Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MCM Exam 2 > Cell Cycle, Apoptosis, and Cancer > Flashcards

Cell Cycle, Apoptosis, and Cancer Flashcards

1
Q

Stage of cell cycle were chromosome
duplication/segregation (start of cycle) and cytokinesis begins (end)

A

M Phase (M=Mitotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phases of Interphase

A

G1, S, G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stage of cell cycle outside of normal dvision

A

G0 Phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What phase does the RNA and protein synthesis needed for DNA replication occur.

A

Gap 1 phase of Interphase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phase of cell cycle where DNA stability is analyzed

A

Gap 2 (G2) phase of Interphase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Stage which ensures division is all set to happen (mitochondria are lined up, attached to the mitotic spindle, etc.)

A

M1 (Mitosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Descrete timepoint that exists if limiting growth factors occur.

At what time does this happen as well?

A

Restriction point

2hrs before S phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prior to going into the S phase, this checkpoint occurs if there is DNA damage.

A

G1 checkpoint (occurs end of G1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Checkpiont that occurs if DNA replication did not occur ideally.

A

G2 checkpoint (occurs end of G2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do mitogens induce moving from G1 into the S phase?

A

Down stream in pathway Rb becomes phosphoralated

Rb normally sequesters E2F.

When phosphoralated it allows E2F to bind to DNA and allows the cell cycle to continue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does Rb regulate itself and drive passed the G1 checkpoint?

A

It promotes Cylin A and Cyclin E synthesis which further phosphoralate Rb and allow the cycle to continue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are cyclins?

A

Cyclins bind to Cyclin Dependent Kinase to allow them to be active. They rise and fall dependent on stage of cell cycle.

DOES NOT FULLY ACTIVATE

Division increases them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What in addition to cyclins do you need to activate Cyclin dependent kinases?

A

Cyclin-activating kinases (CAK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are two examples of CDK1 inhibitors?

A

p27Kip1 or WEE1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is the T-loop of CDK1 influinced by cyclin and CAK.

A

The t-loop blocks the active site.

Cyclin binds and allows it to move partially.

CAK binds in addition and moves it completely.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three main ways to regulate CDK1 activity?

A

Phosphorylation of CDK

Binding of CKI (p27 or WEE1)

Proteolysis with proteasomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where does CAK phosphorylate CDK1

A

On the “cave site”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does WEE1 inhibit CDK1

A

Through phosphorylateing the “roof site”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does cdc25 do to CDK1?

A

Dephosphorylates the roof site (if phosphralated by inhibitory enzyme) to activate it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Does p27 phosphoralate CDK1?

A

No, it binds to CDK1 and cyclin complex preventing them from being active.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When in cell cycle events does p27 inhibit CDK1?

A

Early events.

(G1 to S)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is mitotic division signaled to anaphase?

What is the key ubiquitin ligase invloved?

A

Cyclin turnover, it is ubiquitinated by anaphase promoting complex (APC/C) also know as cyclosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What cyclins are targeted by APC/C

A

S and M cyclins (A and B)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does normal p53 do?

What is it requlated by?

A

Signals for apotosis.

In healthy normal cells it is ubiquinated by MDM2

25
Q

What molecule does p53 increase in transcription rate?

What does this do?

A

p21

p21 binds and inactivates CDK1 causing cell cycle arrest.

26
Q

Type of cell death where ligand binds to receptor.

27
Q

What ligands are used in Extrinsic cell death?

A

Fas and TNF alpha

28
Q

Type of cell death originating from the mitochondria.

29
Q

How are caspases activate?

A

Protease cleavage at certain sites to form a heterodimer with large and small subunits.

30
Q

What are example(s) of intiator caspases?

What are example(s) of executioner caspases?

A

Caspase 8 & 9

Caspase 3,6,7

31
Q

What is a major family of regulatory proteins in apoptosis?

A

The BCL2 family

32
Q

How does BAX (Bcl family) regulate apoptosis

A

In its inactive form it exists on the mitochondirial membrane. Upon activation it aggregates to form a channel that allows cytc to spill out into the cytosol and assist in apoptosis.

