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MCM Exam 2 > Cell Cycle, Apoptosis, and Cancer > Flashcards

Cell Cycle, Apoptosis, and Cancer Flashcards

1
Q

Stage of cell cycle were chromosome
duplication/segregation (start of cycle) and cytokinesis begins (end)

A

M Phase (M=Mitotic)

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2
Q

Phases of Interphase

A

G1, S, G2

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3
Q

Stage of cell cycle outside of normal dvision

A

G0 Phase

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4
Q

What phase does the RNA and protein synthesis needed for DNA replication occur.

A

Gap 1 phase of Interphase

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5
Q

Phase of cell cycle where DNA stability is analyzed

A

Gap 2 (G2) phase of Interphase

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6
Q

Stage which ensures division is all set to happen (mitochondria are lined up, attached to the mitotic spindle, etc.)

A

M1 (Mitosis)

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7
Q

Descrete timepoint that exists if limiting growth factors occur.

At what time does this happen as well?

A

Restriction point

2hrs before S phase

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8
Q

Prior to going into the S phase, this checkpoint occurs if there is DNA damage.

A

G1 checkpoint (occurs end of G1)

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9
Q

Checkpiont that occurs if DNA replication did not occur ideally.

A

G2 checkpoint (occurs end of G2)

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10
Q

How do mitogens induce moving from G1 into the S phase?

A

Down stream in pathway Rb becomes phosphoralated

Rb normally sequesters E2F.

When phosphoralated it allows E2F to bind to DNA and allows the cell cycle to continue.

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11
Q

How does Rb regulate itself and drive passed the G1 checkpoint?

A

It promotes Cylin A and Cyclin E synthesis which further phosphoralate Rb and allow the cycle to continue.

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12
Q

What are cyclins?

A

Cyclins bind to Cyclin Dependent Kinase to allow them to be active. They rise and fall dependent on stage of cell cycle.

DOES NOT FULLY ACTIVATE

Division increases them

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13
Q

What in addition to cyclins do you need to activate Cyclin dependent kinases?

A

Cyclin-activating kinases (CAK)

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14
Q

What are two examples of CDK1 inhibitors?

A

p27Kip1 or WEE1

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15
Q

How is the T-loop of CDK1 influinced by cyclin and CAK.

A

The t-loop blocks the active site.

Cyclin binds and allows it to move partially.

CAK binds in addition and moves it completely.

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16
Q

What are the three main ways to regulate CDK1 activity?

A

Phosphorylation of CDK

Binding of CKI (p27 or WEE1)

Proteolysis with proteasomes

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17
Q

Where does CAK phosphorylate CDK1

A

On the “cave site”

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18
Q

How does WEE1 inhibit CDK1

A

Through phosphorylateing the “roof site”

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19
Q

What does cdc25 do to CDK1?

A

Dephosphorylates the roof site (if phosphralated by inhibitory enzyme) to activate it.

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20
Q

Does p27 phosphoralate CDK1?

A

No, it binds to CDK1 and cyclin complex preventing them from being active.

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21
Q

When in cell cycle events does p27 inhibit CDK1?

A

Early events.

(G1 to S)

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22
Q

How is mitotic division signaled to anaphase?

What is the key ubiquitin ligase invloved?

A

Cyclin turnover, it is ubiquitinated by anaphase promoting complex (APC/C) also know as cyclosome

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23
Q

What cyclins are targeted by APC/C

A

S and M cyclins (A and B)

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24
Q

What does normal p53 do?

What is it requlated by?

A

Signals for apotosis.

In healthy normal cells it is ubiquinated by MDM2

25
Q

What molecule does p53 increase in transcription rate?

What does this do?

A

p21

p21 binds and inactivates CDK1 causing cell cycle arrest.

26
Q

Type of cell death where ligand binds to receptor.

A

Extrinsic

27
Q

What ligands are used in Extrinsic cell death?

A

Fas and TNF alpha

28
Q

Type of cell death originating from the mitochondria.

A

Intrinsic

29
Q

How are caspases activate?

A

Protease cleavage at certain sites to form a heterodimer with large and small subunits.

30
Q

What are example(s) of intiator caspases?

What are example(s) of executioner caspases?

A

Caspase 8 & 9

Caspase 3,6,7

31
Q

What is a major family of regulatory proteins in apoptosis?

