PCol of Chemo Flashcards Preview

Oncology > PCol of Chemo > Flashcards

Flashcards in PCol of Chemo Deck (78):
1

How do Small Molecule Inhibitors work?

A. Block the growth factor receptor at the receptor site

B. Block an allosteric site on growth factor receptors

C. Block tyrosine kinase activity at the receptor site or away from the receptor site

D. Irreversibly bind to the receptor binding site and prevent ligand interaction

C. Block tyrosine kinase activity at the receptor site or away from the receptor site

As you can see in the picture the medications are working at the level of the tyrosine kinases and NOT at the receptor binding site

2

How do Monoclonal Antibodies work? (Select all)

A. Directly inhibits binding site at the growth factor receptor

B. Directly inhibits tyrosine kinases within the cell

C. Directly binds to allosteric sites on growth factor receptors

D. Binds to the natural ligand of a growth factor receptor

A. Directly inhibits binding site at the growth factor receptor

D. Binds to the natural ligand of a growth factor receptor

Monoclonal antibodies can bind to the growth factor receptor site such as EGFR (Epidermal Growth Factor Receptors) or it can bind directlyl to the ligand responsible for activating the growth  (factor receptor. An example of this would be VEGF (Vascular Endothelial Growth Factor) being bound to the monoclonal antibody and being unable to bind to its VEGFR receptor now. 

3

Which of these medications is a mono-clonal antibody? (select all)

A. Gefitnib

B. Trastuzumab

C. Lapatinib

D. Panitumumab

E. Certuximab

B. Trastuzumab

D. Panitumumab

E. Certuximab

Mab= mono clonal antibody

4

Which of these medications is a Small Molecule Inhibitor? (select all)

A. Gefitnib

B. Lapatinib

C. Pertuzumab

D. Erlotinib

E. Trastuzumab

A. Gefitnib

B. Lapatinib

D. Erlotinib

nib= small molecule inhibitor 

I think of nibble as in small bites

5

Which of these medications are categorized as Growth Factor Receptor Antagonists? (select all)

A. Gefitinib

B. Trastuzumab

C. Imatinib

D. Panitumumab

E. Certuximab

A. Gefitinib- EGFR kinases

B. Trastuzumab- HER-2

D. Panitumumab-EGFR

E. Certuximab- EGFR

6

Which of these medications competitivelyl inhibits EGFR tyrosine kinases? (Select All)

A. Gefitinib

B. Trastuzumab

C. Imatinib

D. Erlotinib

E. Lapatinib

A. Gefitinib

D. Erlotinib

E. Lapatinib

7

Which of the following is a mechanism of resistance to Gefitinib? (Select All)

A. Tumors that are not uniquely dependent on EGFR

B. Poor drug penetration

C. Drug efflux mechanisms 

D. Tumor mutates to only rely on EGFR overexpression to achieve cellular growth

E. T790M mutation

D. Tumor mutates to only rely on EGFR overexpression to achieve cellular growth

The previous mechanisms are all mechanisms of ressitance except for this one. Gifitnib was found to be very beneficial in patients who overexpressed EGFR (mutation) because the drug works at the EGFR tyrosine kinases and blocks them from phosphorylating. So if the tumor only relies on EGFR for replication then this is not a mechanism of resistance against this particular drug, Gefitinib.

8

What is the MOA of Gefitinib? (select all)

A. Competitive inhibitor of EGFR tyrosine kinase

B. Prevention of ATP phosphorylation

C. Cell cycle arrest at the G0/G1 boundary 

D. Binds to the EGF ligand and prevents its binding to the EGFR receptor

E. Binds to the receptor pocket of EGFR and prevents ligand binding and activation

A. Competitive inhibitor of EGFR tyrosine kinase

B. Prevention of ATP phosphorylation

C. Cell cycle arrest at the G0/G1 boundary

Remember that Gefitinib is a small molecule inhibitor meaning that it binds competitively to the EGFR tyrosine kinase. It is competeing with ATP for that tyrosine kinase binding pocket so if Gefitnib binds to that binding pocket instead of ATP then phosphorylation cannot happen. if there is no phosphorylation then the kinase pathway cannot be activated and the cell cycle will be arrested. 

