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4 CAN > 5 Oncogenes > Flashcards

5 Oncogenes Flashcards

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1
Q

What is an oncogene?

A

a gene that has the potential to cause cancer when mutated or overexpressed

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2
Q

What do the gene products of proto-oncogenes function as?

A

growth factors
growth factor receptors
signal transduction molecules
transcription factors

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3
Q

What is the significance of oncogenic dominance?

A

only one allele needs to be mutated for the oncogene phenotype

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4
Q

What are the 4 key mechanisms of oncogene activation?

A 
point mutation
amplification of genomic DNA region
chromosome translocation (proto-oncogene under different control, or joining 2 genes together)
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5
Q

Oncogenic Ras mutations invariably involve missense mutations affecting which 3 codons?

What is the significance of these?

A

G12
G13
Q61

these amino acids are close to the GTP pocket in the Ras protein

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6
Q

What do Ras mutations do?

A

decrease GTP hydrolysis

lock Ras in an active GTp-bound state

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7
Q

What are the 2 common EGFR mutations?

A

frame deletion aa747-752

missense mutation L858R

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8
Q

What is the effect of frame deletion aa747-752 with EGFR?

A

change in protein conformation

prolongs active dimer configuration

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9
Q

What is the effect of missense mutation L858R?

A

increases kinase activity 50-fold

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10
Q

What is MYCN amplification associated with?

A

neuroblastoma

very poor outcomes

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11
Q

What is C-Myc amplification associated with?

A

small cell lung cancer
breast cancer
ovarian cancer
oesophageal cancer

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12
Q

What is cyclin 01 amplificaiton associated with?

A

breast cancer

oesophageal cancer

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13
Q

What is EGFR amplification associated with?

A

glioblastoma

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14
Q

Name 2 mechanisms of MYCN amplification in neuroblastoma

A

extrachromosomal copies of MYCN (double minutes)

multiple copies of MYCN on same chromosome

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15
Q

When might N-Myc protein expression be increased?

A

neuroblastomas in MYCN gene amplification

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16
Q

In what proportion of glioblastoma cases is EGFR amplified?

A

30-50%

17
Q

Name a key genetic hallmark of Burkitt lymphoma

A

translocations involving c-Myc

18
Q

Where is Burkitt lymphoma derived from?

A

germinal centre B lymphocytes

19
Q

Name 3 chromosomal involving c-Myc associated with BL

A

T(8;14) - MYC-IgH
T(2;8) - MYC-IgKappa
T(8’22) - MYC-IgLambda

20
Q

What does a T(8;14) translocation do?

A

places IgH enhancer adjacent to c-MYC

the powerful IgH enhancer drives c-Myc protein overexpression

21
Q

What does C-Myc do?

A

binds with a partner protein (MAX) an then binds to DNA, recruiting RNA polymerase activating gene expression

(transcription factor)

22
Q

What is BCL2-IgH translocation associated with?

A

follicular lymphoma

23
Q

What is BCL2?

What is the significance of this?

A

pro-survival gene counteracting apoptosis

overexpresison allows tumour cells to become chemo-resistant

24
Q

What hallmark is associated with chronic myeloid leukaemia?

A

22,9 translocation to form BCR-ABL

25
Q

Name 4 oncogenes encoding tyrosine kinases

A

BCR-ABL
EGFR
ALK
MET

26
Q

How would you treat cancers caused by oncogenes encoding tyrosine kinases?

A

TKIs

27
Q

Name a specific inhibitor of the BCR-ABL TK

How does it work?

A

Gleevec

competitive inhibitor of ATP binding to active site

28
Q

Name 2 first generation TKIs targeting EGFR

A

gefitinib

erlotinib

29
Q

Name 2 second generation TKIs targeting EGFR

A

Afatinib

Dacomitinib

30
Q

Name a third generation TKI targeting EGFR

A

Osimertinib

31
Q

How do first generation TKIs work?

A

competitive ATP-mimics

32
Q

What problem is associated with first generation TKis?

A

frequent drug resistance

T790M mutation increases the ability to bind ATP again

33
Q

How do second generation TKI work?

A

irreversible binding in the ATP pocket

34
Q

How do third generation TKI work?

A

bind more avidly to EGFR T790M mutations than wild-type EGFR

4 CAN (21 decks)

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