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MoD > 21 Carcinogenesis 2 > Flashcards

21 Carcinogenesis 2 Flashcards

1
Q

What is the function of caretaker genes?

A

Maintain genetic stability by repairing damaged DNA and replication errors.

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2
Q

What are the two types of tumour suppressor genes?

A

Gatekeepers and caretakers.

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3
Q

What are the roles of gatekeeper genes?

A

Negatively regulate cell cycle + proliferation.

Positively regulate apoptosis + cell differentiation.

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4
Q

What are the most common mechanisms for the 2nd required for TSG inactivation? (4).

A

Chromosomal non-disjunction.
Gene conversion.
Mitotic recombination.
Promoter hypermethylation.

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5
Q

Which gene is involved in retinoblastoma?

What type of TSG is it?

A

RB1.

Gatekeeper.

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6
Q

Which gene is involved in Li-Fraumeni syndrome?

What type of TSG is it?

A

p53.

Gatekeeper/caretaker.

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7
Q

Which gene is involved in FAP?

What type of TSG is it?

A

APC.

Gatekeeper.

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8
Q

Which genes are involved in familial breast cancer?

What type of TSG is it?

A

BRCA1, BRCA2.

Caretaker.

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9
Q

Which gene is involved in HNPCC?

What type of TSG is it?

A

hMLH1, hMSH2.

Caretaker.

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10
Q

What are the functions of proto-oncogenes? (4).

A

Promote cell proliferation, survival, angiogenesis and regulation of apoptosis.

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11
Q

Are mutated porto-oncogenes dominant or recessive to the normal copy?

A

Dominant.

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12
Q

Are mutated tumour suppressor genes dominant or recessive to the normal copy?

A

Recessive.

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13
Q

What are the three mechanisms of oncogene activation?

A

Translocation to a transcriptionally active site.
Point mutation.
Amplification.

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14
Q

What is the minimum number of genetic alterations needed to transform a normal cell to a neoplastic cell?

A

3.

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15
Q

What are the genetic changes seen in the progression of colon carcinoma? (5).

A 
Loss of APC.
DNA hypermethylation.
Activation of K-ras.
Loss of 18qTSG.
Loss of p53.
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16
Q

What are the hallmarks of cancer cells? (6).

A 
Self sufficiency in growth signals.
Insensitivity to anti-growth signals.
Tissue invasion and metastasis.
Limitless potential for replication.
Sustained angiogenesis.
Apoptosis evasion.
17
Q

How do neoplastic cells become independent of growth signals? (4).

A

EGFR overexpression.
EGFR mutation.
Ras mutation.
B-Raf mutation.

18
Q

How does a RAS mutation lead to independence from growth signals?

A

RAS in EGFR pathway.

Prevents dephosphorylation by GAP, and so becomes permanently active.

19
Q

How do neoplastic cells become resistant to anti-growth signals?

A

Rb protein usually inhibits progression from G1 to S phase of cell cycle. -ve growth factors activate it.
Inactivation results in resistance to -ve growth factors.

20
Q

How do tumour cells achieve immortality?

A

Over expression of telomerase enzyme maintains telomere length indefinitely.

21
Q

What are telomeres?

A

Hexanucleotide repeat sequences. Shorten with each cell division, giving cells a finite replicative lifespan.

22
Q

What is the most common gene mutated in human cancers?

A

TP53.

23
Q

How do neoplastic cells become resistant to apoptosis?

A

TP53 mutation.

24
Q

What is the function of TP53?

A

Induces cell cycle arrest to allow repair of DNA damage.

Induces apoptosis if too much damage.

25
Q

How does angiogenesis occur in tumours?

A

Hypoxia stimulates HIF-1 transcription factor, inducing vascular endothelial growth factor (VEGF). VEGF actively recruits endothelial cells to construct new capillaries.

26
Q

At what size do tumours start angiogenesis?

A

2mm in diameter.

27
Q

How do tumours become invasive/metastatic? (At a genetic level).

A

Mutation/hypermethylation of E-cadherin prevents expression. Results in epithelial-mesenchymal transition (EMT). Mesenchymal cells are motile and secrete proteases, allowing them to break through membrane.

28
Q

What is the CA-125 serum antigen used for? (3).

A

Identifying type of ovarian cancer.
Monitoring treatment success.
Detecting relapse.

29
Q

Which AML translocations are associated with good prognoses?

A

t(8;21)
t(15;17)
inv(16)

30
Q

Which AML translocations are associated with bad prognoses?

A

t(11q23)

complex karyotype

31
Q

What does HER2 code for?
Change found in breast cancer?
Targeted drug?

A

+ve growth factor receptor.
Over expression.
Herceptin.

MoD (21 decks)

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