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MCM Test 2 self > Cell Cycle, Apoptosis, Cancer > Flashcards

Cell Cycle, Apoptosis, Cancer Flashcards

1
Q

Cell types

A

Permanent - remain in Go, cannot be regenerated
*cardiac muscle, neurons, RBCs
Stable (quiescent) - in Go, but can re-enter cycle at G1 if GFs are present
*hepatocytes, epithelium of kidney -> Regeneration of damaged tissue
Labile - never enter Go, always replicating
*gut epithelium, skin, hair follicles, bone marrow

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2
Q

Which stage is CDK 4 and CDK 6 active and what cyclin binds to it?

A

beginning of Go
Mitogen (growth factor) dependent
Activated by cyclin D

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3
Q

During which phase is CDK2 active and what cyclin binds it?

A

End of G1
Mitogen independent
Bound by cyclin E

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4
Q

During which please is CDK1 and CDK2 active and what cyclin binds it?

A

S phase

bound by cyclin A

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5
Q

During which phase is CDK1 active and which cyclin binds it?

A

G2 phase

Bound by Cyclin B

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6
Q

Pathway to proceed past G1 checkpoint

A 
Mitogen/growth factor present 
RAS pathway 
MAPK -> enter nucleus 
Expression of Myc (gene regulating ptn)
Increased CYCLIN D concentration
Binds CDK 4,6
Phosphorylation of RB -> released EF2 
Cell cycle progression
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7
Q

Apoptosis - Extrinsic pathway

A

Death signal from outside of the cell (tumor necrosis factor, FAS ligand)
Receptor recruits pro-caspases 8 & 10
Pro-caspases are cleaved/activated -> caspases 8 & 10 (“initiators”)
Activate Caspases 3 & 7 (“executioners”)
Apoptosis

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8
Q

How are the extrinsic and intrinsic apoptosis pathways linked?

A

Caspase 8 —>
Activates Death domain protein (BID) —>
Activates BAX and BAK —>
Cause mito to release cytochrome C

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9
Q

Apoptosis intrinsic pathway

A

Intrinsic stimuli (DNA damage, ER stress, hypoxia, metabolic stress)
Activates BAX and BAK
mito —> release cytochrome C —> cytosol
Activates apoptosis peptidase activating factor (Apaf1)
Apoptosome forms
Activates Caspase 9
Activates Caspase 3 & 7 (“executioners”)
Apoptosis

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10
Q

How is RAS related to cancer?

A

RTK -> RAS pathway
RAS mutation (glycine -> valine) —> RAS pathway always ON
* oncogenic
* gain of function mutation

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11
Q

Which pathway mutation results in glioblastomas?

A

Deletion in EDF receptor

  • type of receptor tyrosine kinase (RTK)
  • oncogenic
  • gain of function mutation
  • pathways is ALWAYS ON
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12
Q

Which pathway mutation results in breast cancer (HER2)?

A

HER2 is a RTK
Valine -> glutamate mutation in HER2 (RTK)
Pathway is ALWAYS ON -> breast cancer

  • oncogenic
  • gain of function mutation
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13
Q

How do mutations in tumor suppressors lead to cancer?

A
  • loss of function mutations
  • need two defective copies of the gene (loss of heterozygosity)
  • mutations in proteins that suppress the cell cycle
    - p53
    - p21
    - RB (retinoblastoma) - sequesters EF2
    - BRCA gene
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14
Q

What activates p53?

What inhibits p53?

A

ACTIVATION:
- phosphorylation activates/stabilizes it —> expression of p21

INHIBITION:
Mdm2 (ubiquitin-like protein) -> targets p53 for degradation

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15
Q

What increases cyclin concentrations?

What decreases it?

A

INCREASES
- expression of Myc (transcription factor)

DECREASES
cyclosomes “anaphase-promoting complexes” (APCs)
—> ubiquination -> degradation

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16
Q

What activates Cyclin Dependent Kinases (CDKs)?

What inhibits CDKs?

A

ACTIVATION

  • increased cyclin levels
  • CDK-activating kinases (phosphorylate CDKs)
  • ** need to bind cyclin and P —> fully active
  • Cdc25 phosphatase (can remove extra P)

INHIBITION

  • decreased cyclin levels
  • p21
  • WEE kinase (2P —> inactive)
  • p27 protein (uncompetitive inhibitor - binds after cyclin & P have bound CDK)
17
Q

How does Human Papilloma Virus (HPV) cause cancer?

A

Inserts itself into the genome
Proto-oncogenes -> Oncogenes

E6 binds p53 -> p53 degradation
E7 binds RB -> EF2 is released -> cell cycle progression

18
Q

Gleevec

  • mechanism of action
  • cancer it treats
A

Binds ptn involved in leukemia (Brc/c -Abl enzyme) -> phosphorylates it
Enzyme inactivation
No leukemia

19
Q

Herceptin

  • cancer it treats
  • mechanism of action
A
  • breast cancer, HER2 mutation
  • Herceptin is Ab against HER2 receptor -> inactivates HER2 (RTK)
  • also leads to endocytosis of the receptor -> degradation
20
Q

Erbitux

  • cancer it treats
  • mechanism of action
A

Glioblastomas

Ab against EGF receptor (RTK) ->
Prevents ligand binding

21
Q

How do cytotoxic antibodies treat cancer?

A

Intercalated b/t bases of DNA -> inhibits synthesis

Affects S phase and G2 phase

22
Q

How do antimetabolites prevent cancer?

A

Inhibit enzymes in S phase

Methotrexate
5-fluorouracil

23
Q

Mitotic inhibitors

A

Affect M phase
Arrest cells in metaphase

Docetaxel
Paclitaxel

MCM Test 2 self (11 decks)

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