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Bio of Cancer > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what are immediate early genes

A

react right away to GF

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2
Q

What are delayed early genes

A

Occurs with a lag

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3
Q

What do tyrosine phosphorylations do

A

control location of cytoplasmic signaling proteins and therefore their actions

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4
Q

Use the structure of Src to explain tyrosine phosphrylation

A

SH1- interacts with substrate to cause enzymatic reaction
SH2- docking site for protein signal pathway
SH3- stabalize binding site

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5
Q

What are the three major pathways of RAS

A

Ras-RAf
PI3K
Ral-GEF

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6
Q

What is the RAS-Raf pathway

A

map kinases pathway

results in chromatin remodeling, proteing synthesis or transcription

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7
Q

What is the PI3K pathway

A

Stimulates Akt/PKB

inhibits apoptosis, stimulates protein synthesis, stimulates cell proliferation, progression of cell cycle

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8
Q

What is the Ral-GEF pathway

A

causes alteration sin cytoskeleton that allow cell to divide and affect cell mobility

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9
Q

Explain an example of direct signaling

A

Jak-STAT pathway- activation of Jak leads to STAT dimerization and migration to nucleus

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10
Q

What is direct signaling

A

receptor migrates directly to nucleus

not cascade like

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11
Q

What are integrins

A

interact with cytoskeleton

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12
Q

What is integrin signaling

A

transmit signaling through focal adhesion kinase proteins

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13
Q

What types of pathways does integrin signaling activate

A

pathways to decline likelihood of apoptosis

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14
Q

What triggers anoikis

A

lack of binding to ECM

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15
Q

what is anoikis

A

a form of apoptosis that activates caspase-3

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16
Q

Describe the Wnt-Beta-Catenin pathway

A

If wnt is bound, B-catenin evades degradation and goes to the nucleus and turns on proliferation expression by binding to Tcf/Lef

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17
Q

Explain the G-protein coupled Receptors pathway

A

B-arrestin activates kinases for cell proliferation and survival
alpha activates Raf/Ras, gamma and beta activate PI3K, Raf/Ras, src

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18
Q

explain the nuclear factor KB pathway

A

bound to inhibitor

when phosphorylated, inhibitor is degraded and moves to nucleus to activate cell growth and division

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19
Q

Explain the notch pathway

A

interaction with ligand cleaves off fragment of notch and goes to necleus for cell proliferation

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20
Q

NF-KB pathway can cause what cancers

A

breast, lymphomas, myelomas

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21
Q

Notch pathway can cause what cancers

A

cervical, colon, prostate, and lung

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22
Q

Explain the patched-smooth pathway

A

when smooth is activated, allows Gli into the nucleus uncleaved to promote transcription

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23
Q

Patched-smooth pathway can cause what cancers

A

basal cell carcinoma, glioblastomas

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24
Q

what are dual address pathways

A

something exists in the cytoplasm and gets moved to the nucleus to become transcription factors

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25
Q

what are the types of dual adress pathways

A 
Jak-STAT
Wnt-B-catenin
Nf-KB
Notch
Patch-smooth
TGF-B
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26
Q

Explain the TGF-B pathway

A

Smad heterotrimeric complex goes to nucleus to associate with transcription factors

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27
Q

TGF-B pathway is associated with what cancers

A

almost all carcinomas

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28
Q

Examples of negative feedback loops to regulate signal pathways

A

Ras binding to GTP causes sprouty to inhibit SH2 and Raf
Ras bound to Gap stops Ras
Gli moving to nucleus makes more patched and inhibits smooth

29
Q

Examples of positive feedback loops to regulate signal pathways

A

activation of PKC degrades NF1 which allows RAs to become active

30
Q

Ways to cause cancer through pathways

A

alter intrinsic activity of signaling molecules
alter concentration of signaling molecules
alter localization of signaling molecules