33
Q

What spills out from the mitochondria during cell death in addition to cytc?

34
Q

How is the Apotosome formed?

A

Through binding of Cytc with Apaf1

35
Q

What does the apotosome (Cytc/Apaf1 complex) activate?

36
Q

What constitutes a Proto-oncogene?

A

Things that regulate cell growth and division:

Growth factors

GF receptors and hormones

Transcription factors

Signal transducers

37
Q

How are oncogenes formed?

A

Gain of function mutations in proto-oncogenes

Too much product

Alternative product (oncoproteins)

38
Q

What is a mutation happens to proto-oncogene HER2 and what kind of Cancer is it commonly found in?

A

HER2 has a tyrosine kinase domain and is active upon binding a ligand. It becomes NEU upon mutation and is activated without a ligand.

Breast cancer

39
Q

What does EGF receptor become as an oncogene?

What disease does this become?

A

EGFRvIII (tyrosine constitutively active)

Glioblastoma

40
Q

What does BCR fuse with as a gain of function mutation due to translocation?

What disease is this related to?

A

ABL

Chronic Mylogenous Leukemia

41
Q

How is Retinoblasoma formed?

A

One mutation exists in the RB1 gene on one allele. Second allele is hit resulting in the disease as RB1 no longer exists.

(Tumors in both eyes may form)

42
Q

Sporadic Retinoblastoma

A

Mutation in 2 RB genes

Super Rare

43
Q

What are the functions of Tumor Supressor genes?

A

Repress cell cycle progression

Promote apoptosis

Couple DNA damage with the cell cycle

44
Q

BRCA is associated with what cancer?

A

Its a tumor supressor associated with breast cancer

45
Q

TP53 or p53 is associated with what cancers?

A

a. 65% of colon cancers
b. 30-50% of breast cancers
c. 50% of lung cancers

46
Q

PTEN- Phosphatase and tensin homolog is associated with what cancer?

A

%70 of prostate cancers

PTEM

47
Q

APC- Adenomatous polyposis coli is associated with what cancers?

A

Colon cancer

48
Q

What are the functions of Metastasis Suppressor proteins?

A

Prevent tumor cells from despersing

Block loss of contact inhibition

Inibit tumor metastasis

49
Q

Describe the development of cancer and the “multi hit hypothesis”

A
  1. Mutation occurs in cell
  2. This cell proliferates.
  3. Multiple mutations in tumor supressor genes
  4. Mutations in metastisis inhibitory proteins / other modifications
  5. Metastisis
50
Q

10 fundamental things of cancer

A
  1. Growth Signals
  2. Evade growth supressors
  3. Metastasis
  4. Immortality (through replication)
  5. Angiogenisis
  6. Resist Death

7. Disregulate cell energetics

  1. Aviod Immune
  2. Inflammation
  3. Genome instability
51
Q

How can HPV cause cancer?

A

Can cause degredation of p53 through E6

Can cause sequesteration of RB through E7

52
Q

Agents that block or supress DNA replication.

A

Alkalating Agents - everything

Anti-metabolites - S phase

Topoisomerase I Inhibitors - S phase

Topoisomerase II Inhibitors - S phase, G2 phase, and M

Citotoxic antibodies - S phase and G2 phase

Mitotoxic inhibitors - M phase

53
Q

Drug used to block HER2 and Neu?

How does it work?

A

Herceptin

Acts as an antibody that blocks cleavage, dimerization, activates antibody dependent cytotoxisity, causes endocytosis.

54
Q

Drug used to block BCR-ABL protein?

A

Gleevic

Competitively binds to where the ATP binds

55
Q

What drug inhibits EGF?

56
Q

G1 phase CDK and Cyclins

A

Cylcin D

CDK4

CDK5

57
Q

CDK and Cyclin for G1/S phase

A

Cyclin E

CDK2

(Inhibited by CKI)

58
Q

Cyclin and CDK for S phase

A

Cyclin A

CDK2

Inhibited by CKI

59
Q

Cyclin and CDK for M Phase

A

Cyclin A and Cyclin B

CDK1

MCM Exam 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions