Quiz 6 (oncology) Flashcards Preview

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Flashcards in Quiz 6 (oncology) Deck (62):
1

Geftinib drug target

EGFR

2

Erlotinib drug target

EGFR

3

Afarinib drug target

EGFR

4

Crizotinib drug target

Receptor tyrosine kinase/ALK

5

Ceritinib drug target

Receptor tyrosine kinases/ALK

6

Cetuximab drug target

EGFR/KRAS

7

Panitumumab drug target

EGFR/KRAS

8

Which oncology meds are used for colorectal cancer?

Cetuximab
Panitumumab

9

Which oncology med is used for head and neck cancer?

Cetuximab

10

What are the majority of oncology meds used for?

Lung cancer

11

EGFR activation leads to cell ____

proliferation

12

What are the 2 types of lung cancer classifications?

Non-Small Cell Lung Cancer
Small Cell Lung Cancer

13

Which type of lung cancer is more common?

Non-Small Cell Lung Cancer (NSCLC)

14

What is traditional first-line therapy for NSCLC?

Platinum-based chemotherapy

15

Activation/inactivation of EGFR causes cancer?

activation

16

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

TKI Inhibitors

17

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

Chemotherapy

18

What is the structure of EGFR?

Crosses cell membrane
Abs bind outside
Tyrosine kinase inhibitor intracellular

19

What do TKIs do?

Inhibit phosphorylation by tyrosine kinase

20

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

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

21

Which EGFR mutations indicate susceptibility to TKI?

in exons 18, 19, 21

22

Which EGFR mutations indicate resistance to TKIs?

in exon 20

23

What mutation in exon 19 causes susceptibilty to TKIs?

Deletions

24

What mutation in exon 21 causes susceptibility to TKIs?

L858R mutation

25

What are the EGFR tyrosine kinase inhibitors?

Gefitinib
Erlotinib
Afatinib

26

Erlotinib and afatinib are most effective with ___ EGFR expression

higher

27

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

False - fast-track approval has failed

28

When are erlotinib and afatinib first-line treatment?

exon 19 deletions
exon 21 (L858R) substitution mutations

29

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

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

30

Which meds are antibodies against overexpressed EGFR?

Cetuximab
Panitumumab

31

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

KRAS mutations

32

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

True - EGFR signaling is upstream of KRAS

33

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

EGFR-expressing colon cancer; KRAS mutant negative

34

ALK mutation is fusion of the ____ gene to ____

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

35

What are the ALK inhibitors?

Crizotinib
Ceritinib

36

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

Crizotinib

37

Crizotinib increases he risk of ___ adverse effect over chemotherapy

hepatotoxicity (increased LFTs)

38

When is ceritinib used?

If crizotinib fails

39

What ADE with ceritinib?

Increased LFTs

40

What is the mechanism of mercaptopurine?

inhibits purine nucleotide synthesis

41

What gene is associated with mercaptopurine?

TPMT

42

What gene is associated with irinotecan?

UGT1A1

43

What is the MOA of irinotecan?

Inhibits topoisomerase I

44

___ TPMT activity increases the risk of _____ toxicity

Low; mercaptopurine toxicity

45

What is mercaptopurine toxicity?

Myelosuppression (reduced WBC, RBC, platelets)

46

When is irinotecan used?

Metastatic colorectal cancer

47

What is the active metabolite of irinotecan?

SN-38

48

___ inactivates SN-38

UGT1A1/6/9

49

Which UGT1A1 allele decreases function?

*28

50

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

Neutropenia and severe (deadly) diarrhea

51

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

Reduce by 1 dose level

52

Is genotyping for UGT1A1 normally done?

No - no clear dosing guidelines

53

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

Tumor suppressor genes

54

What is loss of heterozygosity?

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

55

Heritable retinoblastama is autosomal dominant or recessive?

Dominant

56

Herital retinoblastoma is normaly bilateral or unilateral?

Bilateral

57

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

Heritable

58

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

TRUE

59

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

Cell cycle regulation

60

P53 prevents cell from completing cell cycle if what?

DNA or cell is damaged

61

How does p53 stop cell cycle if damage is minor?

Halts until it can be repaired

62

How does p53 stop cell cycle if damage is major?

If it cannot be repaired, commits apoptosis