Cytotoxic and Targeted Therapy (Monoclonal Antibodies) MCQs

Pharmacology · 102 free questions with answers & explanations.

1. Imatinib revolutionized CML treatment by targeting the BCR-ABL kinase. The mechanism by which resistance develops most commonly to imatinib is:
2. Trastuzumab (Herceptin) is used in HER2-positive breast cancer. Its primary mechanism of antitumor action is:
3. Immune checkpoint inhibitors (nivolumab, pembrolizumab) targeting PD-1 cause immune-related adverse events. The organ most frequently affected in severe immune-related adverse events is:
4. Imatinib (Gleevec) revolutionized CML treatment. Resistance to imatinib most commonly arises through which mechanism, and what is the preferred next-line agent?
5. Pembrolizumab (anti-PD-1 monoclonal antibody) causes immune-related adverse events (irAEs). Which mechanism is responsible for pembrolizumab-induced hypophysitis?
6. Imatinib is a BCR-ABL tyrosine kinase inhibitor for CML. Resistance develops in most patients over time. The most common mechanism of imatinib resistance in CML is:
7. Pembrolizumab is a PD-1 checkpoint inhibitor. Its immune-related adverse effects (irAEs) share a common pathophysiology. The mechanism of irAEs is:
8. Venetoclax, approved for CLL and AML with specific mutations, induces apoptosis by a mechanism distinct from classical cytotoxics. Its target and primary clinical risk is:
9. Imatinib is a BCR-ABL tyrosine kinase inhibitor. The T315I mutation ('gatekeeper mutation') in BCR-ABL causes resistance because:
10. Bevacizumab is an anti-VEGF monoclonal antibody used in solid tumours. Its primary anti-tumour mechanism is:
11. Immune checkpoint inhibitor (anti-PD-1, e.g., pembrolizumab) associated pneumonitis as an immune-related adverse event is BEST managed initially with:
12. Pembrolizumab exerts its anti-tumour effect by blocking PD-1 on T cells. The downstream signalling consequence of PD-1 activation that pembrolizumab reverses is:
13. Imatinib resistance in CML due to the T315I mutation (gatekeeper mutation) in BCR-ABL is overcome by which third-generation tyrosine kinase inhibitor?
14. Trastuzumab deruxtecan (T-DXd) is an antibody-drug conjugate for HER2-positive breast cancer. Its mechanism of killing HER2-low expressing cells beyond the target cell ('bystander killing') is unique to its payload. What property of the payload enables this?
15. Imatinib revolutionised the treatment of CML. Resistance to imatinib most commonly arises from which mechanism, and which second-generation TKI overcomes this?
16. Pembrolizumab is an anti-PD-1 antibody used in multiple cancers. The predictive biomarker that most reliably identifies patients likely to respond to anti-PD-1 therapy in solid tumours is:
17. Trastuzumab (anti-HER2 antibody) is used in HER2-positive breast cancer. Its mechanism of action beyond inhibiting HER2 dimerisation includes which important immune effector function?
18. Imatinib resistance in CML most commonly arises from T315I point mutation in BCR-ABL. Ponatinib is specifically designed to overcome T315I resistance because:
19. A patient with HER2-positive breast cancer is treated with trastuzumab emtansine (T-DM1). The mechanism of tumor selectivity of T-DM1 compared to free DM1 (maytansine derivative) is that:
20. Pembrolizumab's mechanism of action in cancer immunotherapy involves blocking the PD-1/PD-L1 checkpoint. The reason PD-1 blockade is more effective than PD-L1 blockade in some tumors relates to the fact that PD-1 also interacts with:
21. KRAS G12C mutation is now a targetable oncogenic driver. Which drug specifically targets this mutation and what is its unique mechanism?
22. Which mechanism of resistance is most commonly observed in patients with BCR-ABL1-positive CML who develop resistance to dasatinib?
23. A patient with metastatic melanoma develops immune checkpoint inhibitor-related pneumonitis while on pembrolizumab. Management with steroids is initiated. Which mechanism specifically explains why pembrolizumab causes autoimmune adverse effects?
24. Imatinib (Gleevec) resistance in CML most commonly develops through ABL kinase domain point mutations. The T315I ('gatekeeper') mutation confers resistance to imatinib, dasatinib, and nilotinib. Which third-generation BCR-ABL inhibitor was specifically developed to overcome T315I?
25. Trastuzumab (anti-HER2) combined with pertuzumab for HER2+ breast cancer — what is the rationale for combining two HER2-targeted antibodies with different binding epitopes?
26. Pembrolizumab and nivolumab are PD-1 checkpoint inhibitors. A patient develops immune-related pneumonitis grade 3 (severe). What is the FIRST-LINE management, and why are systemic steroids used rather than drug-specific antidotes?
27. Imatinib resistance in CML arising from the BCR-ABL T315I (gatekeeper) mutation is best treated with:
28. Pembrolizumab, an anti-PD-1 monoclonal antibody, causes immune-related adverse events (irAEs) because:
29. Venetoclax (ABT-199) is a highly selective BCL-2 inhibitor used in CLL. The tumor lysis syndrome risk with venetoclax is particularly high because:
30. Imatinib resistance in CML after initial response most commonly develops through which mechanism, and which drug is used to overcome it?
