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Therapeutics P3 Semester 1 > Exam 1 - Oncology (kinase inhibitors) > Flashcards

Exam 1 - Oncology (kinase inhibitors) Flashcards

1
Q

what is unique about the action of the tamoxifen as compared to Fluvestrant?
a. it leads to ER degradation
b. it holds ER out of the nucleus
c. it ejects ER from the cell
d. it activates ER in bone

A

d. it activates ER in bone

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2
Q

which of the following is not a hormone responsive cancer type?
a. breast
b. ovarian
c. prostate
d. endometrial

A

b. ovarian

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3
Q

which of the following is used only in the postmenopausal setting?
a. Letrozole
b. Tamoxifen
c. Leuprolide
d. Raloxifene

A

a. Letrozole

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4
Q

which compound acts directly on AR?
a. Leuprolide
b. Abiraterone
c. Degarelix
d. Enzalutamide

A

d. Enzalutamide

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5
Q

molecular causes of cancer

A

cancer is a breakdown of cellular maintenance that may be manifested by several causes
signal transduction through kinases drives proliferation

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6
Q

do better therapeutic agents target one kinase pathway or multiple?

A

multiple

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7
Q

kinases are _____

A

highly abundant proteins

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8
Q

9 tyrosine kinase inhibitors

A

imatinib
ibrutinib
dasatinib
ceritinib
lenvatinib
tofacitinib
ruxolitinib
lapatinib
pazopanib

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9
Q

4 serine/threonine kinase inhibitors

A

palbociclib
trametinib
vemurafenib
dabrafenib

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10
Q

2 dual protein kinase inhibitors

A

regorafenib
sorafenib

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11
Q

do kinase inhibitors have diverse or similar structures

A

diverse

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12
Q

genomic DNA from lung cancer biopsies are tested via ____ for a particular mutation of EGFR
if positive, these pts will go on ______ therapies

A

PCR, anti-EGFR

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13
Q

substrate for every kinase

A

ATP

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14
Q

what makes tyrosine a good (and common) target of several kinases?

A

can be phosphorylated at -OH group

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15
Q

other targets of kinases

A

serine, threonine, and lipids

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16
Q

cell signaling is ____ (complex or simple)

A

complex

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17
Q

describe the general structure of kinases

A

N and C groups connected by a hinge region
activation loop controls access to the active site

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18
Q

3 types of kinase inhibitors and differences btwn them

A

type 1: bind to active conformation of kinase
type 2: bind and stabilize the inactive conformation of kinase
type 3: occupy an allosteric pocket outside of the ATP-binding pocket

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19
Q

competitive vs. covalent inihbitors

A

competitive inhibitors compete with ATP in a reversible fashion
covalent is irreversible (stronger bond)

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20
Q

which amino acid is not a target of phosphorylation?
a. tyrosine
b. serine
c. threonine
d. alanine

A

d. alanine (only has methyl side group, not as reactive)

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21
Q

what is the source of the phosphate that gets transferred onto a substrate by a kinase?
a. SAM
b. DNA
c. RNA
d. ATP

A

d. ATP

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22
Q

most commonly mutated growth factor in lung cancer

A

EGFR

23
Q

T/F: Gefitinib. requires genetic test before prescribing

A

T

24
Q

Gefitinib and Erlotinib indication

A

EGFR mutant metastatic NSCLC

25
Q

Gefitinib (IRESSA) and Erlotinib fxn thru ____ kinase activity

A

tyrosine

26
Q

EGFR signaling induces cell ____. inhibition of kinase activity turns ___ signal to _____

A

proliferation, off, proliferate

27
Q

AE of Gefitinib and Erlotinib

A

fatigue, rash, diarrhea

28
Q

Afatinib (Gilotrif) indication

A

EGFR mutant NSCLC

29
Q

Afatinib (Gilotrif) is what type of inhibitor

A

covalent inhibitor of all ErbB receptors

30
Q

Explain how EGFR inhibitor associated skin rash can be a good thing

A

If rash seen (normally on chest/neck area), pts tend to respond better to therapy and live longer

31
Q

T790M mutation is associated with drug _______ (resistance or sensitivity)

A

resistance (this one specifically causes resistance to Gefitinib)

32
Q

L858R is commonly associated with drug _______ (resistance or sensitivity)

A

sensitivity

33
Q

drug to give pt if T790M mutation found

A

Osimertinib (third gen. EGFR inhibitor)

34
Q

type of bond Osimertinib forms

A

covalent

35
Q

Lapatinib (Tykerb) MOA

A

small molecule tyrosine kinase inhibitor that blocks HER2 and EGFR signaling

36
Q

Lapatinib (Tykerb) indication

A

approved (in combo with capecitabine) for tx of advanced metastatic breast cancer in pts whose cancer has progressed on other therapies

37
Q

Lapatinib (Tykerb) bond (and what it binds to)

A

reversible inhibitor of EGFR and HER2Lapatinib (Tykerb) indication

38
Q

Lapatinib (Tykerb) is selective for HER2 or EGFR?

A

HER2

39
Q

SE of Lapatinib (Tykerb)

A

NVD
- watch for sx of CHF too

40
Q

Tucatinib (Tukysa) use

A

for tx of HER2+ breast cancer
-2nd line therapy

41
Q

FLT3 inihibitors
-1st gen: ______ is _____ kinase inhibitor

A

midostaurin is broad

42
Q

FLT3 inihibitors
-2nd gen: ______ is _____ kinase inhibitor

A

crenolanib is more specific

43
Q

FLT3 inihibitors
-type 2: ______ is _____ kinase inhibitor

A

Quizartinib is specific for ITD mutations

44
Q

Imatinib (Gleevec) MOA and reasoning

A

type 2 small molecule inhibitor of the Abl tyrosine kinase. activity of Bcr-Abl chimeric protein is constitutively active which results in malignancy
-primarily treats CML

45
Q

Imatinib (Gleevec) AE

A

N/V
fluid retention and edema
neutropenia and thrombocytopenia frequent but mild
resistance is constant battle

46
Q

Ponatinib (Iclusig) use

A

BCR-Abl inhibitor effective against all major mutant forms of BCR-Abl

47
Q

drug approved for ALK mutation in NSCLC who have progressed or are intolerant to crizotinib

A

Alectinib (Alecensa)

48
Q

Trametinib (Mekinist) MOA

A

inhibits kinase activity of MEK1 and MEK2
-type 3 inhibitor

49
Q

cannot use what drug if pt has history of BRAF inhibitor therapy

A

trametinib

50
Q

Trametinib (Mekinist) AE

A

rash
diarrhea
lymphedema

51
Q

Acalabrutinib

A

2nd gen covalent BTK inhibitor
-more potent and more selective than 1st gen ibrutinib
-indication is B cell lymphoma (MCL and CLL)

52
Q

rapamycin analogues

A

-aka: Sirolimus
-mTOR is a serine-threonine kinase
-inhibits immune response by blocking IL-2 signaling tranduction

53
Q

T/F: Everolimus inhibits mTORC1 and mTORC2

A

F, only mTORC1

54
Q

biggest problem with kinase inhibitors

A

resistance
-they are not curative therapy

Therapeutics P3 Semester 1 (16 decks)

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