31
Q

what occurs at the G1 check point

A

look for DNA damage

32
Q

what occurs at the S phase checkpoint

A

make sure DNA only replicated once

33
Q

what occurs at the G2 checkpoint

A

is DNA replication complete

34
Q

what occurs at the mitosis checkpoint

A

are chromatids properly assembled

35
Q

What happens at the R-point

A

the cell no longer responds to mitogenic GFs and TGF-B

36
Q

what is cyclin D controlled by

A

macrphages, pathways

37
Q

why are there three types of Cyclin D

A

different version induced by different pathways

38
Q

inhibitors of Cyclin/CDKs

A

TGF-B, Akt/PKB, p21, p27

39
Q

What are the three pRBs and what are their functions

A

p130 imposes Go quiescence
pRB regulates progression through G1
p107 regulates late G1/S

40
Q

what does hyperphosphorylation of pRB do

A

discourages transcription

41
Q

What do E2F/pRB complexes do

A

modify chromatin conformation and discourage transcription

42
Q

explain the pRB pathway

A

mitogen - receptor Ras- cyclins and e-pRB inactivation or E2F activation - S phase

43
Q

how does Myc affect pRB

A

increases transcription of proteins that inactivate pRB
increases transcription of E2F family genes
increases transcription of proliferation inhibitors

44
Q

Role of Cyclin D

A

interacts wiht estrogen receptor and TFs to control gene expression

45
Q

Role of Cyclin E

A

may help regulate centrosom duplication

46
Q

Examples of dominant mutations

A

ras, myc point mutations, receptor mutations that cause constant signaling, proto-oncogenes

47
Q

examples of recessive mutations

A

tend to be tumor supressos genes

48
Q

retinoblastoma tumor supress gene example

A

dominant phennotype, recessive genotype

needs to lose both copies for cancer development

49
Q

what are ways LOH can occur

A 
mitotic recombination
gene conversion during DNA repair
deletion
nondisjunction
translocations
50
Q

how do we detect LOH

A

RFLPs track loss of paternal or maternal allel
PCR
overlapping deletions

51
Q

How can you inactivate a tumor suppressor

A

methylation of CpG in promoter

52
Q

What are the major tumor suppressor genes

A

Rb and p53

53
Q

Why is p53 mutated easily

A

because needs all 4 copies to work properly

54
Q

what does p53 control

A

apoptosis, DNa repair, blocking of angiogenesis and cell cycle arrest

55
Q

What are the four hallmarks of apoptosis

A

Membrane blebbling
Pyknosis
DNA fragmentation
Formation of apoptotic bodies

56
Q

Ways to detect apoptosis

A

Phosphatidylserine on membrane

Tunel assay
Antibody to activate cascade 3

57
Q

What causes intrinsic apoptosis

A

DNA damage, low o2 , uv damage

58
Q

Explain intrinsic apoptosis

A

Cytochrome C with apaf1 plus procaspase makes the wheel of death

59
Q

What causes extrinsic apoptosis

A

Death receptors and death ligands

60
Q

Explain extrinsic apoptosis

A

Form timers that activate FADD

Procaspase cleaved to caspase turns into executioner procaspases

Then extrinsic and intrinsic come together

61
Q

What proteins open and close the cytochrome C channels

A

Bcl2 keeps channels closed

Bax/bak open channels up

62
Q

what is the hayflick limit

A

the amount of times a cell can divide

63
Q

what are reasons cells stop dividing

A

accumulated oxidative damage

cell counts its division amounts

64
Q

when does a cell enter crisis

A

when the cell goes past the Hayflisk limit

when less than 3,000 base pairs

65
Q

What happens in crisis

A

BFB cycles build then the telomeres snap whereever

66
Q

How does cancer save telomeres

A

telomerase

ALT

67
Q

how do cells escape crisis

A

expression of telomerase

68
Q

Why are mice good models for telomeres

A

have longer telomeres

69
Q

How do BFB cycles contribute to cancer

A

genetic instability

inactivates p53

Bio of Cancer (4 decks)

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