31. Trastuzumab (anti-HER2) combined with pertuzumab provides superior benefit in HER2-positive breast cancer compared to trastuzumab alone because:
32. Pembrolizumab, an anti-PD-1 checkpoint inhibitor, can cause immune-related adverse events (irAEs). A patient develops grade 3 immune-related hepatitis 8 weeks after starting pembrolizumab for NSCLC. The correct management is:
33. Imatinib resistance in chronic myeloid leukemia (CML) most commonly occurs via which mechanism, and which second-generation TKI overcomes most but NOT the T315I ('gatekeeper') mutation?
34. Pembrolizumab and nivolumab are anti-PD-1 monoclonal antibodies used in cancer immunotherapy. Immune-related adverse events (irAEs) in these drugs are caused by which mechanism?
35. Osimertinib is a third-generation EGFR-TKI effective against the T790M resistance mutation. When osimertinib resistance develops via a C797S mutation, which combination treatment rationale applies?
36. Trastuzumab emtansine (T-DM1) exemplifies antibody-drug conjugate (ADC) design. Which pharmacological concept explains why T-DM1 causes less systemic toxicity than free emtansine (DM1)?
37. Pembrolizumab and nivolumab are PD-1 checkpoint inhibitors. Immune-related adverse events (irAEs) are their main toxicity. Which cytokine pathway is primarily responsible for pembrolizumab-induced pneumonitis?
38. Imatinib (a BCR-ABL tyrosine kinase inhibitor) resistance in CML commonly develops due to which mutation?
39. Trastuzumab (anti-HER2 monoclonal antibody) exerts its antitumour effect through which mechanism?
40. Pembrolizumab and nivolumab treat cancer by blocking which checkpoint inhibitory pathway?
41. Venetoclax is used in CLL and AML. Its mechanism of action is:
42. A patient with CML on imatinib develops resistance due to T315I 'gatekeeper' mutation. Which drug overcomes this specific mutation, and why does T315I confer resistance to imatinib, dasatinib, and nilotinib?
43. Pembrolizumab is a PD-1 checkpoint inhibitor used in solid tumours. A patient develops pembrolizumab-induced immune checkpoint myocarditis. The immunological mechanism of this irAE involves:
44. Imatinib, a tyrosine kinase inhibitor, achieves selectivity for the BCR-ABL oncoprotein (in CML) by:
45. Trastuzumab (Herceptin) causes cardiac toxicity (cardiomyopathy) that is different from anthracycline cardiotoxicity because:
46. Rituximab, a monoclonal antibody used in B-cell lymphomas and autoimmune diseases, targets:
47. Methotrexate causes mucositis and bone marrow suppression as dose-limiting toxicities. 'Leucovorin rescue' given after high-dose MTX administration works by:
48. Pembrolizumab and nivolumab are immune checkpoint inhibitors targeting PD-1. Their immune-related adverse effects (irAEs) — colitis, thyroiditis, pneumonitis, hepatitis — are best managed with:
49. Imatinib mesylate revolutionized treatment of CML. Its mechanism of action is best described as:
50. Trastuzumab (Herceptin) is used in HER2-positive breast cancer. Its mechanism involves:
51. Bevacizumab is a monoclonal antibody used in colorectal cancer. It targets which molecule?
52. Imatinib (a BCR-ABL tyrosine kinase inhibitor) is used for CML. The T315I gating mutation of BCR-ABL confers resistance to imatinib, dasatinib, and nilotinib. Which drug overcomes T315I resistance?
53. Trastuzumab (anti-HER2 monoclonal antibody) mediates anti-tumour effects through which primary mechanism in HER2-overexpressing breast cancer?
54. Pembrolizumab is an anti-PD-1 checkpoint inhibitor used for various cancers. Its immune-related adverse events (irAEs) are predominantly mediated by:
55. Imatinib (Gleevec) revolutionised CML treatment by inhibiting which molecular target?
56. A 55-year-old woman with HER2-positive breast cancer receives trastuzumab (Herceptin). Which mechanism of action correctly describes trastuzumab's anti-tumour effect?
57. Cyclophosphamide is an alkylating agent that requires hepatic bioactivation. The active metabolite responsible for its cytotoxic and immunosuppressive effect is:
58. Pembrolizumab is a programmed cell death protein 1 (PD-1) inhibitor used in various cancers. Immune-related adverse events (irAEs) are common. Which irAE is most immediately life-threatening and requires immediate high-dose corticosteroid therapy?
