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Microbio > cell cycle and cancer > Flashcards

cell cycle and cancer Flashcards

1
Q

eukaryotic cell cycle master controllers are a few protein ___ that contain what 2 subunits

A

protein kinases
cyclin, catalytic subunit (cyclin-dependent kinase [CDK])

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2
Q

cell cycle phases

A

G1 (first gap)
S (sythesis)
G2 (second gap)
M (miotic - prophase, metaphase, anaphase, telophase)
Go (resting phase)

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3
Q

what phases count as interphase and how long does it take vs how long does mitosis last

A

G1,S,G2 (16-24 hrs)
mitosis - 1-2 hr

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4
Q

G1
S
G2
M

A

G1 - grow, synthesize RNA and proteins for DNA synthesis
S - chromosome replication
G2 - rapid growth and protein synthesis
M - cell division

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5
Q

-Initiates mitosis
-Gradual condensation of chromosomes
-Disintegration and eventual disappearance of the nucleolus
-Beginning of formation of miotic spindle
-Centrosomes (pair of microtubule organizing centers) from which microtubules radiate
-Centrosomes gradually move to take up positions at poles of cell
-Separation of centrosomes

A

Prophase

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6
Q

-Enters when nuclear membrane breaks up
-Chromosomes disperse within the cell and attach via kinetochores, to microtubules of the mitotic spindle
-Chromosomes begin to move toward a point midway between the spindle poles
-Chromosomes continue to condense throughout this stage
-Microtubules attach to chromosomes
-Chromosome forms 2 kinetochores at centrosome

A

Pro-metaphase

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7
Q

-Chromosome algin in the metaphase plate
-Chromosome reach maximal condensation
-Chromosomes become arranged at the equatorial plane of the cell
-Chromosome of a divind human cell is most readily analyzed at the metaphase stage of mitosis

A

Metaphase

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8
Q

-Chromatids separate words opposite poles
-Begins abruptly when the chromosomes separate at the centromere
-Sister chromatids of each chromosome now become independent daughter chromosomes, which move to opposite poles of the cell

A

Anaphase

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9
Q

-New nuclear envelop forms
-Chromosomes unfold back into chromatin
-Nucleoli reappearance
-Cell continues to elongate
-Chromosomes begin to decondense from their highly contracted state
-Nuclear membrane begins to reform around each of the 2 daughter nuclei and each nucleus gradually resumes its interphase appearance

A

Telophase

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10
Q

cytokinesis

A

separation of the 2 daughter cells

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11
Q

cell cycle checkpoint in mitosis

A

anaphase is blocked if chromatids are not properly assembled on mitotic spindle

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12
Q

R point

A

decide to continue or go G0

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13
Q

B-CDK1 what phase

A

M phase

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14
Q

D-CDK4/6 what phase

A

G1 phase

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15
Q

E-CDK2 what phase

A

G1 and S phase

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16
Q

A-CDK2 what phase

A

S phase

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17
Q

A-CDK1 what phase

A

S and G2 phase

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18
Q

CDK inhibitors suppress the formation of what

A

tumors (are tumor suppressor proteins)

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19
Q

INK4 proteins (inhibitors of CDk4) affect what

A

CDK4/6

20
Q

cip/kip proteins affect what

A

CDK1/2

21
Q

members of INK4 proteins

A

p16INK4A, p15INK4B, p18INK4C, p19INK4D

22
Q

members of cip/kip proteins

A

p21CIP1 (or p21Waf1), p27Kip1, p57Kip2

23
Q

mitogens do what to inhibitors

A

proliferative (inhibits the inhibtors) (favor cell cycle advance)

24
Q

antiproliferative do what to inhibitors

A

activate inhibitors (block cell cycle)

25
Q

Rb protein initially inhibits what

A

E2F acitvity

26
Q

stimulation of G0 cells with mitogens induces expression of what

A

CDK4, CDK6, D-type cyclins, E2F transcription factor

27
Q

in the presence of mitogens, what does cyclin D-CDK4/6 do

A

phosphorylates Rb protein

28
Q

E2F does what

A

stimulates gene transcription

29
Q

phosphorylated or unphosphorylated Rb is inhibiting E2F

A

phosphorylated Rb is not inhibiting E2F

30
Q

Rb is a what type of protein

A

tumor supressing protein

31
Q

important hallmark of cancer

A

evading growth supressors

32
Q

what is mutated in several cancers

A

p53

33
Q

what are the two prototypical tumor suppressor genes

A

p53 and Rb

34
Q

p21Cip1 is activated by what

A

p53

35
Q

what is p53 trying to do, and so what happens if its mutated

A

halt cell cycle if theres damage
if its mutated, proliferation keeps going w the damage

36
Q

ATM and ATR are what and do what

A

protein kinases
sense DNA damage and trigger cell cycle arrest

37
Q

how can cancer cells spread

A

through blood and lymphatic systems

38
Q

what causes sustaining proliferative signaling

A

growth factors
autocrine proliferative stimulation

39
Q

Rb

A

tumor supressor protein

40
Q

p53

A

tumor supressor protein

41
Q

TGF-B

A

antiproliferative protein

42
Q

NF2/Merlin

A

tumor suppressor protein, orchestrates contact inhibition

43
Q

loss of normal p53 important why

A

p53 is a critical damage sensor (usually apoptosis would occur)

44
Q

extrinsic apoptosis pathway

A

bind to cell surface receptors-death receptors (DRs)

45
Q

intrinsic apoptosis pathway

A

involves damage to nuclear DNA as well as mitochondria
triggered by agents such as ROS

46
Q

necrosis

A

release proinflammatory signals into the surrounding tissue environment, and immune inflammatory cells can be tumor promoting due to fostering angiogenesis, cancer cell proliferation and invasiveness

47
Q

necrotic cells can release

A

Microbio (12 decks)

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