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Cancer Biology > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

apoptosis

A

programmed cell death

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2
Q

p53

A

homotetramer transcription factor for apoptosis genes and repair mechanisms (binds DNA and responds to stress/damage)

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3
Q

describe why it is important to know that p53 is a homotetramer

A

only 1/16 of all possible combos is functional because need all 4 WT and no mutation

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4
Q

why is it better to have the p53+/- genotype than the p53+/m

A

absent, phenotype is mostly normal but mutation, the phenotype is that there is no p53 function

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5
Q

p53 turns on what genes…

A

mdm2, cell cycle arrest genes (p21/27), DNA repair genes, apoptosis genes

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6
Q

stressors that can turn on p53

A

lack of nucleotides, UV radiation, ionizing radiation, oncogene signaling, hypoxia, blockage of transcription

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7
Q

why is it an advantage that p53 is constantly expressed in all cells all the time

A

energy consuming but beneficial because it allows rapid response to stress and a fast way to turn off proliferation

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8
Q

mdm2 function

A

regulates p53 via negative feedback

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9
Q

how does mdm2 regulate p53 via negative feedback

A
  • lots of copies of p53
  • some p53 P even when not stressed so p53 binds DNA—> translate Mdm2 protein
  • Mdm2 then feeds back and initiates degradation of un-P p53 by ubiquitination
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10
Q

when is p53 P

A

stress

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11
Q

how is was signaling involved in p53 expression and function

A

GF–> Ras–> Mapk/Erk1/2 —> proliferation

overaction GF/Ras signaling will increase Mdm2 expression so there will be very little or no p53 and no regulation

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12
Q

how can we prevent the consequence of overactive Ras signaling and not enough p53

A

ARF (only transcribed if signaling on “too long”)

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13
Q

describe ARF signaling pathway

A

ARF negatively regulates Mdm2 and therefore helps p53 because p53 won’t be inhibited by Mdm2

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14
Q

TFs for ARF

A

E2F when Rb hyper P

Erk 1/2 (AP1 and Ets)

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15
Q

how does ARF inhibit Mdm2`

A

binds Mdm1 and hides/sequesters Mdm2 into nucleus–> Mdm2 and ARF can’t bind p53, so p53 will accumulate, allows p53 to get P by stress sensing kinase

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16
Q

apoptosis vs necrosis

A

apoptosis: neat and ordered, usually doesn’t impact neighboring cells, everything stays contained in plasma membrane
necrosis: a lot of cells, messier (explosion), broad neg impacts –> inflammation

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17
Q

extrinsic apoptosis

A
  • death receptor proteins
  • no mitochondria
  • death signal from diff cell
  • no p53
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18
Q

intrinsic apoptosis

A
  • mitochondria
  • stuff inside cell signal apoptosis
  • p53
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19
Q

explain how cancer cells get past apoptosis

A

apoptosis in early stages of cancer develop is important (50% cancer has mut p53) so big advantage for cancer cells to lose intrinsic apoptosis because able to survive and reproduce

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20
Q

initiator vs executioner caspases

A

initiator only cuts proteases and executioner cuts other procaspases and cuts death substrates

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21
Q

cell with no p53 activation

A

receives survival signals, has stable Bcl-2 levels, cytochrome C in mitochondria

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22
Q

cell with p53 activation

A

induce p53 to transcribe Bax

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23
Q

Bax

A

can form a pore to release cytochrome C, pro-apoptotic

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24
Q

Bcl2

A

anti-apoptotic, binds to Bax to prevent it from forming a pore

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25
Q

what happens when there is more Bax than Bcl2?

A

apoptosis, Bax prefers to bind to Bcl2 than the mitochondrial membrane but when not enough Bcl2, forms pores so cytochrome C is released into the cytoplasm to induce apoptosis

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26
Q

what happens once cytochrome C leaves the mitochondria and is in the cytoplasm?

