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Pgx > Oncology PGx > Flashcards

Oncology PGx Flashcards

1
Q

What type of mutation does cancer usually have?

A

Somatic usually, germ and somatic second, Germ-line last

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2
Q

5 year survival for Colorectal cancer?

A

64%

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3
Q

5 year survival for mCRC

A

14%

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4
Q

What is KRAS?

A

Proto-oncogene

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5
Q

what happens if KRAS is on?

A

GTPase state and propagate cell growth and differentiation

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6
Q

What is K-ras?

A

It can be intercellular as well

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7
Q

When do you give a EGRF inhibitor?

A

KRAS -
Cant give is positive

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8
Q

What codon is activated in KRAS mutation?

A

12,13 or 61

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9
Q

What happens when you bind EGFR?

A

Attaches cell surface and turns off the tumor like environment

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10
Q

Is EGRF therapy given alone?

A

No always in combo with a chemotherapy

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11
Q

Do we have toxic and dosing data for KRAS positive pt given EGFR?

A

No

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12
Q

KRAS mutation on what codon for mCRC cant receive what?

A

Codon 12 and 13 and can’t get EGFR therapy

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13
Q

What do you give if they have KRAS mutation?

A

Sotorasib NSCLC

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14
Q

What is BCR-ABL?

A

The fuse of 2 gene (9 and 22) and when fused it shortens one called the Philadelphia chromosome

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15
Q

Effect of BCR-ABL?

A

Speeds up cell division and block DNA repair

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16
Q

What are the 3 symptoms phase of CML

A

Chronic - mild or no
Accelerated - symptoms
Blast - severe symptoms

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17
Q

what is first generation TKI and what does it do?

A

Gleevac (imatinib) - prolongs survival and events
Doesn’t cure and goes back to chronic state

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18
Q

How does CML develop imatinib resistant?

A

BCR-AML point mutation bc of amplification and over expression
Cause point mutation in ATP binding site

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19
Q

What is IC50?

A

Lower the better for mutations

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20
Q

What is T315I?

A

ATP binding site point mutation that is important for drugs

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21
Q

What are the 4 mutations we look for in CML and which ones do we worries about?

A

P-loop, ATP binding site, Catalytic domain, A-loop
P-loop and ATP binding site most common

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22
Q

When do we test CML pt?

A

Accelerated or blast phase

23
Q

When to test when on mediation for CML?

A

See fails or resistance to imatinib
Same with 2nd gen dasatinib or nilotinib

24
Q

Which drug do i give with mutation T315I?

A

3 or 4th gen ( ponatibnib or asciminib)
FDA approve for this mutation

25
Q

Where are V299L, T315A, and F317L/V and what drug do i give

A

ATP binding site mutations and i give Nilotinib over dasatinib

26
Q

Where are Y253H, E255K/V and F359V/Cand what drug do i give

A

Y and E are P loop and F is a catalytic domain
Give Dasatinib over Nilotinib

27
Q

What is HER2 or ERBB2?

A

Givens a worst prognosis and over expressed

28
Q

How does Trastuzamab work and when do I use

A

Binds to HER 2 and use only if + for HER 2

29
Q

What are the 2 test that find HER2?

A

FISH and Hercept test

30
Q

6-MP and TPMT what are the alleles?

A

3A, 3C and 2

31
Q

What does the Allele changes in TPMT do?

A

Decrease Allele activities

32
Q

What type of SNP is TPMT?

A

Non-Synonymous

33
Q

How does TPMT cause toxicity?

A

Usually make 6 - MeMP but since it is decreased you make 6-TGN which is toxic and drive effectively

34
Q

CPIC guidelines for Homo-TPMT?

A

Reduce 10 fold 75-10
give 3 times a week

35
Q

CPIC for hetero-TPMT?

A

Reduce dose 30-80%

36
Q

What is FDA recommendation for TPMT testing?

A

Recommends testing
HOMO- reduce initial dose
HETERO - monitor

37
Q

What SNP is NUDT15?

A

Non-synonymous C>T
Loss of function
*2 and *3

38
Q

What does NUDT15 do?

A

Converts 6-TGN to less toxic form
Loss of function more cytotoxic effects

39
Q

CPIC for HOMO-NUDT15?

A

Does to 10mg
Daily

40
Q

CPIC for Hetero-NUDT15

A

30-80% reduction

41
Q

Impact of TPMT and NUD15 on OS?

A

NONE

42
Q

What is Tamoxifen for?

A

Prodrug too
SERM for ER+ and PR+

43
Q

What is need for Tamoxifen to worK?

A

2D6 and Endoxifen

44
Q

What does 2D6 *10, 17 and 41 do?

A

Double digits decreased

45
Q

What does 2D6 *3, 4, 5 and 6 do?

A

Loss of activity

46
Q

What does 2D6 *1xn and 2xn do?

A

Can be a ultra metabolized

47
Q

Should we test for tamoxifen?

A

No recommended bc no OS for null but inconsistencies

48
Q

CPIC for DPYD NM?

A

No change

49
Q

CPIC for DPYD IM?

A

Reduce does based on activity score
1- 50%
1.5 - 25-50%

50
Q

CPIC for DPYD PM?

A

Avoid use

51
Q

Why do we test DPYD and is it worth it?

A

Yes bc hospiliztion have been related to these toxicities
Rn cost neutral soon cost effective
Not required rn
5-FU

52
Q

UGT1A1*28 does what?

A

Reduce enzyme activity for the drug Irotecan

53
Q

What factors do i consider when dosing Irotecan and why?

A

UGT1A1*28 and strong CYP3A4 inhibitors bc of the dose reduction provides a safer profile for neutropenia

Pgx (5 decks)

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