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MCM Exam 2 > (7) Cell Cycle, Apoptosis and Cancer > Flashcards

(7) Cell Cycle, Apoptosis and Cancer Flashcards

1
Q

Broad overview of the cell cycle?

A
  1. Cell growth and chromosome replication
  2. Chromosome segregation
  3. Cell division
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2
Q

What are the stages of the cell cycle?

A
  1. The S Phase (Synthesis)

2. The M Phase (Mitosis)

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3
Q

Insert stages of the cell cycle here!!!

A

Slide 7

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4
Q

The Stages of the cell cycle:

What occurs in MITOSIS (M):

A
  • Nuclear division (mitosis) at the beginning

- Cell division (cytokinesis) at the end

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5
Q

The Stages of the cell cycle:

What occurs in interphase?

A

(G1): Gap 1 phase; RNA and protein synthesis needed for DNA replication

(S): DNA synthesis

(G2): Gap 2 phase- DNA stability is checked

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6
Q

The Stages of the cell cycle:

What occurs during Go phase?

A

Occurs during POOR NUTRIENT/enviornmental conditions

–> Cells withdraw from cell cycle

*Also occurs following terminal differentiation in certain tissue types

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7
Q

The Stages of the cell cycle:

What are restriction points/checkpoints for?

A

A discrete timepoint where “errors” are checked

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8
Q

The Stages of the cell cycle:

___ Restriction point
___ Checkpoints

A

one restriction point; 3 checkpoints

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9
Q

The Stages of the cell cycle:

What happens if growth factors are limiting?

A

Growth factors are limiting

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10
Q

The Stages of the cell cycle:

Progression following exit from restriction point (R) is growth factor _________

A

independent

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11
Q

The Stages of the cell cycle:

G1 checkpoint

Occurs in response to:

A

DNA Damage

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12
Q

The Stages of the cell cycle:

G2 checkpoint

Purpose?

A

Verify complete genomic duplication

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13
Q

The Stages of the cell cycle:

Metaphase checkpoint

Purpose?

A

Ensures chromosomes attached to mitotic spindle

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14
Q

Cell cycle is activated by ______

A

growth factors

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15
Q

Retinoblastoma (Rb) and Cyclin activity: Describe

A

Rb and E2F are associated with each other. Cyclin D-CDK4 and Cyclin D-CDK6 can hyperphosphorylate RB to dissociate it from E2F…

Then, E2F can actively transcribe

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16
Q

____________ drives cells from G1 to S phase of the cell cycle

A

Rb Phosphorylation

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17
Q

Once E2F is actively transcribing, what does it produce?

A

Cyclin E: cell cycle goes from G1 to S phase

Cyclin A: S phase can occur

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18
Q

Retinoblastoma protein is known as a __________ protein

A

tumor suppressor

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19
Q

What are activators of cyclin-CDK activity?

A

-Binding of cyclin to CDK causes only PARTIAL activation

***FULL activation=CDK activating kinase (CAK)

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20
Q

What are inhibitors of Cyclin-CDK activity?

A
  • p27

- WEE1

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21
Q

Cdk-activating kinase (CAK) and the T-Loop

What’s its role?

A

T-loop is a region of CDK that blocks active site

  • T-loop moves out of active site after cyclin binding
  • CAK phosphorylates T-loop which FULLY activates enzyme
22
Q

What specific cyclins help the passage of cells through the restriction point in late G1 phase?

A

Cyclin D-CDK4

CyclinD-CDK6

23
Q

What are the methods to regulate Cyclin-Cdk activities?

A
  1. Phosphorylation of CDK
  2. Binding of CKI (p27/WEE1)
  3. Proteolysis of cyclins
24
Q

What can make a Cyclin-CDK complex fully active after being hyperphosphorylated?

A

CDC25 phosphatase

25
Q

p53 is the…

A

“Guardian of the genome”

-A transcription factor

26
Q

p53

In the absence of DNA damage…

A

MDM2 degrades p53

27
Q

p53

In the presence of DNA damage…

A

Activates protein kinases that phosphorylate p53 (*ACTIVATES)

  • Increased transcription of p21
  • CKI
28
Q

Extrinsic pathway:

What is the caspase associated?

A

Procaspase 8 –> Caspase 8

29
Q

Extrinsic pathway:

AKA?

A

Death receptor pathway;

triggered by binding of external death ligand

30
Q

Extrinsic pathway:

What are examples of external death ligands?

A

Fas ligand, TNFalpha (tumor necrosis factor)

31
Q

Extrinsic pathway:

What happens after caspase 8 becomes active?

A

Activates caspases -3, -6, -8

32
Q

Intrinsic pathway:

AKA?

A

Mitochondrial pathway

33
Q

Intrinsic pathway:

What causes it?

A

Triggered by:

Growth factor withdrawal, DNA damage, cell cycle defects

34
Q

Intrinsic pathway:

How does it happen?

A

Cytochrome C released by stressed mitochondria, binds to n

35
Q

Intrinsic pathway:

How does it happen?

A

Cytochrome C released by stressed mitochondria

Binds to an adaptor protein (APAF-1)

Leads to Apoptosome

Recruits Caspase 9

36
Q

Intrinsic pathway:

What can facilitate?

A

*Proapoptotic

BAX

BAK

p53

37
Q

Intrinsic pathway:

What can inhibit?

A

*Antiapoptotic

BCL-2

BCL-xl

38
Q

How can a proto-oncogene be converted to oncogenes?

A

3 mechanisms

  1. Point mutation/deletion
  2. Gene amplification
  3. Chromosomal translocation
39
Q

What is an example of a common oncogene?

A

HER2 Receptor

OVEREXPRESSED HER2, observed in many breast cancers

40
Q

What is the major example of a tumor suppressor with a clinical correlation in the lecture?

A

Retinoblastoma (Rb)

41
Q

What is the difference b/w sporadic retinoblastoma and hereditary?

A

Sporadic= RARE, 2 independent mutations of Rb

Hereditary= Mutation/deletion of one copy of RB1, predisposed to be cancerous

42
Q

What are the functions of tumor suppressors?

A
  • Repress cell cycle progression
  • Promote apoptosis
  • DNA repair proteins (BRCA)
43
Q

Name some other tumor suppressors:

A
  1. RB1 –> Rb
  2. TP53–> p53
  3. PTEN; Phosphatase and tensin homolog
  4. APC; adenomatous polyposis coli
44
Q

What is the function of metastasis suppressors?

A

*Cell adhesion proteins

  • Prevent tumor cells from dispersing
  • Block loss of contact inhibition
  • Inhibit tumor metastasis
45
Q

T/F

You can get cancer from a single hit of a tumor suppressor gene

A

FALSE!

You need multiple pathways to fail in order to cause cancer

46
Q

HPV:

E6 binds to

A

p53

47
Q

HPV:

p53 binds to

A

E6

48
Q

HPV:

E7 binds to

A

Rb

49
Q

HPV

Rb binds to

A

E7

50
Q

What does GLEEVEC do?

A
  • Competitive inhibitor of Bcr/c-Abl enzyme which is derived from the philadelphia chromosome 22/9 translocation, which stops the cell cycle
  • Anti-cancer
51
Q

What is the mechanism of Erbitux?

A

EGF INHIBITOR

MCM Exam 2 (13 decks)

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