Cell Cycle, Apoptosis, and Cancer Flashcards

1
Q

What are the stages of the cell cycle?

A

G1/G0->S->G2->M

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2
Q

What is done during G1/G0?

A

G1: RNA and protein synthesis/ cell growth
G0: Cells withdrawn from cell cycle, defective cells

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3
Q

What happens during S phase?

A

DNA is synthesized and replicated to form homologs (2 chromosomes)

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4
Q

What happens during M phase?

A

Mitosis occurs: (prophase, metaphas, anaphase, telophase) nuclear division at the beginning and cell division (cytokinesis) at the end

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5
Q

What occurs during G2?

A

DNA stability is checked

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6
Q

What is interphase?

A

G1, S, and G2

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7
Q

What are restiction points and checkpoints and where are they located for the cell cycle?

A

They are a discrete timepoint where ‘errors’ are checked.
Restriction: before S phase
Checkp: After restriction before S, end of G2, beginning of Metaphase

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8
Q

What is the main job of restriction point before S?

A

If growth factors of cell are limited, restriction occurs and removed cell from cycle

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9
Q

What occurs at G1 checkpoint before S?

A

If there is DNA damage, pulls cell from cycle and trys to fix or goes to trash

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10
Q

What occurs at G2 checkpoint before M?

A

G2 verifies complete genomic duplication, if errors cell is pulled from cycle

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11
Q

What occurs at metaphase checkpoint during M?

A

This checkpoint ensures chromosomes are attached to the mitotic spindle

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12
Q

What does cyclin (protein) and cyclin dependent kinases do in cell proliferation?

A

Activated by many things, they phosphorylate retinoblastoma (Rb) which releases E2F, which is needed to enter S phase from G1.

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13
Q

What are cyclin E and A needed for?

A

E: so that cell cycle can transition from G1 to S phase
A: so that S phase can occur

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14
Q

Why is cyclin important to CDKs and what are their main role?

A

CDK without cyclin are inactive, with cyclin binded, CDKinase is activated to phosporylate substrates so cell cycle can continue/not

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15
Q

What is required for full activation of cyclin/CDK?

A

CDK-activating kinase (CAK!) (phosphorylates)

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16
Q

How is cyclin/cdk inhibited?

A

p27 and WEE1 inhibit, or cyclin cut off by proteasomes

17
Q

Where can Cyclin D-CDK4 and cyclin D- CDK6 be found?

A

They are found in G1 and help pass cells through the restiction point

18
Q

How does p27 inhibit cyclin/cdk

A

Binds to both and inactivates

19
Q

How does WEE1 inhibit cyclin/cdk?

A

WEE1 inhibits by adding another phosphate to the (roof site) and inactives cdk.

20
Q

how is WEE1 phosphorylation reversed?

A

CDC25 phosphotase

21
Q

How is Cyclin S and M activity downregulated to move into anaphase?

A

APC (anaphase promoting complex, cyclosome), member of ubiquitin fam, is activated, ubiquinating S and M, which signals for destruction by proteosomes, CDK inactivated, moves cells to anaphase

22
Q

What is p53, what activates it, and what does it activate?

A

p53 is the guardian of the genome, a trasncription factor.

It is activated by protein kinases (which is activated by DNA damage), and is regulated by MDM2

It activates transcription gene of p21

23
Q

How is p21 important to the cell cycle?

A

binds to cyclin cdk to inactivate, inactivating G1 and S phase, keeping Rb active, and E2F sequestered to it

24
Q

What is the extrinsic pathway for apoptosis?

A

Ligand binds to death receptor (FAS or TNFalpha), activates procaspase8 to active caspase-8, activates Caspases 3,6&7, APOPtosis

25
Q

What is the intrinsic pathway for apoptosis?

A

DNA damage activates p53 & BAX/BAK, BAX makes ports which causes mito cyto C to leak out and bind APAF-1, forming Apoptosome, which activates caspase 9, activating caspases 3,6,7 and apoptosis

26
Q

What is BCL2 and BAX? What happens if cancer gets a hold of these?

A

BCL2 inhibits apoptosis, BAX activates apoptosis. If cancer is active, will upregulated BCL2 and downregulate BAX so cancer cells survive!

27
Q

What is a oncogene?

A

a gene that normally promotes cell cycle

28
Q

What is a tumor suppressor gene and what does it do?

A

a gene that inhibits cell cycle, promotes apoptosis, couple DNA damage to cell cycle

29
Q

what happens if a protooncogene is mutated by point mutation, deletion or translocation?

A

Known as “Gain of function” become oncogene which increases expression

30
Q

What is an example of an oncogene, and its mutation?

A

HER2 receptor, a point mutation changes valine to glutamine= NEU. which allows kinase to remain active even when to ligand. results in breast cancer (Ras)

31
Q

Example of a tumor suppressor gene, and mutation?

A

Rb, because binds E2F to stop cell division. can cause cararacts when mutated and gets ‘second hit’

32
Q

What do metastasis supressors do, example?

A

Cell adhesion proteins

  1. prevent tumor cells from dispersing
  2. block loss of contact inhibition
  3. inhibit tumor metastasis
33
Q

What are the steps/mutations that lead to metastasized cancer?

A

Loss of APC, Mutation in Ras to always be on (oncogene), loss of tumor suppressor, loss of p53 activity, metastasis :(

34
Q

What are the 6 hallmarks of cancer?

A
  1. Ability to grow alone (HER2)
  2. Tumor suppressor failure
  3. Invading and metastasis
  4. Telomerase up activation
  5. Angiogenesis
  6. Resisting cell death from apoptosis (mutated BAX)
35
Q

Describe viral oncogene to transformed cell

A

Protooncogene, infected by virus, attacks and hijacks cell, Virus replicates and protooncogene turns into oncogene. infects normal cell, turning to tumor cell

36
Q

HPV mechanics?

A

E6 binds p53(loss of t sup.) , E7 binds Rb (releases E2F), activates cell cylce/proliferation

37
Q

What do alkylating agents do compared to antimetabolites?

A

Alkylating block DNA replication

Antimetabolites inhibits S phase

38
Q

What do cytotoxic antibiotics do compared to mitotic inhibitors?

A

Cytotoxic intercalate between DNA bases to inhibit S/G2 phase
Mitotic arrest cells in mitosis during metaphase

39
Q

What do Topo I inhibitors do compared to Topo II?

A

Topo I inhibitors result in tangled DNA=S phase

Topo II inhibitors result in tangled DNA in G2 phase