A
  • cytochrome C forms apoptosome

- apoptosome will cleave procaspase–> caspase

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27
Q

extrinsic apoptosis steps

A
  • signal from neighboring cell
  • extrinsic signals lead to cytochrome C being released
  • apoptosome
  • initiator and executioner caspases
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28
Q

what kind of signal leads to extrinsic apoptosis

A

either small protein or cell surface protein on killing cell

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29
Q

targeted therapies

A

trying to kill cancer cells and not healthy cells

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30
Q

target therapy for cancer cells that are avoiding apoptosis

A

inhibit Bcl2

  • prevent from binding pro-apoptotic
  • useful for cancer cells overexpress Bcl2 (drug in binding pocket so pro-apoptotic go into mitochondria instead of bind bcl2)
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31
Q

why does cancer occur?

A
  • drug resistance
  • avoid intrinsic/extrinsic
  • mutation eliminate protein in pathway (pro-apoptotic, etc)
  • mutations lead to a lot of variation
  • natural selection
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32
Q

what is the problem that occurs at the end of replication?

A

after each round of replication of linear DNA, the DNA will be a bit shorter, ds ends of linear DNA look like ds breaks, nuclease destroy end linear DNA

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33
Q

what is the solution to the end replication problem?

A

telomeres and telomerase

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34
Q

telomere DNA

A

long 3’ end of dsDNA, short repeated seq allows for looping

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35
Q

telomere protein

A

facilitate the looping, hide 5’ and 3’ ends so not degraded, repeated hexamer seq, regulate telomerase function

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36
Q

telomerase RNA

A

hTR

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37
Q

telomerase protein

A

hTERT

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38
Q

job of telomerase protein

A

synthesize DNA, 6 nucleotides at a time to extend 3’ end DNA, then DNA poly and primer can extend 5’ end

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39
Q

which cells have telomerase?

A
  • stem cells (long lived, replicate a lot)
  • some immune cells (T cells and B cells during infection need a lot)
  • germ cells (long lived)
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40
Q

once telomere is gone…

A

end of DNA looks like ds break which leads to p53 activation and apoptosis

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41
Q

once telomere is gone but no p53 present

A

fusion of unprotected chromosome ends, chromosome break, crisis, cell death even without p53 or cancer cell turns on telomerase

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42
Q

define hyperplasia

A

a lot of normal cells

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43
Q

evidence for why cancer takes decades to develop

A

30 year lag between increase in cigarette consumption and increase in smoking related lung cancer, autopsies

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44
Q

colon cancer multi-step tumorigenesis

A

normal epithelium–>(loss of APC) hyper plastic epithelium—> (DNA hypomethylation) early–> (activation of K-ras) intermediate adenomas–> (loss of 18q TSG) late –> (loss of p53) carcinoma–> invasion and metastasis

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45
Q

common mutations in colon cancer

A
  • loss of APC TSG function (too much epithelial cell prolif)
  • DNA hypomethylation
  • oncogene activation of Ras
  • loss of unknown TSG
  • loss of p53
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46
Q

DNA hypomethylation colon cancer mutation

A

problems with regulation of gene expression, DNA methylation makes it more difficult to express a region of DNA

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47
Q

oncogene activation of Ras colon cancer mutation

A

Ras is “on” when it shouldn’t be, too much prolif, p53 activate

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48
Q

step wise cancer

A

initiating mutation (1st clonal expansion)-> second mutation (2nd clonal)—> –> increase mutation rate due to fast rate of prolif–> multiple independent mutations (multiple parallel clonal expansions–> sub pop gain ability to metastasize –> metastatic cancer

49
Q

step wise cancer and natural selection

A

each step inc ability for cancer cells to survive and reproduce, “most fit” metastasize

50
Q

acute inflammation

A

short time period, caused by infection, goes away after immune system eliminates virus/bacteria

