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Bio of Cancer > Exam 2 > Flashcards

Exam 2 Flashcards

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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
what are the types of dual adress pathways
``` Jak-STAT Wnt-B-catenin Nf-KB Notch Patch-smooth TGF-B ```
26
Explain the TGF-B pathway
Smad heterotrimeric complex goes to nucleus to associate with transcription factors
27
TGF-B pathway is associated with what cancers
almost all carcinomas
28
Examples of negative feedback loops to regulate signal pathways
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
Examples of positive feedback loops to regulate signal pathways
activation of PKC degrades NF1 which allows RAs to become active
30
Ways to cause cancer through pathways
alter intrinsic activity of signaling molecules alter concentration of signaling molecules alter localization of signaling molecules
31
what occurs at the G1 check point
look for DNA damage
32
what occurs at the S phase checkpoint
make sure DNA only replicated once
33
what occurs at the G2 checkpoint
is DNA replication complete
34
what occurs at the mitosis checkpoint
are chromatids properly assembled
35
What happens at the R-point
the cell no longer responds to mitogenic GFs and TGF-B
36
what is cyclin D controlled by
macrphages, pathways
37
why are there three types of Cyclin D
different version induced by different pathways
38
inhibitors of Cyclin/CDKs
TGF-B, Akt/PKB, p21, p27
39
What are the three pRBs and what are their functions
p130 imposes Go quiescence pRB regulates progression through G1 p107 regulates late G1/S
40
what does hyperphosphorylation of pRB do
discourages transcription
41
What do E2F/pRB complexes do
modify chromatin conformation and discourage transcription
42
explain the pRB pathway
mitogen - receptor Ras- cyclins and e-pRB inactivation or E2F activation - S phase
43
how does Myc affect pRB
increases transcription of proteins that inactivate pRB increases transcription of E2F family genes increases transcription of proliferation inhibitors
44
Role of Cyclin D
interacts wiht estrogen receptor and TFs to control gene expression
45
Role of Cyclin E
may help regulate centrosom duplication
46
Examples of dominant mutations
ras, myc point mutations, receptor mutations that cause constant signaling, proto-oncogenes
47
examples of recessive mutations
tend to be tumor supressos genes
48
retinoblastoma tumor supress gene example
dominant phennotype, recessive genotype | needs to lose both copies for cancer development
49
what are ways LOH can occur
``` mitotic recombination gene conversion during DNA repair deletion nondisjunction translocations ```
50
how do we detect LOH
RFLPs track loss of paternal or maternal allel PCR overlapping deletions
51
How can you inactivate a tumor suppressor
methylation of CpG in promoter
52
What are the major tumor suppressor genes
Rb and p53
53
Why is p53 mutated easily
because needs all 4 copies to work properly
54
what does p53 control
apoptosis, DNa repair, blocking of angiogenesis and cell cycle arrest
55
What are the four hallmarks of apoptosis
Membrane blebbling Pyknosis DNA fragmentation Formation of apoptotic bodies
56
Ways to detect apoptosis
Phosphatidylserine on membrane Tunel assay Antibody to activate cascade 3
57
What causes intrinsic apoptosis
DNA damage, low o2 , uv damage
58
Explain intrinsic apoptosis
Cytochrome C with apaf1 plus procaspase makes the wheel of death
59
What causes extrinsic apoptosis
Death receptors and death ligands
60
Explain extrinsic apoptosis
Form timers that activate FADD Procaspase cleaved to caspase turns into executioner procaspases Then extrinsic and intrinsic come together
61
What proteins open and close the cytochrome C channels
Bcl2 keeps channels closed Bax/bak open channels up
62
what is the hayflick limit
the amount of times a cell can divide
63
what are reasons cells stop dividing
accumulated oxidative damage cell counts its division amounts
64
when does a cell enter crisis
when the cell goes past the Hayflisk limit when less than 3,000 base pairs
65
What happens in crisis
BFB cycles build then the telomeres snap whereever
66
How does cancer save telomeres
telomerase ALT
67
how do cells escape crisis
expression of telomerase
68
Why are mice good models for telomeres
have longer telomeres
69
How do BFB cycles contribute to cancer
genetic instability inactivates p53

Bio of Cancer (4 decks)

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