in front of srong promoer

28
Q

how t diagnose c-myc rpoblems

A

FISH

see mny repeats-double minute chromasomes?

also can see small dots where notmal should be

29
Q

c-myc disease

A

burkitt lymphoma

tumor of b lymphoytes
-powerful enchancer to make b lymphoytes

translocate c-myc into hat region-much more trx

30
Q

c abl disease+ how diagnose+etiology

A

CML

philidelphia chromasome

translocation of 9 to 12, small p[art of 22 breaks off (philidelphia)-other part goes onto chromaosme 9
-attaches behind BCR-no more protein kinase to turn on (contintuivilty active)

31
Q

BCR

A

breakpint cluster reion-on chromasome 22

-creates protein that does nto have to be activated

32
Q

c abl structure

A

sh-src homology-oncogene withprotein kinase activity

sh2/3-regulatory-inhibit kinase untl they are modifed by activatd inhibitor

sh1-portien kinase domain

activation loop-poly peptidee chain in sh1 domain that occludes active site-can be phophorylated toallow substrateto bind
——add 2 oligomerzed bcr in front-activate kinase that can do whatever it wants now

33
Q

gleevec

A

binds to and stabilies inactive confomrmatin of c-abl

34
Q

oncogene addiction

A

glevec

main component of cancer driving pathay makes a bottleneck-this gene becomes the king becuase others are gotten rid of because this one is the best for abnromal environemt-target this gene

35
Q

ras + GAP abilites

A

active when bound t GTP, inactive at GDP

  • two gap actvites (intrinsic and extrenisc by GAPs (like NF1)
  • intrinsic is not as effecient as GAPs
  • need both to ensure ras sigals properly
36
Q

GEF

A

replaces GDP by GTP

37
Q

GAP

A

gtpases-ras (intrinsicly) and NF1

switches GTP to GDP

38
Q

proteins with ras homology domain

A

alot-results in cell growh, cell adheion, ant apop, membrane traffic, etc.

39
Q

oncogenic mutation in ras

A

gly 12 and gln 61
0reudece GAP (gtpase) activty of ras
0spends more time active

BMS 2 (41 decks)

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