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MCM > Cell Cycle, Apoptosis, and Cancer > Flashcards

Cell Cycle, Apoptosis, and Cancer Flashcards

1
Q

When is the restriction point (R), and what happens there?

A

2 hours prior to S phase (in G1)

if growth factors are limiting –> restriction occurs

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2
Q

What two proteins in HPV cause cancer?

A

E6 and E7

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3
Q

What happens in the G0 phase?

A

poor nutrient/environmental conditions –> cell withdraws from cell cycle

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4
Q

What do proto-oncogenes normally code for?

A

growth factors
receptors for GFs and hormones
Transcription factors
(basically anything promoting cell growth and division)

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5
Q

What is p53

A

transcription factor that is activated when DNA is damaged –> activates p21 –> keeps Rb hypophosphorylated and sequesters E2F so you can’t move into S phase
Promotes apoptosis = tumor suppressor

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6
Q

What does CDC25 phosphatase do?

A

Undoes WEE1 phosphorylation of C-CDK complex to reactivate it

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7
Q

When do topoisomerase I inhibitors work?

A

S, G2, and M phases

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8
Q

What does E6 in HPV inhibit?

A

p53

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9
Q

What are the checkpoints?

A

R, G1, G2, Metaphase

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10
Q

What is APC/C?

A

anaphase promoting complex/ cyclosome
a ubiquitin ligase enzyme that adds polyubiquitin to cdk-cyclin complex –> cyclin degrades –> signals change to anaphase

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11
Q

What type of protein is APC?

Mutations in it are linked to what type of cancer?

A

adenomatous polyposis coli = tumor suppressor

colon cancer

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12
Q

What does the SH2 domain on GRB-2 do?

A

binds to phosphorylated tyrosine residues on an RTK

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13
Q

What are 2 common toxins that cause p53 mutations?

A

activated benzopyrene in cigarette smoke and aflatoxin, a fungal metabolite in moldy grain and peanuts

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14
Q

What happens in the G2 phase?

A

DNA stability is checked

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15
Q

How do alkylating agents work to treat cancer?

A

block DNA replication

affect all phases of cell cycle

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16
Q

How to antimetabolites work to treat cancer?

A

inhibit enzymes involved in DNA synthesis

S phase

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17
Q

What is Erbitux?

A

treats colorectal cancer

mAb directed against EGF receptor that is over-expressed in colorectal cancer

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18
Q

What triggers metaphase to anaphase?

A

cyclin turnover

APC/C degrades cyclin to help do this

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19
Q

What is the order of the cell cycle?

A

G0 G1 –> S –> G2 –> M

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20
Q

What happens in the M phase

A

Mitosis
Chromosome separation
Cell division

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21
Q

What happens in the G1 checkpoint?

A

occurs in response to DNA damage

timing similar to R (2 hours before S)

22
Q

What happens in hereditary retinoblastoma?

A

mutation/deletion of once copy of RB1 is inherited –>

cells are predisposed to be cancerous –> some mutation occurs to eliminate last good copy –> cancer

23
Q

How can viruses cause cancer?

A

During virus replication, accidentally incorporates a human proto-oncogene into its genome –> mutation turns it into an oncogene –> virus can now transform normal cells and cause cancer

24
Q

Which enzyme is missing in many somatic cells that causes their senescence?

A

telomerase - maintains telomere length

w/out it, telomeres shrink and cells will eventually die

25
Q

What type of mutations turn proto-oncogenes into oncogenes?

A

gain of function mutations –>
increased expression of protein products
expression of altered protein (oncoprotein) that doesn’t respond to normal signal

26
Q

What is cyclin A essential for?

A

so that S phase can occur

27
Q

What happens in the G1 phase?

A

RNA and protein synthesis needed for DNA replication

28
Q

What does p27 do?

A

Inhibits cyclin-CDK by binding to it

29
Q

What do small G-proteins do, and what is their significance with cancer?

A

monomeric G proteins that have GTPase activity (RAS); control cell proliferation; apoptosis, and a lot of other stuff; mutations can lead to cancer

30
Q

How to cytotoxic antibiotics work to treat cancer?

A

intercalate between bases in DNA to inhibit DNA synthesis

S phase and G2 phase

31
Q

What type of protein is p53?

A

Tumor suppressor

32
Q

What types of cancers do mutations in p53 cause?

A

65% of colon cancers
30-50% of breast cancers
50% of lung cancers
others

33
Q

What does Herceptin do?

A

treats breast cancer; is a monoclonal Ab for HER2/NEU

34
Q

What does E7 in HPV inhibit?

A

Rb

35
Q

What do metastasis suppressors do?

A

cell adhesion proteins that prevent tumor cells from dispersing and block loss of contact inhibition

36
Q

How to mitotic inhibitors work to treat cancer?

A

Arrest cells in mitosis during metaphase

37
Q

What happens in the metaphase checkpoint?

A

ensures chromosomes are attached to mitotic spindle

38
Q

How are gain of function mutations in proto-oncogenes passed on?

A

autosomal dominant

39
Q

What is HER2?

A

Proto-oncogene that, when mutated, results in overexpression of HER2
observed in many breast cancers

40
Q

What type of protein is PTEN?

Mutations in it are linked to what type of cancer?

A

tumor suppressor

Prostate cancer

41
Q

What does WEE1 Kinase do?

A

Inhibits Cyclin-CDK complex by hyperphosphorylating it

42
Q

What type of mutations screw up tumor suppressors?

A

loss of function

43
Q

What happens in the S phase?

A

DNA Synthesis

44
Q

What type of protein is retinoblastoma (Rb)?

A

tumor suppressor

45
Q

What does cyclin E do?

A

gets cell from G1 to S

46
Q

How are loss of function mutations in tumor suppressor genes passed on?

A

autosomal recessive

only need 1 good copy to function

47
Q

What happens in G2 checkpoint?

A

Verify complete genomic duplication

48
Q

What is Gleevec?

A

treats chronic myelogenous leukemia

binds to active site of ABL tyrosine kinase and inhibits its activity

49
Q

What is the most common base change in p53 that causes cancer?

A

G –> T transversion

50
Q

What is p21?

A

tumor suppressor that inhibits cyclin-CDK by keeping Rb hypophosphorylated so E2F is sequestered and can’t go into S phase

MCM (14 decks)

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