9

Gefitinib works well in patients with:

A. T790M gene mutation

B. Underexpressed EGFR

C. Overexpressed EGFR

D. Mutated EGFR with altered tyrosine kinases

C. Overexpressed EGFR

Since Gefitinib works at the tyrosine kinases of EGFR receptors then an overexpressed EGFR receptors will be succeptible to GIfitnib since it is able to block phosphorylation at the level of the kinases. 

10

Which of these mutations can a tumor undergo that will actually increase Gefitinib activity responsiveness? (Select All)

A. L858R Tyrosine Kinase mutation

B. T790M Tyrosine Kinase mutation

C. d746:753 Tyrosine Kinase mutation

D. TLK58 Tyrosine Kinase mutation

A. L858R Tyrosine Kinase Mutation

C. d746:753 Tyrosine Kinase Mutation

 

T790M is actually a tyrosine kinase mutation that Gefitnib AND Erlotinib have less of an effect on. They are mechanisms of resistance. 

11

T/F

Erlotinib is inneffective against the tyrosine kinase mutation T790M

T

12

Which of the following receptor tyrosine kinases is inhibited by Lapatinib? (select all)

A. ErbB1 (EGFR)

B. HER-3

C. ErbB2 (HER-2)

D. ErbB3

A. ErbB1 (EGFR)

B. ErbB2(HER-2)

13

Which of the following statments is true regarding HER-2 (ErbB-2)?

A. Generates a weaker signaling cascade when it dimerizes with another HER-2 receptor

B. Generates a weaker signaling cascade when it dimerizes with an EGFR receptor that is bound to an EGF.

C. Generates a much stronger signaling cascade when it binds to the ligand EGF and dimerizes with another HER-2

D. Generates a much stronger signaling cascade when it dimerizes with an EGFR receptor that is bound to an EGF.

D. Generates a much stronger signaling cascade when it dimerizes with an EGFR receptor that is bound to an EGF.

 

HER receptors do not bind directly with EGF. Instead they will dimerize with an EGFR receptor that already has EGF bound to it. When HER and EGFR dimerize they will produce a much stronger signaling cascade that drives cellular replication in comparison to an EGFR receptor dimerizing with another EGFR receptor. Thats what makes HER-2 receptors so dangerous and problematic.

14

T/F

HER-2 Receptors are constituitvelyl (always) expressed in normal cells.

False

HER-2 receptors are typically only expressed in breast tumors. In other words something has to happen to the cell that causes it to express that type of receptor. 

15

Which of these medications is a monoclonal antibody that blocks EGFR receptor kinases? (Select All)

A. Certuximab

B. Trastuzumab

C. Pertuzumab

D. Panibumumab

A. Certuximab

D. Panibumumab

16

Which of these Small Molecule inhibitors blocks EGFR ONLY? (Select All)

A. Gefitinib

B. Lapatinib

C. Erlotinib

D. Certuximab

A. Gefitinib

C. Erlotinib

 

Lapatinib does block EGFR BUT it also blocks HER-2. 

17

Which of these Monoclonal antibodies blocks HER-2 receptors? (Select All)

A. Certuximab

B. Trastuzumab

C. Panitumumab

D. Pertuzumab

B. Trastuzumab

D. Pertuzumab

18

Which of these Small Molecule Inhibitors blocks both EGFR and HER-2? 

A. Gefitinib

B. Erlotinib

C. Lapatinib

D. Pertuzumab

C. Lapatinib

19

Which of the following Growth Factor Receptor Antagonists has the ability to block ONLY EGFR (Select All)

A. Gefitinib

B. Cetuximab

C. Erlotinib

D. Pertuzumab

E. Lapatinib

F. Panitumumab

A. Gefitinib

B. Cetuximab

C. Erlotinib

D. Panitumumab

20

Which of the following Growth Factor Receptor Antagonists is able to block either HER-2 receptors or HER-2 receptor kinases? (Select All)

A. Lapatinib

B. Erlotinib

C. Cetuximab

D. Trastuzumab

E. Pertuzumab

A. Lapatinib

D. Trastuzumab

E. Pertuzumab

21

Both Cetuximab and Panitumumab are are monoclonal antibodies that block EGFR. The advantage of Panitumumab is that it is ___. 

