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MCM Final > Cell Cycle, Apoptosis, Cancer > Flashcards

Cell Cycle, Apoptosis, Cancer Flashcards

1
Q

What is the purpose of the G1 phase of the cell cycle?

A

RNA and protein synthesis needed for DNA replication

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2
Q

What is the purpose of S phase of the cell cycle?

A

DNA synthesis occurs

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3
Q

What is the purpose of G2 phase of the cell cycle?

A

DNA stability is checked

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4
Q

In what phase of the cell cycle might the cells withdraw due to poor nutrients/environmental conditions?

A

G0 phase

[this also occurs following terminal differentiation in tissues like neurons, cardiac muscle, RBCs]

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5
Q

What are the 3 checkpoints of the cell cycle?

A

G1 CP = towards end of G1, occurs in response to DNA damage

G2 CP = towards the end of G2, verifies complete genomic duplication

Metaphase CP = ensures chromosomes attached to mitotic spindle

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6
Q

What is the restriction point of the cell cycle?

A

Occurs 2 hrs prior to S phase

If growth factors are limiting, restriction will occur

Once through the (R) point, progression of the cell cycle is growth factor-independent

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7
Q

What are some of the growth factors that affect the cell cycle prior to the restriction point?

A 
EGF
FGF
GMCSF
HGH
IL-1
PDGF
TGF-B
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8
Q

_____ is a TF that drives cell proliferation by increasing G1-CDK levels

These CDKs phosphorylate _______, which releases sequestered _____ - the TF that drives cells from G1 to S phase

A

Myc

Rb; E2F

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9
Q

What effect does hypophosphorylated Rb have on the cell cycle?

A

Hypophosphorylated Rb is active, and blocks the G1 to S transition by remaining bound to E2F

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10
Q

What effect does hyperphosphorylated Rb have on the cell cycle?

A

Rb is inactive and allows the G1/S transition by releasing E2F

Involves Cyclin D-CDK4 and Cyclin CDK6

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11
Q

When E2F is released from Rb, transcription of what 2 genes can occur?

A

Cyclin E, so that cell can transition from G1 to S

Cyclin A, so that S phase can occur

(Cyclin E-CDK2 and Cyclin A-CDK2 keep Rb in a hyperphosphorylated state)

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12
Q

________ are proteins that interact with and regulate CDK activity. They are required for CDKs to be active, and their expression rises and falls during the cell cycle

A

Cyclins

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13
Q

Binding of cyclin to CDK causes partial activation. What is needed for full activation?

A

CDK-activating kinase (CAK)

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14
Q

What are the 2 primary inhibitors of CDK?

A

p27 = CKI that binds both Cdk and Cyclin (primarily regulates early in cell cycle)

Wee1 kinase = phosphorylates roof site

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15
Q

Wee1 kinase adds a phosphate to the roof site of the Cdk-cyclin complex. What enzyme is capable of removing that phosphate and reversing the inhibition?

A

CDC25 phosphatase

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16
Q

Which cyclin-Cdks are active during G1 phase?

A

Cyclin D-CDK4
Cyclin D-CDK6

Helps passage of cells through restriction point in late G1 phase

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17
Q

Which cyclin-CDKs are active during the G1/S transition?

A

Cyclin E-CDK2

Helps the cells at the end of G1 to commit to DNA replication and enter S phase

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18
Q

Which cyclin-CDKs are active during S phase?

A

Cyclin A-CDK2

Necessary for initiation of DNA synthesis

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19
Q

Which cyclin-CDKs are active during M phase?

A

Cyclin A-CDK1
Cyclin B-CDK1

Necessary for nuclear division during mitosis

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20
Q

Cyclin turnover is responsible for the progression from metaphase to anaphase.

The key regulator of this process is _______, aka cyclosome.

A

APC/C - member of the ubiquitin ligase family

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21
Q

Ubiquitin exists in all eukaryotic cells, attaches to _____ residues on target proteins, and is a signal dependent destruction signal

A

Lysine

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22
Q

What 2 cyclins must be downregulated in order to move into anaphase of the cell cycle?

A

S-Cyclin and M-Cyclin

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23
Q

What are the steps that need to be taken in order for S- and M-cyclins to be downregulated to move into anaphase of the cell cycle?

A

APC/C activation by Cdc20 –> APC/C ubiquitinates S and M-cyclins so that they are targeted for destruction by proteosome

Absence of cyclins inactivates Cdks

24
Q

______ is a transcription factor that is normally degraded by the proteosome in quiescent cells and is considered to be “guardian of the genome”

A

p53

25
Q

What effect does DNA damage have on p53 activity?

A

Increases protein kinase activity –> p53 is stabilized and activated by phosphorylation leading to increased transcription of p21 CKI –> cell cycle arrest

26
Q

How does p21 cause cell cycle arrest?

A

Binds and inactivates cyclin-CDK complexes for G1/S and S, keeping Rb hypophosphorylated (active) which sequesters E2F

27
Q

p21 is a CKI that is primarily associated with the inhibition of _______

A

CDK2

[although it is capable of inhibiting all cyclin/CDK complexes]

28
Q

What are the 2 potential pathways for apoptosis?

