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MCB II Block 1 > Cancer II > Flashcards

Cancer II Flashcards

1
Q

static cell population ex

A

nerve cell
skeletal
cardiac muscle
erythrocyte

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2
Q

static cell, once they are differentiated

A

they wont’ go through cel cycle

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3
Q

now and then divider ex

A

hepatocytes

fibroblast

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4
Q

now and then diver, about dividng

A

they arent usually but if a wound occurs they will be stimulated to go into cell cycle

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5
Q

stem cell ex

A

spermatogonia

epithelial stem cell

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6
Q

stem cell cell cycle

A

constantly dividing short half life

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7
Q

cell cycle

A

G1 S G2 M

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8
Q

interphase what stages

A

G1 S G2

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9
Q

cytokinesis

A

splitting of one cell into two daughter cells

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10
Q

growth phase

A

interphase

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11
Q

G1 to S phase is important

A

checkpoint

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12
Q

restriction point or

A

R point

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13
Q

R point

A

*

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14
Q

if no growth factor signaling in G1

A

when cell exits mitosis it comes into G1 if there are no growth factors being secreted it will exit cell cycle and go into G0

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15
Q

up until restriction point cells are sensitive to

A

growth factor and antigrowth factor signaling

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16
Q

some growth factor secreted and then it stops

A

cell will go into G0

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17
Q

if there’s enough growth factor signling that cell gets to restriction point, it’s known as the

A

point of no return

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18
Q

once a cell passes a restriction point

A

it’s too late to stop going through the self cycle or it will kill itself by apoptosis. it can no longer go to G0 and just be

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19
Q

G1 to S phase is past the

A

R point

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20
Q

once it’s past the R point the cell can still

A

repair damage

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21
Q

prophase

A

genome starts condensing

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22
Q

prometaphse

A

breakdown of nuclear envelope

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23
Q

metaphse

A

sister chromatidds lined up in center of spindle

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24
Q

anaphse

A

pull sister chromatids apart to opposite pulls

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25
Q

important checkpoint in mitosis

A

metaphse to anaphse transition

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26
Q

metaphase to anaphase checkpoint is important for preventing

A

anaploidy

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27
Q

telphase

A

nuclear envelopes reforme

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28
Q

ctokinesis

A

cell splits to two daughter cells

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29
Q

to get from metphase and anaphase need activation of what protein

A

APC/C

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30
Q

APC/C

A

anaphase promoting complex or cyclesome

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31
Q

when cell is in G1 how many copies of chrom.