A. Chimeric

B. Humanized

C. Human

D. Animal

C. Human

Here is a chart that summarizes how you can tell the difference between chimeric, humanized and human

22

T/F

The advantage of Certuximab has over Panitumumab is that a patient taking certuximab will have less of an allergic response in comparison to a patient taking Panitumumab

False

Certuximab is chimeric so it is not completely human like Panitumumab is. The more human-like the monoclonal antibody is the less likely it will produce an allergic response in the patient. 

23

Which of the following statments is true regarding Trastuzumab? (Select All)

A. Chimeric mouse/human monoclonal antibody

B. Binds to EGFR receptors 

C. Binds to HER-2 receptors

D. Can induce antibody-dependent cellular cytotoxicity

E. Can inhibit angiogenesis

A. Chimeric mouse/human monoclonal antibody

C. Binds to HER-2 receptors

D. Can induce antibody-dependent cellular cytotoxicity

E. Can inhibit angiogenesis (she mentioned this)

Antibody-dependent cellular cytotoxicity is possible because the monoclonal antibody binds to the HER-2 receptors and targets the cell for destruction by natural cytotoxic cells in the body. This is it's additional function but its primary function is that it disrupts receptor cell signaling to stop cellular replication. 

24

What is the main clinical toxicity of Trastuzumab that requires a baseline test before administration of the drug?

A. Nephrotoxicity

B. Hepatotoxicity

C. Neurotoxicity

D. Cardiotoxicity

D. Cardiotoxicity

This especially can occur if given with anthracyclines

25

Which other monoclonal antibody is Pertuzumab sometimes used in conjunction with?

A. Certuximab

B. Trastuzumab

C. Panitumumab

D. Gefitinib

B. Trastuzumab

The way I remember this is that they are the only two monoclonal antibodies that bind to HER-2 receptors so they can be used in conjunction. 

26

Why is Pertuzumab used in conjunction with Trastuzumab?

A. Pertuzumab blocks EGFR receptors only and Trastuzumab blocks HER-2 receptors only.

B. Pertuzumab blocks HER-2 receptors only and Trastuzumab blocks EGFR receptors only.

C. Pertuzumab and Trastuzumab both bind at different target regions of the EGFR receptor and therefore complement each others activity at the receptor. 

D. Pertuzumab and Trastuzumab both bind at different target regions of the HER-2 receptor and therefore complement each others activity at the receptor. 

D. Pertuzumab and Trastuzumab both bind at different target regions of the HER-2 receptor and therefore complement each others activity at the receptor. 

27

Increased toxicity is reported when giving Erlotinib or Gefitnib with CYP3A4 ___.

A. Inducers

B. Inhibitors

B. Inhibitors

CYP3A4 is the major metabolic pathway for Erlotinib and Gefitinib so blocking the enzyme will cause accumulation of the drug and cause toxicity. 

28

Which of these Small Molecule Inhibitors is meant to block ABL(Select All)

A. Imatinib

B. Dasatinib

C. Gefitinib

D. Erlotinib

E. Nilotinib

A. Imatinib

B. Dasatinib

E. Nilotinib

When going through the answer choices be sure to identify as much as you can about each drug that is the wrong answer to refresh your knowledge. 

