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SFM Quiz 2 (mine) > (L14) Cell Cycle, Cancer, and Cell Death > Flashcards

(L14) Cell Cycle, Cancer, and Cell Death Flashcards

1
Q

What are the molecular regulators of the cell cycle? L14 S15

A

Cyclins:

-levels increase or decrease during certain times of cell cycle indicating the current phase

Cyclin dependent kinase (CDK):

  • kinases that are active when bound to their specific cyclin
  • kinase activity regulates relevant enzymes for the current phase of cell cycle

Cyclin dependent kinase inhibitor (CKI):

-inhibit CDKs

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2
Q

How are CDKs regulated?

L14 S18

A

Requires cyclin binding

Three phosphorylation sites:

  • 1 activating (T-loop)
  • 2 inactivating
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3
Q

What are the main cyclins?

L14 S17

A
  • A
  • B
  • D
  • E
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4
Q

What are the major inhibitory regulators of the cell cycle?

L14 S22

A

p21:

-adds inhibitory phosphate to CDKs

p27

p16/INK4

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5
Q

What events trigger entry into cell cycle?

What is the transcripition factor for this and what does it stiumulate?

L14 S23

A

Mitogen binds receptor which activates Ras by replacing GDP with GTP.

Ras-GTP activates RAF, RAF phosphorylates MEK, MEK phosphorylates MAP, and MAP phosphorylates Myc.

Myc is a transcription factor that:

  • stimulate cyclin D transcription
  • stimulates p27 degradation
  • stimulates E2F transcription
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6
Q

What is the R point in the cell cycle?

L14 S25

A

Restriction point or G1 checkpoint

It occurs during late G1 and after the cell proceeds through, it is commited to dividing.

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7
Q

What cyclin/CDK complex allows for progression through the R point?

What is the mechanism?

L14 S17;25

A

Cylcin D-CDK4/6

Hypophosphorylates Rb (retinoblastoma protien) which inhibits E2F

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8
Q

What cyclin/CDK complex allows for progression through the G1 ► S checkpoint?

What is the mechanism?

L14 S17;24

A

Cylcin E-CDK2

Hyperphosphorylates pRb causing it to release E2F. E2F causes transcription of more cylin E and E2F, amplifying the process.

Initiates assembly of pre-replicaiton complex.

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9
Q

What cyclin/CDK complex allows progression through S phase?

What is the mechanism?

L14 S17;27

A

Cyclin A-CDK2

Stabilizes replicaiton complex.

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10
Q

What cyclin/CDK complex allows progression from S ► G2?

What does this compelx do?

L14 S17;25

A

Cyclin A-CDK1

Stimulates production of cyclin B.

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11
Q

What cyclin/CDK complex allows progression from G2 ► M?

What is the mechanism?

L14 S17;28

A

Cyclin B-CDK1

Activates CDC25 phosphorylase which activates more CDK1.

Initiates mitotic spindle assembly.

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12
Q

What is the function of CDC25?

L14 S19;28;30

A

Phosphorylase that removes inhibiting phosphates from CDKs.

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13
Q

What are ATM and ATR?

What pathways do they activate?

L14 S29-30;32

A

Both are kinases that are activated when DNA damge is detected.

p53 pathway:

  • ATM/ATR phosphorylates Mdm2 causing it to release p53
  • p53 activates p21
  • p21 places inhibitory phosphate on CDKs

Chk pathway:

  • ATM/ATR phosphorylate Chk, activating it
  • Chk phosphorylates CDC25, inactivating it
  • without CDC25, inhibitory phosphates are not removed from CDK
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14
Q

Differentiate between the terms tumor, neoplasm, and cancer.

L14 S35

A

Tumor:

-space occupying lesion

Neoplasm:

-abnormal growth caused by abnormal gene regulation

Cancer:

-malignant neoplasm

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15
Q

What are the stages of carcinogenesis?

