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CTMD LOMO > Apoptosis/DNA damage > Flashcards

Apoptosis/DNA damage Flashcards

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1
Q

Programmed necrosis mechanism

A

Consumption of NAD+ through PARP-dependent modification –> ADP-ribose
- Leads to NAD+ depeltion and inhibition of glycolysis, no ATP so pump doesn’t work and sodium can’t leave cell, water rushes in and it bursts

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2
Q

IHC to detect apoptosis

A

best method, antibodies used for specific caspases

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3
Q

propidium iodide and cell sorting to detect apoptosis

A

PI intercalates DNA and is fluorescent
- DNA content analyzed using flow cytometry
< 2N have lost DNA content due to DNA fragmentation

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4
Q

Annexin V staining

A

PS found on outer leaflet during apoptosis, stain with antibodies

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5
Q

TUNEL

A

labeling nicks in DNA

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6
Q

extrinsic pathway ligands

A

TNFalpha
TRAIL
Fas

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7
Q

unique extrinsic caspase initiators

A

8, 10

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8
Q

caspase initiators for both intrinsic and extrinsic

A

2, 9

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9
Q

effector caspases

A

3, 6, 7

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10
Q

IAPs

A

IAP1, IAP2, XIAP, Livin

- inhibit effector and initiator caspases

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11
Q

Pro-death Bcl-2 proteins: effectors

A

BAK and BAX

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12
Q

Pro-death Bcl-2 proteins: BH3- only

A

BID, BIM, PUMA

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13
Q

BH-3 only activators

A

BID, BIM, PUMA

  • bind and neutralize pro-survival Bcl-2 family members
  • promote BAX and BAK oligomerization and pore formation –> cyt c release
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14
Q

BH3-only sensitizers

A

BAD, BIK, NOXA…. etc

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15
Q

BAX and BAK functions

A

oligomerize to form pore in mitochondria, release of cyt C

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16
Q

pro-survival Bcl-2 proteins

A

bind and sequester BAX and BAK

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17
Q

BID

A

extrinsic, activated in response to death receptors

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18
Q

BIM, PUMA

A

intrinsic,
BIM activated in response to MT stress
PUMA activated in response to p53

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19
Q

apoptosome

A

cyt C binds Apaf1, these then bind pro-caspase 9 to cleave and activate it, triggering caspase cascade

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20
Q

5 proteins released from mitochondria

A
  1. cyt c: forms apoptosome
  2. AIF: triggers chromatin condensation, DNA deg, disrupts ETC
  3. Smac/Diablo: inhibit IAPs
  4. Omi/HtrA2: inhibit IAPs
  5. Endo G: endonuclease that cleaves DNA
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21
Q

One of most common events to occur during oncogenesis

A

upregulation ofNF-kappa B activity: upregulates gene products that block apoptosis

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22
Q

damage by UVB

A

pyrimidine dimers

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23
Q

damage by UVA

A

free radicals

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24
Q

ionizing radiation/X rays

A

DS breaks in DNA strands or SS

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25
polycyclic hydrocarbons
bulky adducts
26
direct DNA repairs uses...
MGMT
27
NER
fixes dimers and adducts
28
BER
uses glycosidase enzymes to remove abnormal bases
29
NHEJ
- DNA ligase IV, cofactor XRCC4 - can introduce mutations - no template
30
HR
- requires template
31
MMR
- defects cause slippage (HNPCC)
32
TLS
- last resort, super error prone | - kinda shitty polymerases, but betta than nathan
33
XP
NER
34
HNPCC
MMR MIN proximal polyp, subtle
35
familial breast ovarian cancer
DS DNA repair
36
FA
interstrand crosslink repair/translesional synthesis
37
Nijmegen Breakage Syndrome
ds DNA repair | NBS1 gene
38
Li Fraumeni
- mutation in p53 and chk2 genes
39
AT
ATM gene
40
Bloom and Werner Syndrome
mutations in RECQ DNA helicase | hyperrecombination
41
FAP
APC gene numerous polyps in distal colon, severe CIN
42
GFs expressed by cancer cells
PDGF: glioblastomas HGF: numerous cell types VEGF: angiogenesis
43
Receptor tyrosine kinases
HER-2 MET EGFR c-KIT
44
BRAF-V600
seen in melanomas
45
Gleevac/imatinib
blocks kinase domain of tyrosine kinase
46
Rituximab
immunotherapy | * antibody against CD20 receptor found on B cells (immunosuppresion)
47
Tamoxifen
- receptor antagonist for estrogen | * good for bones, bad for endometrium, good for breast ca
48
Arimidex
hormonal | non-steroidal aromatase inhibitor
49
Side effects of radiation
Early: mucositis, infertility Late: fibrosis, secondary cancers
50
3 common side effects of chemotherapy
alopecia, GI, bone marrow suppression
51
MDR gene
multi-drug resistance gene, encodes P-glycoprotein, involved in tumor cell resistance to drugs pumps out chemo drug
52
how much of tumor mass can be stroma
90% of cells
53
Two mechanisms for stromal incorporation into tumor
1. incorporates pre-existing stroma | 2. induces stromal differentiation
54
xenografts
immunodeficient mice, can't see stromal contributions
55
chemical carcinogenesis
carcinogen exposure
56
implantable murine tumors
line derived from spontaneous cancer in mouse
57
genetic mouse models
mice develop tumors over time, progressive developmental model similar to humans
58
chronic inflammatory diseases and cancer susceptibility
Barrett's esophagus: esophageal ulcers/gastritis: gastric cancer IBS: colorectal cancer
59
TAMs
macrophage, function dysregulated in cancer
60
MDSCs
myeloid derived suppressor cells * suppress anti-tumor responses mediated by other immune cells
61
CAFs
cancer associated fibroblasts * encourage tumor growth, angiogenesis, inflammation, metastasis
62
EMT
epidermal to mesenchymal transition E --> N cadherins, promotion of migration - upregulate mesenchymal markers increase in proteolytic enzymes spindly mesenchymal shape
63
angiogenesis
new vessels from pre-existing
64
vasculogenesis
de novo formation of endothelial cells from mesoderm cell precursors
65
angiogenic switch
can be controlled by hypoxia
66
MMPs
effector of EMT, good for tumors that want to metastasize
67
TIMPs
inhibit MMPs
68
tissue tropism
non-random tissue preference for site of metastasis
69
CAM use by cancer patients
75% in conjunction with conventional therapy

CTMD LOMO (14 decks)

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