29

Which of these Small Molecule Inhibitors is meant to block ABL? (Select All)

A. Lapatinib

B. Dasatinib

C. Bosutinib

D. Erlotinib

E. Ponatinib

F. imatinib

B. Dasatinib

C. Bosubinib

E. Ponatinib

F. Imatinib

30

Which of these Small Molecule Inhibitors is better suited to bind to Wild-Type ABL? (Select All)

A. Imatinib

B. Bosutinib

C. Nilotinib

D. Dasatinib

E. Ponatinib

C. Nilotinib

D. Dasatinib

31

Which of the following is true regrding the medication Imatinib? (Select All)

A. Inhibits ABL and BCR-ABL

B. Binds at the ATP binding site on ABL

C. Stablizes the ABL in an open (inactive) conformation

D. Inhibits PDGFR

E. Inhibits KIT

A. Inhibits ABL and BCR-ABL

B. Binds at the ATP binding site on ABL

D. Inhibits PDGFR

E. Inhibits KIT

It stabilizes the ABL in the closed inactive state NOT the open state. 

32

What is the name of the hyperactive form of ABL?

A. TCR-ABL

B. TCA-ABL

C. BCR-ABL

D. BCC-ABL

C. BCR-ABL

33

T/F

BCR-ABL have a higher incidence of causing intestinal tumors 

True

34

What are the types of BCR-ABL? (Select All)

A. Random-Type

B. Wild-Type

C. Variant-Type

D. Pred-Type

 

B. Wild-Type

C. Variant-Type

35

Which of the following statments is true regarding KIT? (Select All)

A. Its oncogene is called C-Kit

B. Its oncogene can cause higher incidence of Gastrointestinal Stromal Tumors (GIT or GIST)

C. Uses EGF as its ligand for activation

D. Kit is a cytokine receptor expressed on hematopoietic stem cells

E. Requires Stem Cell factor as its ligand for activation

A. Its oncogene is called C-Kit

B. Its oncogene can cause higher incidence of Gastrointestinal Stromal Tumors (GIT or GIST)

D. Kit is a cytokine receptor expressed on hematopoietic stem cells

E. Requires stem cell factor and its ligand for activation. 

36

Imatinib uses CYP3A4 as its major form of metabolism. We can expect to see toxicities when this medication is given with CYP3A4___.

A. Inhibitors

B. Inducers

A. Inhibitors

37

Which of the following is true regarding the Mechanism of Resistance to Imatinib? 

A. Acquired resistance against Imatinib includes the reduced drug affinity for the kinase BCR-ABL

B. Primary resistance is a common form of resistance for Imabinib after years of use

C. Acquired resistance against Imatinib includes the enahced drug affinity for the kinase BCR-ABL

D. Acquired resistance against Imatinib is the development of the T790M gene mutation. 

A. Acquired resistance against Imatinib includes the reduced drug affinity for the kinase BCR-ABL

T790 is an acquired affinity that is seen in Erlotinib and Gefitnib NOT Imatinib

38

Imatinib is only able to bind to BCR-ABL when it is in the ___-loop conformation.

A. Open

B. Closed

B. Closed

39

Which of these are clinical toxicities of Imatinib? (Select All)

A. Neutropenia

B. Hepatotoxicity

C. Neurotoxicity

D. Thrombocytopenia

A. Neutropenia

D. Thrombocytopenia

40

Which of the following are advantages of Dasatinib and Nilotinib in comparison to Imatinib? (Select All)

A. Dasatinib and Nilotinib have better affinity for the ATP-Binding site in ABL when it is in the open conformation

B. Dasatinib and Nilotinib have greater affinity against Wild-Type BCR-ABL kinases.

C. Dasatinib and Nilotinib are able to bind to the ATP-Binding site in ABL irrespective of the conformation state (open or closed)

D. Dasatinib and Nilotinib are have greater affinity against Variant-Type BCR-ABL kinases 

B. Dasatinib and Nilotinib have greater affinity against Wild-Type BCR-ABL kinases.

C. Dasatinib and Nilotinib are able to bind to the ATP-Binding site in ABL irrespective of the conformation state (open or closed)

41

Which of the following are advantages of Bosutinib and Ponatinib in comparison to Imatinib? 