51
Q

chronic inflammation

A

long time period, infections can’t be cleared, autoimmune problems

52
Q

multi-step tumorigenesis and hep B

A
  • immune cells enter liver
  • immune cells prolif and tell liver cells to prolif
  • release ROS
  • tumor initiating mutations can occur
53
Q

autoimmunity - hepatitis B virus:

A
  • infects liver cells (chronic inflammation)

- high rates liver cancer

54
Q

autoimmunity- chron’s disease/UC/IBD

A
  • chronic inflammation in gut

- high rates colon cancer

55
Q

inflammation on molecular level

A

pathogen–>

1) immune cells prolif (immune cells produce and respond GF)
2) immune cells to site infection
3) immune cells kill pathogen or pathogen infected cells (secrete apoptosis mol)

56
Q

cytokines are

A

GF that tell immune cells and epithelial cells to prolif

57
Q

chronic inflammation and cytokines

A

high levels of IL6/TNFa

1) DNA damage (DNA rep mistake)
2) constant prolif of epithelial

58
Q

immune cells create

A

ROS to kill pathogen but this leads to DNA damage

59
Q

cancer stem cells

A
  • not necessarily normal stem cells that have turned into cancer stem cells
  • cells that prolif to give rise to more and more tumor cells
  • most resistant to treatment
60
Q

cancer stem cell sub-population

A

acquire mut that allows them to be really good at prolif

61
Q

genomic integrity

A

2 copies of each 23 chromosomes functional

62
Q

loss of genomic integrity

A

DNA repair mechanisms messed up and apoptosis not happening

63
Q

normal cells DNA damage

A

p53 activation (halt cell cycle, repair, apoptosis)

64
Q

cancer cells DNA damage

A

loss of p53 common or problems downstream p53

65
Q

dsDNA break

A

HDR, NHEJ

66
Q

HDR

A

homology directed repair

67
Q

NHEJ

A

non homologous end joining

68
Q

dsDNA break can lead to

A

chromosomal translocation (proto-onco)

69
Q

HDR

A
  • end S/G2
  • need sister chromatid pairing
  • use undamaged sister chromatid as template to repair damaged chromatid
  • involves BRCA1/2 proteins
70
Q

when can HDR not happen?

A

without BRCA1/2 or if dsDNA break during G1 so no sister for template

71
Q

NHEJ

A
  • randomish bp

- worse than HDR but not as bad as 2 diff chromosomes getting stitched together (happens if >1 ds break present)

72
Q

aneuploidy

A

abnormal # chromosomes

73
Q

aneuploidy caused by

A

DNA damage or mitosis problems

74
Q

why is aneuploidy bad?

A

loss of TSG, LOH mech and gain copies of proto-oncogenes

75
Q

what are some problems that can lead to aneuploidy?

A
  • mis-attach microtubules to kinetochores
  • chromosomal translocation (due to NHEJ)
  • abnormal number kinetochores
76
Q

spindle assembly checkpoint

A

metaphase to anaphase transition

-chromosomes won’t pull apart until all evenly connected to mitotic spindles

77
Q

spindle assembly checkpoint not effective

A

chromosomes don’t pull apart correctly and aneuploidy occurs

78
Q

how does the spindle assembly checkpoint work

A
  • sister chromatids attached with protein called cohesion

- once cohesin degraded, chromatids pull apart

79
Q

“signaling” pathway of SAC

A

CDC20 activated by cyclins/CDks –> degrades securin which is in binding pocket of separate but once degraded separase can degrade cohesion –> chromatids pull apart

80
Q

all chromatids have to be attached evenly before

A

cohesin degraded

81
Q

what inhibits CDC20?

A

BUBR1

82
Q

mutation with BUBR1

A

SAC broken and advantageous for cancer cells because leads to aneuploidy

83
Q

how does BUBR1 inhibit CDC20?