A

The BCL2 family

32
Q

How does BAX (Bcl family) regulate apoptosis

A

In its inactive form it exists on the mitochondirial membrane. Upon activation it aggregates to form a channel that allows cytc to spill out into the cytosol and assist in apoptosis.

33
Q

What spills out from the mitochondria during cell death in addition to cytc?

A

Ca2+

34
Q

How is the Apotosome formed?

A

Through binding of Cytc with Apaf1

35
Q

What does the apotosome (Cytc/Apaf1 complex) activate?

A

Caspase-9

36
Q

What constitutes a Proto-oncogene?

A

Things that regulate cell growth and division:

Growth factors

GF receptors and hormones

Transcription factors

Signal transducers

37
Q

How are oncogenes formed?

A

Gain of function mutations in proto-oncogenes

Too much product

Alternative product (oncoproteins)

38
Q

What is a mutation happens to proto-oncogene HER2 and what kind of Cancer is it commonly found in?

A

HER2 has a tyrosine kinase domain and is active upon binding a ligand. It becomes NEU upon mutation and is activated without a ligand.

Breast cancer

39
Q

What does EGF receptor become as an oncogene?

What disease does this become?

A

EGFRvIII (tyrosine constitutively active)

Glioblastoma

40
Q

What does BCR fuse with as a gain of function mutation due to translocation?

What disease is this related to?

A

ABL

Chronic Mylogenous Leukemia

41
Q

How is Retinoblasoma formed?

A

One mutation exists in the RB1 gene on one allele. Second allele is hit resulting in the disease as RB1 no longer exists.

(Tumors in both eyes may form)

42
Q

Sporadic Retinoblastoma

A

Mutation in 2 RB genes

Super Rare

43
Q

What are the functions of Tumor Supressor genes?

A

Repress cell cycle progression

Promote apoptosis

Couple DNA damage with the cell cycle

44
Q

BRCA is associated with what cancer?

A

Its a tumor supressor associated with breast cancer

45
Q

TP53 or p53 is associated with what cancers?

A

a. 65% of colon cancers
b. 30-50% of breast cancers
c. 50% of lung cancers

46
Q

PTEN- Phosphatase and tensin homolog is associated with what cancer?

A

%70 of prostate cancers

PTEM

47
Q

APC- Adenomatous polyposis coli is associated with what cancers?

A

Colon cancer

48
Q

What are the functions of Metastasis Suppressor proteins?

A

Prevent tumor cells from despersing

Block loss of contact inhibition

Inibit tumor metastasis

49
Q

Describe the development of cancer and the “multi hit hypothesis”

A
  1. Mutation occurs in cell
  2. This cell proliferates.
  3. Multiple mutations in tumor supressor genes
  4. Mutations in metastisis inhibitory proteins / other modifications
  5. Metastisis
50
Q

10 fundamental things of cancer

A
  1. Growth Signals
  2. Evade growth supressors
  3. Metastasis
  4. Immortality (through replication)
  5. Angiogenisis
  6. Resist Death

7. Disregulate cell energetics

  1. Aviod Immune
  2. Inflammation
  3. Genome instability
51
Q

How can HPV cause cancer?

A

Can cause degredation of p53 through E6

Can cause sequesteration of RB through E7

52
Q

Agents that block or supress DNA replication.

A

Alkalating Agents - everything

Anti-metabolites - S phase

Topoisomerase I Inhibitors - S phase

Topoisomerase II Inhibitors - S phase, G2 phase, and M

Citotoxic antibodies - S phase and G2 phase

Mitotoxic inhibitors - M phase

53
Q

Drug used to block HER2 and Neu?

How does it work?

A

Herceptin

Acts as an antibody that blocks cleavage, dimerization, activates antibody dependent cytotoxisity, causes endocytosis.

54
Q

Drug used to block BCR-ABL protein?

A

Gleevic

Competitively binds to where the ATP binds

55
Q

What drug inhibits EGF?

A

Erbitux

56
Q

G1 phase CDK and Cyclins

A

Cylcin D

CDK4

CDK5

57
Q

CDK and Cyclin for G1/S phase

A

Cyclin E

CDK2

(Inhibited by CKI)

58
Q

Cyclin and CDK for S phase

A

Cyclin A

CDK2

Inhibited by CKI

59
Q

Cyclin and CDK for M Phase

A

Cyclin A and Cyclin B

CDK1

MCM Exam 2 (14 decks)

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