A. Bosutinib and Ponatinib have greater affinity for the Variant-Type BCR-ABL

B. Bosutinib and Ponatinib have greater affinity for the Wild-Type BCR-ABL

C. Bosutinib and Ponatinib are able to inhibit the T790 gene variant of BCR-ABL

D. Bosutinib and Ponatinib are able to inhibit VEGFR kinases as well.

A. Bosutinib and Ponatinib have greater affinity for the Variant-Type BCR-ABL

42

What is the distinc advantage Ponatinib has over the other BCR-ABL kinase inhibitors?

A. Inhibits the T790M Variant-gene of ABL

B. Inhibits angiogenesis

C. Inhibits the T315I mutant ABL

D. Has increase binding affinity for the Wild-Type BCR-ABL

C. Inhibits the T315I mutant ABL

43

Which of the following is classified as a Small Molecule Antagonist? (Select All)

A. Gefitnib

B. Erlotnib

C. Imatinib

D. Trastuzumab

E. Pertuzumab

F. Dasatinib

A. Gefitinib

B. Erlotinib

C. Imatinib

D. Dasatinib

44

Which of the following Small Molecule Inhibitors is able to block Wild-Type BCR-ABL? (Select All)

A. Dasatinib

B. Erlotinib

C. Gefitinib

D. Bosutinib

E. Nilotinib

A. Dasatinib

E. Nilotinib

45

Which of these medications is able to bind to Variant-Type ABL that has undergone the T325I mutation?

A. Bosutinib

B. Lapatinib

C. Pertuzumab

D. Cetuximab

E. Ponatinib

E. Ponatinib

46

Sorafenib is able to inhibit which of the following? (Select All)

A. EGFR kinases

B. C-RAF

C. B-RAF

D. VEGFR-2

E. PDGFR-B

B. C-RAF

C. B-RAF

D. VEGFR-2 (Vascular Endothelial Growth Factor Receptor)

E. PDGFR-B (Platelet-Derived Growth Factor Receptor)

47

Sorafenib is also known as an ___ inhibitor because it also blocks ___.

A. Platelet, VEGFR-2

B. Angiogenesis, VEGFR-2

C. Angiogenesis, PDGFR-B

D. Clotting factors, PDGFR-B

B. Angiogenesis, VEGFR-2

Aside from being a RAF inhibitor it is also an Angiogenesis inhibitor and is classified accordingly. 

48

What is the MOA of Everolimus?

A. Inhibition of RAF-C

B. Inhibition of RAF-B 

C. Inhibition of EGFR kinases

D. Inhibition of RAS

E. Inhibition of mTOR

E. Inhibtion of mTOR

49

Which of the following medications is a Proteosome Inhibitor?

A. Sorafenib

B. Gefitinib

C. Trastuzumab

D. Bortezomib

D. Bortezomib

50

Which proteosome is responsible for the breakdown of Ubiquitinated proteins and is blocked by Borteozomib? 

A. Proteosome 30S

B. Proteosome 26S

C. Proteosome 15S

D. Proteosome 5S

B. Proteosome 26S

51

What is the overall effect of using a proteosome inhibitor? (Select All)

A. Preventing the degredation of pro-apoptotic factors

B. Increasein Neoplastic cell degredation via apoptosis

C. Increases the turnover rate of cells in the cell cycle

D. Decreases the affinity of neoplastic cell degredation

A. Preventing the degredation of pro-apoptotic factors

B. Increasein Neoplastic cell degredation via apoptosis

52

What are the drug interactions with Bortezomib? (select all)

A. Nephrotoxicity

B. Peripheral neuropathy

C. Hepatotoxicity

D. Neutropenia

E. Thrombocytopenia

B. Peripheral Neuropathy

D. Neutropenia

E. Thrombocytopenia

53

Bortezomib shows decreased effectiveness when given with ___. 

A. Grapefruit juice

B. Benazepril

C. Green tea extract

D. Terazosin

C. Green tea extract

Also remember that Bortezomib is metabolized by CYP3A4, 2D6, 2C19 etc. and can be toxic when given with CYP3A4 inhibitors and polymorphisms of any of these enzymes can affect the medication bioavailability. 

