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CTMD LOMO > Apoptosis/DNA damage > Flashcards

Apoptosis/DNA damage Flashcards

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
Q

polycyclic hydrocarbons

A

bulky adducts

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26
Q

direct DNA repairs uses…

A

MGMT

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27
Q

NER

A

fixes dimers and adducts

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28
Q

BER

A

uses glycosidase enzymes to remove abnormal bases

29
Q

NHEJ

A
  • DNA ligase IV, cofactor XRCC4
  • can introduce mutations
  • no template
30
Q

HR

A
  • requires template
31
Q

MMR

A
  • defects cause slippage (HNPCC)
32
Q

TLS

A
  • last resort, super error prone

- kinda shitty polymerases, but betta than nathan

33
Q

XP

34
Q

HNPCC

A

MMR
MIN
proximal polyp, subtle

35
Q

familial breast ovarian cancer

A

DS DNA repair

36
Q

FA

A

interstrand crosslink repair/translesional synthesis

37
Q

Nijmegen Breakage Syndrome

A

ds DNA repair

NBS1 gene

38
Q

Li Fraumeni

A
  • mutation in p53 and chk2 genes
39
Q

AT

40
Q

Bloom and Werner Syndrome

A

mutations in RECQ DNA helicase

hyperrecombination

41
Q

FAP

A

APC gene
numerous polyps in distal colon, severe
CIN

42
Q

GFs expressed by cancer cells

A

PDGF: glioblastomas
HGF: numerous cell types
VEGF: angiogenesis

43
Q

Receptor tyrosine kinases

A

HER-2
MET
EGFR
c-KIT

44
Q

BRAF-V600

A

seen in melanomas

45
Q

Gleevac/imatinib

A

blocks kinase domain of tyrosine kinase

46
Q

Rituximab

A

immunotherapy

* antibody against CD20 receptor found on B cells (immunosuppresion)

47
Q

Tamoxifen

A
  • receptor antagonist for estrogen

* good for bones, bad for endometrium, good for breast ca

48
Q

Arimidex

A

hormonal

non-steroidal aromatase inhibitor

49
Q

Side effects of radiation

A

Early: mucositis, infertility
Late: fibrosis, secondary cancers

50
Q

3 common side effects of chemotherapy

A

alopecia, GI, bone marrow suppression

51
Q

MDR gene

A

multi-drug resistance gene, encodes P-glycoprotein, involved in tumor cell resistance to drugs
pumps out chemo drug

52
Q

how much of tumor mass can be stroma

A

90% of cells

53
Q

Two mechanisms for stromal incorporation into tumor

A
  1. incorporates pre-existing stroma

2. induces stromal differentiation

54
Q

xenografts

A

immunodeficient mice, can’t see stromal contributions

55
Q

chemical carcinogenesis

A

carcinogen exposure

56
Q

implantable murine tumors

A

line derived from spontaneous cancer in mouse

57
Q

genetic mouse models

A

mice develop tumors over time, progressive developmental model similar to humans

58
Q

chronic inflammatory diseases and cancer susceptibility

A

Barrett’s esophagus: esophageal
ulcers/gastritis: gastric cancer
IBS: colorectal cancer

59
Q

TAMs

A

macrophage, function dysregulated in cancer

60
Q

MDSCs

A

myeloid derived suppressor cells

  • suppress anti-tumor responses mediated by other immune cells
61
Q

CAFs

A

cancer associated fibroblasts

  • encourage tumor growth, angiogenesis, inflammation, metastasis
62
Q

EMT

A

epidermal to mesenchymal transition
E –> N cadherins, promotion of migration
- upregulate mesenchymal markers
increase in proteolytic enzymes

spindly mesenchymal shape

63
Q

angiogenesis

A

new vessels from pre-existing

64
Q

vasculogenesis

A

de novo formation of endothelial cells from mesoderm cell precursors

65
Q

angiogenic switch

A

can be controlled by hypoxia

66
Q

MMPs

A

effector of EMT, good for tumors that want to metastasize

67
Q

TIMPs

A

inhibit MMPs

68
Q

tissue tropism

A

non-random tissue preference for site of metastasis

69
Q

CAM use by cancer patients

A

75% in conjunction with conventional therapy

CTMD LOMO (14 decks)

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