A

BUBR1 attached to chromatids and kinetochore, once spindles present BUBR1 removed by kinetochore and no longer inhibiting

84
Q

over expression of BUBR1

A

no aging, random mistakes such as BUBR1 accidentally falling off prevented and decrease aneuploidy because fewer random mistakes

85
Q

heterotypic signaling

A

signals being shared between diff cell types

86
Q

carcinoma

A

epithelial originating cancer

87
Q

cell types involved in carcinoma

A 
cancer cells
stromal/mesenchymal cells (non cancer, non epithelial, support)
fibroblasts (create ECM)
endothelial (form blood vessels)
macrophages (support tumors)
88
Q

what signals are sent from non-cancer cells to cancer cells?

A
  • growth and survival
  • angiogenic
  • signals that allow for metastasis
  • cancer cells need to grow blood vessels and move
89
Q

what signals allow for metastasis

A
  • require non cancer

- ability for epithelial cell to move

90
Q

angiogenic signals

A

growing new blood vessels

91
Q

non cancerous wound healing main steps

A

wound–>damage vasculature–> bleeding –> recruit platelets–> blood clot

92
Q

non cancerous wound healing, what happens between damage vasculature and bleeding?

A

hypoxia

93
Q

hypoxia in non cancer leads to

A

VEGF production

94
Q

VEGF

A

recruits macrophages and leads to angiogenesis

95
Q

macrophages (non-cancer)

A

degrade ECM, release sequestered GF, lead to EMT

96
Q

after recruiting platelets in non-cancer what happens?

A

release PDGF which tells fibroblasts and endothelial cells to grow new blood vessels

97
Q

what is a key difference between non-cancer and cancer carcinoma cells

A

cancer go through EMT but not MET so they remain invasive and metastasize

98
Q

angiogenesis

A

used for wound healing, growth, pregnancy

99
Q

angiogenesis is important for

A
  • growth of new blood vessels
  • deliver O2, nutrients
  • take away CO2, waste
100
Q

hypoxic area of tumor

A

cells signal growth of new blood vessels

101
Q

steps to make more blood vessels

A
  • in blood supply, endothelial progenitor cells (EPCs)
  • VEGF recruits EPCs out of circulation and into tissue
  • VEGF tells EPCs to prolif and differentiate into endothelial cells
  • new blood vessels branch off of existing blood vessels
102
Q

anti-angiogenesis therapies

A

anti-VEGF antibody binds VEGF and prevents signaling or drug inhibits VEGF receptors and prevents signaling

103
Q

benign

A
  • not yet metastatic

- still contain in BM

104
Q

malignant

A

metastatic

105
Q

metastasis steps

A

1) leave primary tissue

2) colonize a new tissue

106
Q

leave primary tissue metastasis step

A
  • BM degraded
  • EMT
  • carcinoma cell moves into bloodstream or lymphatic system
107
Q

how is the basement membrane degraded?

A

cancer cells and macrophages secrete an enzyme, MMPs

108
Q

EMT

A

epithelial to mesenchymal transition allows carcinoma cells to move

109
Q

colonize new tissue step

A
  • many cancer cells die in circulation
  • often cancer cells caught in lung capillaries
  • not all cancer cells survive in the new tissue
110
Q

other common sites for cancer cells besides lungs

A

bone, brain, liver

111
Q

which cancer cells don’t die in circulation?

A

hearty ones really good at prolif and survival

112
Q

EMT physical changes

A

motility

113
Q

EMT gene exp changes

A

change from expressing E cadherin to expressing N cadherin

114
Q

E cadherin

A

binds epithelial cells together (tight)

115
Q

N cadherin

A

binds stromal and endothelial cells together (not tight)

116
Q

EMT

A

epithelial stops binding other epithelial because E cadherin signal lost when TGFbeta binds to cells to induce EMT

117
Q

TGFbeta

A
  • stromal cells produce
  • cancer cells can amplify production
  • macrophages can help produce
118
Q

TWIST

A
  • overexpress leads to EMT
  • without twist, a lot of E cadherin
  • with TWIStT, a lot of N cadherin

Cancer Biology (4 decks)

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