54

Which of these Growth Factor Receptor/Growth Factor Ligand combinations is responsible for causing Angiogenesis?

A. EGFR, EGF

B. PDGFR, PDGF

C. VEGFR, VEGF

D. TEGFR, TEGF

C. VEGFR, VEGF

VEGFR= Vascular Endothelial Growth Factor Receptor

VEGF= Vascular Endothelial Growth Factor

Remember that Angiogenesis is the growth of new blood vessels which is new vasculature and the first word in VEGFR is Vascular

55

Which of the following stimulates the production of VEGF? (Select All)

A. Cytokines

B. Over-oxygenation

C. Body's natural homeostasis

D. Hypoxia

E. Growth factors

F. Oncogenes

A. Cytokines

D. Hypoxia

E. Growth Factors

F. Oncogenes

56

Which of these proteins is responsible for regulating the amount of VEGF that is produced? 

A. VHS

B. VHL

C. VEO

D. VOL

B. VHL (Von-Hippel Lindau protein)

VHL is respnosible for ubiquitination of the transcription factor HIF-1a that codes for VEGF (as well as EPO). When HIF-1a is ubiquitinated by VHL protein it is targeted for proteosome destruction. 

VHL is always expressed to regulate VEGF in times of normal bodily function. VHL is not active when the stimuli for VEGF production are present (cytokines, growth factor, hypoxia, oncogenes)

57

T/F

It would be favorable in renal carcinoma for the cancer to mutate VHL and cause its over production.

False

It would mutate VHL for underexpression in order to prevent VHL ubiquitination of VEGF. That way the cancer cell can promote angiogenesis and aquire a blood vessel formation that supplies the tumor with blood. 

58

Which of these medications is an Angiogenesis inhibitor and blocks VEGF (ligand)?

A. Sorafenib

B. Ipilimumab

C. Gefitinib

D. Trastuzumab

E. Bevacizumab

E. Bevacizumab

59

Which of these medications is an Angiogenesis inhibitor that blocks VEGFR receptor kinases? (Select All)

A. Bevacizumab

B. Sorafenib

C. Lapatinib

D. Imatinib

E. Sunitinib

B. Sorafenib

E. Sunitinib

60

Which of these medications are Anbiogenesis Inhibitors that block bFGF? (Select All)

A. Sorafenib

B. Thalidomide

C. Lenalidomide

D. Bevacizumab

B. Thalidomide

C. Lenalidomide

61

What is the suspected MOA of Bevacizumab when it bids to VEGF? (Select All)

A. Induction of tumor hypoxia and starvation

B. Generates large influx of oxygen and causes tumor cell to rupture

C. Increases delivery of chemotherapeutic medications, potentiating their effects

D. Increases affinity for kinases of other medications

A. Induction of tumor hypoxia and starvation

C. Increases delivery of chemotherapeutic medications, potentiating their effects

62

What is the common risk that all Angiogeneisis inhibitor share

A. Risk of clotting

B. Risk of bleeding

C. Risk of DVT

D. Risk of VTE

B. Risk of bleeding

63

Which receptor kinases do Sorafenib and Sunitinib bind to? (Select all)

A. VEGFR

B. B-RAF

C. Kit

D. PDGFR

A. VEGFR

D. PDGFR

They have these in common but they also bind to unique receptor kinases.

Sorafenib also binds to B-RAF

Sunitinib also binds to KIT

64

Regorafenib is an Angiogenesis Inhibitor that is a  Small Molecule Inhibitor that binds to: (Select All)

A. EGFR

B. TIE2-TK

C. VEGFR-2

D. PDGFR-B

B. TIE2-TK

C. VEGFR-2

65

Which of these medications is an Angiogenesis antabonist that is classified as a recombinant fusion protein?

A. Gefitinib

B. Erlotininb

C. Ziv-aflibercept

D. Imatinib

C. Ziv-afliercept

66

How does Ziv-aflibercept prevent Angiogenesis?