A

2 copies

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32
Q

S phase how many copies of chrom

A

2 or 4

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33
Q

G2 phase how many copies of chrom

A

4

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34
Q

if theres enough antigrowth signaling before restrictoin point cell can

A

go into G0

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35
Q

G1→ s phase checkpoint checks for

A

dna damage

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36
Q

restriction point sees if what

A

is envriornment faoriable? is it ok to proceed through cell cycle

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37
Q

DNA damage can activate

A

checkponits at all stages of cell cycle

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38
Q

dna damage activates checkpoints larger through activation of what

A

p53

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39
Q

cyclin-cdk complexes regulate

A

different stages through cell cycle

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40
Q

early G1 what is the first cyclin cdk complex to get activated

A

cyclin D CDK 4

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41
Q

G1 - S phase what cyclin

A

cyclin E CDK 2 complex

42
Q

the cyclin dependent kinases have their name b/c

A

their kinase activity is dependent on the presence of their particular cyclin

43
Q

cyclin CDK 4 is dependent on precense of

A

cyclin D

44
Q

once Cdks are active they will

A

phosphorylate and continue next stage in cell cycle

45
Q

cyclins are called cyclin b/c

A

their expression levels are cyclicle, they are cycling w/ cell cycle

46
Q

cyclin dependent kinases are expressed at what level

A

constantly expressed at same level

but they wont be active until their cyclin expressed

47
Q

anytime cell finishes that cycle the cyclin response for that stage what happens

A

poly-ubiquinated and degraded

48
Q

at the end of m phase there are what regarding cyclins

A

ubiquitin ligase complex that will degrase any remaining cyclins

49
Q

APC/C complex is part of what complex

A

ubiquitin ligase complex responsible of degradation of cyclins

50
Q

draw diff. cycin-CDKs at the different cell cycle they are expressed at

A

pg 18

51
Q

major cyclin complex involved in G1

A

Cyclin D-CDK4
Cyclin D-CDK6
major one is 4

52
Q

once cyclin D-CDK 4

A

phosphorylation of Rb - release E2F which then transcribes cyclin E

53
Q

Cyclin E expression you are past

A

restriction point

54
Q

G1 into S what is the cyclin complex

A

Cyclin E - CDK2 complex

55
Q

CDK2 complex phorphorylates

A

proteins that push it into S phase

56
Q

When cell is in S phase what cyclin complex

A

Cyclin A-CDK2

57
Q

major mitotic cyclin

A

Cyclin B-CDK1

also Cyclin A-CDK1

58
Q

Cyclin B-CDK1 is also called

A

M cyclin-cdk complex or MPF

59
Q

MPF stands for

A

maturation promoting factor

think of it as mitosis promoting factor

60
Q

Draw out external signal to MYC RAS pathway

A

pg 20

RAS - RAF- MEK (look up and draw this out!)

61
Q

what is function of normal Rb

A

inhibits E2F

62
Q

what happens in retinoblastoma

A

No Rb so nothing inhibiting E2F - constantly stimulating proliferation

63
Q

if there’s DNA damage p53 will

A

accumulate

64
Q

p53 is a

A

TF

65
Q

when p53 accumulates it transcribes

A

p21

66
Q

E2F TF transcribes

A

DNA polymerase

Cyclin E

67
Q

what happens in cells to speed up

A

feedback regulation

68
Q

E2F starts to transcribe Cyclin E which activates cdk2, this complex can also phosphorylate

A

any remaining Rb

69
Q

most common primary intraocular malignancy of childhood

A

retinoblastoma

70
Q

metastesis of retinoblastoma usually occur within

A

12 months

71
Q

almost all untreated pts of retinoblastoma die within

A

2 years of disease

72
Q

CDK inhibitors are

A

negative regulators of cell cycle

73
Q

INK4 inhibt

A

kinase 4

74
Q

INKs include

A

p15, p16, p18, p19

75
Q

all the INKs inhibit

A

kinase 4

76
Q

p21

A

can block all the cyclin CDK complexes

77
Q

CIP stands for

A

Cdk inhibitor proteins

78
Q

CIP block

A

all cyclin -cdk complexes

79
Q

p53 can block cell cycle

A

at any stage (via p21)

80
Q

in non-proliferating cell what is Rb doing

A

it is active and bound to E2F, stopping it from continuing which would lead to proliferation

81
Q

in a non-proliferating cell is there is active p16 what does it do

A

it blocks cyclin D CDK4 complex

82
Q

another name for p16

A

CDKN2A

83
Q

TGF beta signaling pathway normally induces transcription of

A

INKs

p15 and p16

84
Q

TFG beta activate

A

SMAD

85
Q

TGF beta blocks

A

cyclin D-CDK4 complex

86
Q

list steps for and draw out for TGF b signalign pathway

A

pg 34

87
Q

TGF beta prevents

A

phosphorylation of pRB and blocks cell cycle progression

88
Q

LFS stands for

A

Li-Fraumeni Syndrome (LFS)

89
Q

Li-Fraumeni Syndrome (LFS)

what is inherited mutation

A

1 mutated p53 allele

90
Q

Li-Fraumeni Syndrome (LFS) have increased risk

A

for developing cancer

91
Q

clinical diagnosis for Li-Fraumeni Syndrome (LFS)

A

sarcoma under age of 45

92
Q

p53 is a

A

tumor suppressor gene

93
Q

what is most frequently mutated gene in human cancer

A

p53

94
Q

what regulates p53

A

lack of nucletodies, UV radation (any DNA damage)
oncogenic signaling
hypoxia
shortening of telomeres

95
Q

by activating p53, what is that saying

A

accumulation of p53

96
Q

p53 is constantly

A

made in cell but then degraded

97
Q

p53 what does it do

A

cell cycle arrest, DNA repair, blocks angiogenesis if high levels then apoptosis

98
Q

p53 first transcriptional target

A

p21

99
Q

very high levels of p53 it will transcribe

A

pro-apoptotic genes to kill cell

100
Q

if there is DNA damage what happens to p53

A

it accumulates due to more phosphorylation which stabilizes the p53

101
Q

p21 can inhibit

A

all the cyclin/CDK complexes

102
Q

in a proliferating cell where will p16 be

A

not active

MCB II Block 1 (12 decks)

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