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Pharmacogenomics > Quiz 6 (oncology) > Flashcards

Quiz 6 (oncology) Flashcards

1
Q

Geftinib drug target

A

EGFR

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2
Q

Erlotinib drug target

A

EGFR

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3
Q

Afarinib drug target

A

EGFR

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4
Q

Crizotinib drug target

A

Receptor tyrosine kinase/ALK

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5
Q

Ceritinib drug target

A

Receptor tyrosine kinases/ALK

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6
Q

Cetuximab drug target

A

EGFR/KRAS

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7
Q

Panitumumab drug target

A

EGFR/KRAS

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8
Q

Which oncology meds are used for colorectal cancer?

A

Cetuximab

Panitumumab

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9
Q

Which oncology med is used for head and neck cancer?

A

Cetuximab

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10
Q

What are the majority of oncology meds used for?

A

Lung cancer

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11
Q

EGFR activation leads to cell ____

A

proliferation

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12
Q

What are the 2 types of lung cancer classifications?

A

Non-Small Cell Lung Cancer

Small Cell Lung Cancer

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13
Q

Which type of lung cancer is more common?

A

Non-Small Cell Lung Cancer (NSCLC)

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14
Q

What is traditional first-line therapy for NSCLC?

A

Platinum-based chemotherapy

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15
Q

Activation/inactivation of EGFR causes cancer?

A

activation

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16
Q

HER1/ErbB1 mutations in EGFR predict _____ may be more effective.

A

TKI Inhibitors

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17
Q

If mutation not present in EGFR, then ____ is more effective.

A

Chemotherapy

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18
Q

What is the structure of EGFR?

A

Crosses cell membrane
Abs bind outside
Tyrosine kinase inhibitor intracellular

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19
Q

What do TKIs do?

A

Inhibit phosphorylation by tyrosine kinase

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20
Q

What factors of a tumor indicate poor prognosis (there are 5)?
EGFR Inhibits all of these

A 
Proliferation
Survival
Angiogenesis (creating its own blood supply)
Migration 
Adhesion
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21
Q

Which EGFR mutations indicate susceptibility to TKI?

A

in exons 18, 19, 21

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22
Q

Which EGFR mutations indicate resistance to TKIs?

A

in exon 20

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23
Q

What mutation in exon 19 causes susceptibilty to TKIs?

A

Deletions

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24
Q

What mutation in exon 21 causes susceptibility to TKIs?

A

L858R mutation

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25
Q

What are the EGFR tyrosine kinase inhibitors?

A

Gefitinib
Erlotinib
Afatinib

26
Q

Erlotinib and afatinib are most effective with ___ EGFR expression

A

higher

27
Q

T/F: Gefitinib had a survival benefit in patients who had high levels of EGFR

A

False - fast-track approval has failed

28
Q

When are erlotinib and afatinib first-line treatment?

A 
exon 19 deletions
exon 21 (L858R) substitution mutations
29
Q

What is the barrier to using genotype guided dosing with TKIs?

A

It’s desired to begin therapy before genotype results are available

30
Q

Which meds are antibodies against overexpressed EGFR?

A

Cetuximab

Panitumumab

31
Q

___ mutations are associated with resistance to TKIs in patients with EGFR mutations

A

KRAS mutations

32
Q

T/F: Activation of KRAS proteins would cause cancer development regardless of EGFR signaling

A

True - EGFR signaling is upstream of KRAS

33
Q

Cetuximumab/Panitumumab are used in patients with ______ colon cancer and _______

A

EGFR-expressing colon cancer; KRAS mutant negative

34
Q

ALK mutation is fusion of the ____ gene to ____

A

ALK to EML4 (which is constitutively promoted, so makes ALK always active)

35
Q

What are the ALK inhibitors?

A

Crizotinib

Ceritinib

36
Q

Which ALK inhibitor is first-line for ALK positive NSCLC patients?

A

Crizotinib

37
Q

Crizotinib increases he risk of ___ adverse effect over chemotherapy

A

hepatotoxicity (increased LFTs)

38
Q

When is ceritinib used?

A

If crizotinib fails

39
Q

What ADE with ceritinib?

A

Increased LFTs

40
Q

What is the mechanism of mercaptopurine?

A

inhibits purine nucleotide synthesis

41
Q

What gene is associated with mercaptopurine?

A

TPMT

42
Q

What gene is associated with irinotecan?

A

UGT1A1

43
Q

What is the MOA of irinotecan?

A

Inhibits topoisomerase I

44
Q

___ TPMT activity increases the risk of _____ toxicity

A

Low; mercaptopurine toxicity

45
Q

What is mercaptopurine toxicity?

A

Myelosuppression (reduced WBC, RBC, platelets)

46
Q

When is irinotecan used?

A

Metastatic colorectal cancer

47
Q

What is the active metabolite of irinotecan?

A

SN-38

48
Q

___ inactivates SN-38

A

UGT1A1/6/9

49
Q

Which UGT1A1 allele decreases function?

A

*28

50
Q

What does decreased UGT1A1 function increase the risk of with irinotecan?

A

Neutropenia and severe (deadly) diarrhea

51
Q

How should you adjust irinotecan dosing for patients with UGT1A1*28?

A

Reduce by 1 dose level

52
Q

Is genotyping for UGT1A1 normally done?

A

No - no clear dosing guidelines

53
Q

Most familiar cancer syndromes are related to tumor suppressor genes or oncogenes?

A

Tumor suppressor genes

54
Q

What is loss of heterozygosity?

A

Losing chromosomes - maybe 23, maybe just part of some of them - but only have 1 copy left of a gene

55
Q

Heritable retinoblastama is autosomal dominant or recessive?

A

Dominant

56
Q

Herital retinoblastoma is normaly bilateral or unilateral?

A

Bilateral

57
Q

Average age at diagnosis is younger for pts with nonheritable or heritable retinoblastoma?

A

Heritable

58
Q

T/F: Retinoblastoma follows the two-hit hypothesis model

A

TRUE

59
Q

The RB1 gene (involved in retinoblastoma) is involved in ______ when normally functioning

A

Cell cycle regulation

60
Q

P53 prevents cell from completing cell cycle if what?

A

DNA or cell is damaged

61
Q

How does p53 stop cell cycle if damage is minor?

A

Halts until it can be repaired

62
Q

How does p53 stop cell cycle if damage is major?

A

If it cannot be repaired, commits apoptosis

Pharmacogenomics (3 decks)

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