A

Extrinsic = death receptor pathway

Intrinsice = mitochondrial pathway

29
Q

What are some triggers for the intrinsic pathway of apoptosis?

A 
Abnormalities in DNA
DNA damage
Lack of O2
Lack of nutrients
Lack of EC survival signals
30
Q

What are some signals that may trigger the extrinsic apoptosis pathway?

A

Removal of survival factors

Proteins of TNF family

31
Q

Caspases are first synthesized as inactive precursors called _________, which are activated by ________ cleavage at specific sites. Caspases then form a ___________ made up of a large and small subunit

A

Procaspases
Protease
heterodimer

32
Q

Which caspases are the “initiators”

A

Caspase 8

Caspase 9

33
Q

What caspase is the “executioner”

A

Caspase 3

34
Q

What is the primary difference between the apoptotic regulators Bcl-2 and BAX?

A

Bcl-2 is anti-apoptotic

BAX is pro-apoptotic

35
Q

In the intrinsic pathway of apoptosis, ______ aggregates in the outer mt membrane, which causes release of Ca++ from the SR, allowing the release of __________ as well as other intermembrane space proteins into the cytosol

A

BAX

Cyt C

36
Q

After Cyt C is released from the intermembrane space, it activates _______ which assembles into the ________ and recruits procaspase 9–> caspase 9, which activates caspase ____

A

Apaf1
Apoptosome
3

37
Q

The transition of a proto-oncogene to an oncogene is considered what type of mutation?

A

Gain of function

[point mutation, deletion, gene amplification, chromosomal translocation]

38
Q

What is a common oncogene in breast cancer?

A

HER2 receptor undergoes Val–>Gln mutation causing receptor dimerization and tyrosine kinase activity can be activated in the absence of ligand

39
Q

What is a common oncogene associated with Glioblastoma?

A

EGF receptor undergoes deletion mutation, causing its receptor tyrosine kinase activity to be constitutively active

40
Q

What common oncogene is associated with Chronic myelogenous leukemia (CML)?

A

BCR-Abl translocation

41
Q

What are the 2 forms of Retinoblastoma, and which one is associated with a loss of heterozygosity?

A

Hereditary (born with 1 good Rb1)
Sporadic (born with 2 good Rb1 copies)

Hereditary form is associated with loss of heterozygosity

42
Q

Which form of Retinoblastoma is associated with the 2-hit hypothesis?

A

Sporadic - since born with 2 good copies of the gene, one must be mutated, then second “hit” for cancer to develop

43
Q

What type of mutations are associated with tumor suppressor genes causing cancer?

A

Loss of function

44
Q

What are some tumor suppressor genes and what cancers are they associated with?

A 
p53 - many cancers
Rb - retinoblastoma
APC - colon cancer
DCC - colon cancer
BRCA1/2 - breast cancer
NF-1 - neurofibromatosis
45
Q

Along with oncogenes and tumor suppressor genes, what is one other type of gene associated with cancer risk?

A

Metastasis suppressor genes, which code for cell-adhesion proteins that prevent tumor cells from dispersing, block loss of contact inhibition, and inhibit tumor metastasis

46
Q

Describe the process of viral oncogenesis

A
  1. Nontransforming virus infects host
  2. Viral genome integrates into host genome adjacent to protooncogene
  3. Virus replicates
  4. Protooncogene mutates into oncogene
  5. Virus containing oncogene infects normal cell, turning it into a tumor cell
47
Q

What are 3 DNA viruses associated with oncogenesis?

A

EBV –> Burkitt Lymphoma

Hep B –> liver cancer

HPV –> cervical and uterine cancer

48
Q

What are 2 RNA viruses associated with oncogenesis?

A

HTLV-1 —> Leukemia

HSV –> Kaposi Sarcoma (common in HIV patients)

49
Q

What is the mechanism of action of the following chemotherapeutic agent:

Alkylating agents

A

Block DNA replication

50
Q

What is the mechanism of action of the following chemotherapeutic agent:

Antimetabolites

A

Inhibit enzymes involved in DNA synthesis

51
Q

What is the mechanism of action of the following chemotherapeutic agent:

Topoisomerase I inhibitors

A

Inhibit topoisomerase I, an enzyme that removes supercoils in DNA

52
Q

What is the mechanism of action of the following chemotherapeutic agent:

Topoisomerase II

A

Inhibits topoisomerase II, an enzymes that resolves tangles in DNA

53
Q

What is the mechanism of action of the following chemotherapeutic agent:

Cytotoxic Antibiotics

A

Intercalate between bases in DNA to inhibit DNA synthesis

54
Q

What is the mechanism of action of the following chemotherapeutic agent:

Mitotic inhibitors

A

Arrest cells in mitosis during metaphase

55
Q

Herceptin is a treatment for breast cancer that targets what?

A

HER2 receptor (or NEU which is mutated version of HER2)

56
Q

Gleevec is a treatment for CML that targets what?

A

Bcr-Abl protein

Binds Bcr-Abl in ATP-binding site, preventing its activation

57
Q

What is the mechanism of Cetuximab (Erbitux) in treating Glioblastoma?

A

Blocks EGF ligand from binding EGF receptor, which would otherwise be necessary for tyrosine kinase activity and cell proliferation

MCM Final (14 decks)

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