L14 S38-42

A

Initiation:

  • irreverisble change in DNA sequence
  • activation of oncogene or inactivation of tumor supressor gene

Promotion:

  • reversible gene activtion or repression
  • cellular selection leads to clonal expansion
  • once threshold is reached, cancer occurs

Progression:

  • it is now cancer
  • continued evolution of cancer for optimal growth
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16
Q

What are oncogenes and what are the 3 types?

L14 S44-46

A

Genes that stimulate cell division and growth

Only needs one copy with enhanced expression (dominant)

Types:

  • cellular proto-oncogenes activated by mutation
  • viral genes that behave like proto-oncogenes
  • viral captured cellular proto-oncogenes
17
Q

What are the types of viral oncogens?

L14 S47

A

Type 1, transducing viruses:

-cellular oncogene carried by retrovirus

Type 2, non-transducing viruses:

-cellular oncogene that is activated by viral insertion

Type 3, non-transducing long latency virus:

-viral protein disrupts normal cell cycle regulation

Type 4:

-viral envolope creates inappropriate signaling

18
Q

What are the main oncogenes?

L14 S51

A
  • growth factors
  • growth factor receptors
  • signal transduction molecule (ras, raf, src)
  • transcription factors (myc)
  • cyclins
  • anti-apoptotic factors
19
Q

What are tumor supressor genes?

L14 S52

A

Genes that repress cell division and growth

Requires both copies to be inactivated; one copy can be inherited as inactivated

20
Q

What are the main tumor supressor genes?

L14 S53

A
  • p53
  • p14
  • p16/INK4A
  • Rb
21
Q

What are the methods of treating cancer?

L14 S59-61

A

Surgery

Radiation (degrades DNA by directly breaking bond or indirectly by creating ROS from water which then break DNA bonds)

Chemotherapy (alkylating agents, intercalating agents, antimetabolites, mitostatic agents, platinum derivatives)

Immunotherapy

22
Q

What are the types of cell death?

L14 S65

A

Apoptosis

Autophagy

Necrosis

Mitotic catastrophe

Senescence

23
Q

What are the morphologic characteristics, cells involved, inflammatory state, and biochemical features of necrosis?

L14 S67-68

A

Morphology:

  • cell membrane: swollen and ruptured
  • cytoplasm: vacuolation and organelle degradation
  • nucleus: karyolysis

Cells: can occur in all cells

Inflamation: Yes

Biochemical features:

-failure of homeostatic mechanisms such as ATP producting, ion transport, or pH balance

24
Q

What are the morphologic characteristics, cells involved, inflammatory state, and biochemical features of apoptosis?

L14 S71-72

A

Morphology:

  • membrane: blebing
  • cytoplasm: fragmentation and shrinkage
  • nucleus: condensation of chromosomes

Cells: mainly hematopoietic cells and liquid tumors

Inflammation: no

Biochemical features:

-loss of membrane asymmetry (externalized phosphatidylserine)

-mitochondrial caspases (caspases 8, 9, and 3)

25
Q

What are the morphologic characteristics, cells involved, inflammatory state, and biochemical features of autophagy?

L14 S78

A

Morphology:

  • membrane: blebing
  • cytoplasm: autophagic vacuoles
  • nucleus: partial condensation

Cells: all

Inflammation: no

Biochemical features:

  • increased lysosomal activity
  • caspase-independent
26
Q

What are the morphologic characteristics, cells involved, inflammatory state, and biochemical features of mitotic catastrophe?

L14 S81-82

A

Morphology:

  • cell membrane: no changes
  • cytoplasm: enlarged (giant cell formation)
  • nucleus: fragmentaiton

Cells: most dividing cells

Inflammation: no

Biochemical features:

-abnormal mitosis leading to delayed cell death

27
Q

What are the morphologic characteristics, cells involved, inflammatory state, and biochemical features of senesence?

L14 S85-86

A

Morphology:

  • membrane: no change
  • cytoplasm: flattening and granulation
  • nucleus: heterochromatic

Cell: all

Inflammation: yes

Biochemical features:

-activation of p53 or p16 pathways that lead to permanent senescence through p21 or Rb respectively

SFM Quiz 2 (mine) (25 decks)

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