A. Binds to VEGFR receptors at the binding site

B. Binds to the ligand VEGF-A and prevents it from reaching the target VEGFR receptor. 

C. Binds to VEGFR kinases and prevent phosphorylation from occuring

D. None of the above

B. Binds to the ligand VEGF-A and prevents it from reaching the target VEGFR receptor. 

67

Which of the following statements is true regarding bFGF is FALSE?

A. Resides in the sub-endothelial extracellular matrix of blood vessels 

B. Stays membrane-bound until activated

C. During wound healing heparin sulfat-degrading enzymes activate bFGF

D. bFGF mediates the formation of new blood vessels.

E. bFGF is utilized by tumor cells in order to degrade blood vessels of the body, causing extensive bleeding.

E. bFGF is utilized by tumor cells in order to degrade blood vessels of the body, causing extensive bleeding.

68

Which of these are Angiogeneis Inhibitors that inhibit bFGF? (Select all)

A. Sorafenib

B. Sunitinib

C. Ziv-aflibercept

D. Thalidomide

E. Lenalidomide

D. Thalidomide

E. Lenalidomide

69

All of the following medications are Angiogenesis inhibitors EXCEPT:

A. Bevacizumab

B. Sunitinib

C. Ziv-Aflibercept

D. Regorafenib

E. Lenalidomide

F. Bortezomib

F. Bortezomib

try identifying the other medication MOAs

70

Which of these medications are Immune Checkpoint Inhibitors?

A. Bevacizumab

B. Ipilimumab

C. Pembrolizumab

D. Nivolumab

E. Rituximab

B. Ipilimumab

C. Pembrolizumab

D. Nivolumab

71

Which of these Immune Checkpoint Inhibitors inhibits CTLA-4 receptors on T-Cells?

A. Ipilimumab

B. Pembrolizumab

C. Nivolumab

D. Rituximab

A. Ipilimumab

72

Which of these Immune Checkpoint Inhibitors binds to PD-1 on the surface of T-Cells? (Select All)

A. Ipilimumab

B. Pembrolizumab

C. Imatinib

D. Sorafenib

E. Nivolumab

B. Pembrolizumab

E. Nivolumab

73

What is the possible MOA of tumor-specific monoclonal antibodies? (Select All)

A. Enhance binding to tumor-specific EGFR

B. Induction of antibody dependent cell-mediated cytotoxicity

C. Induction of apoptosis of the cancer cell

D. Enhance binding to tumor-specific EGFR kinases

B. Induction of antibody depenent cell-mediated cytotoxicity

C. Induction of apoptosis of the cancer cell

74

Which of these medications is a Tumor-Specific Monoclonal Antibody? (Select All)

A. Ipilimumab

B. Bevacizumab

C. Rituximab

D. Trastuzumab

E. Alemtuzumab

C. Rituximab

E. Alemtuzumab

75

Rituximab binds to ___ receptors that are located on ___. 

A. CD52, B-Cells

B. CD20, B-Cells

C. CD52, T-Cells

D. CD20, T-Cells

B. CD20, B-Cells

B-Cell lymphomas express CD20 on their cell surfaces so this medication will allow the binding to that receptor and help target the cancer cell for antibody-dependent cell-mediated cytotoxicity

76

Alemtuzumab binds to ___ receptors on ___ and ___ .

A. CD20, T-Cells and B-Cells

B. CD54, T-Cells and B-Cells

C. CD20, T-Cells and Dendritic cells

D. CD54, T-Cells and Dendritic cells

B. CD54, T-Cells and B-Cells

77

Match the Specialty MoAB with their corrrect identification:

A. Radioactive Isotope

B. Diptheria Toxin

C. Antibiotic Calicheamicin 

1. Gemtuzumab

2. Ibritumomab and Tosimomab

3. Denileukin Diftitox

1: Gemtuzumab= Antibiotic Calicheamicin (C)

2: Ibritumomab and Tosimomab= Radioactive isotope (A)

2: Denileukin Diftitox= Diptheria Toxin

 

We may not need to know which one belongs to which for the test but she does want us to know that the three types of MoABs do exist. 

78