59. Imatinib mesylate (Gleevec) revolutionised CML treatment by specifically targeting:
60. Trastuzumab (Herceptin) is used in HER2-positive breast cancer. Its mechanism of cardiotoxicity (asymptomatic LV dysfunction/heart failure) differs from anthracycline cardiotoxicity because trastuzumab-associated dysfunction is:
61. Imatinib revolutionized treatment of CML. Its mechanism of selective toxicity to CML cells involves:
62. A patient with HER2-positive breast cancer is treated with trastuzumab (Herceptin). Despite initial response, the tumor becomes resistant. Pertuzumab is added, and it provides benefit despite the same resistance because it:
63. Pembrolizumab is used in multiple solid tumors including lung cancer. Its mechanism is:
64. Imatinib mesylate revolutionised the treatment of CML. Its molecular target is the BCR-ABL tyrosine kinase. The mechanism by which imatinib specifically inhibits BCR-ABL is:
65. Bevacizumab is used in metastatic colorectal cancer. It is a monoclonal antibody targeting VEGF-A. The predominant mechanism by which bevacizumab enhances the efficacy of co-administered chemotherapy (beyond direct antitumour effects) is:
66. PARP inhibitors (olaparib, niraparib) selectively kill BRCA1/2-deficient cancer cells by a concept termed 'synthetic lethality.' The mechanism is:
67. Immune checkpoint inhibitors (anti-PD-1/anti-PD-L1) cause immune-related adverse events (irAEs) in multiple organ systems. The pathomechanism of irAEs is:
68. CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib) are approved for hormone receptor-positive (HR+), HER2-negative metastatic breast cancer. Their mechanism of action involves:
69. Imatinib mesylate revolutionised CML treatment. Its mechanism of action is:
70. A 52-year-old woman with HER2-positive metastatic breast cancer is started on trastuzumab. The drug's mechanism of action includes:
71. Pembrolizumab and nivolumab are immune checkpoint inhibitors used in cancer immunotherapy. The immune pathway they target is:
72. Imatinib (Gleevec) revolutionized treatment of CML. Its mechanism of resistance through ABL kinase domain mutation at Thr315 (T315I, the 'gatekeeper' mutation) is significant because:
73. Pembrolizumab is an anti-PD-1 monoclonal antibody used in multiple cancers. Its immune-related adverse events (irAEs) are mechanistically explained by:
74. Trastuzumab (Herceptin) is used for HER2-positive breast cancer. Beyond blockade of HER2 receptor signaling, which additional mechanism of action contributes to its anti-tumor efficacy?
75. A patient with CML is started on imatinib. After 2 years, he develops resistance. The MOST common mechanism is:
76. Trastuzumab (Herceptin) is used for HER2-positive breast cancer. Its mechanism of antitumor activity is BEST described as:
77. Bevacizumab, a VEGF-A monoclonal antibody, is used in colorectal cancer. The most clinically significant adverse effect that must be screened for before initiating therapy is:
78. Imatinib (Gleevec) revolutionised CML treatment by targeting which specific molecular abnormality?
79. A patient with metastatic colorectal cancer is found to have a KRAS wild-type tumour and is given cetuximab (anti-EGFR monoclonal antibody). Why is KRAS wild-type status necessary for cetuximab to be effective?
80. Imatinib (Gleevec) revolutionised CML treatment. Its mechanism of action and the molecular target are:
81. Pembrolizumab is a checkpoint inhibitor approved for several cancers. Its mechanism is:
82. Imatinib mesylate achieves remission in CML by specifically targeting BCR-ABL tyrosine kinase. The mechanism by which it inhibits this kinase is:
83. Rituximab is a chimeric anti-CD20 monoclonal antibody. The predominant mechanism by which rituximab kills B cells in lymphoma is:
84. Imatinib (Gleevec) revolutionised CML treatment. It acts as a competitive inhibitor of the ATP-binding site of BCR-ABL tyrosine kinase. Resistance to imatinib most commonly develops through:
85. Rituximab, an anti-CD20 monoclonal antibody, does NOT affect plasma cells in multiple myeloma because:
86. Pembrolizumab is a checkpoint inhibitor targeting PD-1 (programmed death-1). Its immune-mediated anti-tumour activity results from:
87. Imatinib (gleevec) revolutionized treatment of CML. After years of response, a patient develops resistance. Dasatinib overcomes most imatinib resistance mutations except T315I (gatekeeper mutation). Why does the T315I mutation confer resistance to both imatinib and first-generation TKIs but not ponatinib?
88. Trastuzumab (anti-HER2 monoclonal antibody) is used in HER2-overexpressing breast cancer. A patient develops trastuzumab-related cardiomyopathy. Unlike anthracycline cardiotoxicity, trastuzumab cardiac toxicity is:
89. A 55-year-old woman with HER2-positive metastatic breast cancer is treated with trastuzumab but develops resistance after 18 months. Trastuzumab-deruxtecan (T-DXd) is started as second-line therapy. What structural feature distinguishes antibody-drug conjugates (ADCs) like T-DXd from standard monoclonal antibodies and explains their activity in trastuzumab-resistant tumors?
90. Imatinib (STI-571) revolutionized CML treatment. After decades of use, patients on imatinib occasionally develop resistance. The most common mutation causing imatinib resistance in BCR-ABL positive CML is the T315I 'gatekeeper' mutation. What third-generation TKI specifically overcomes this mutation?
91. A 50-year-old man with non-small cell lung cancer (NSCLC) tests positive for EGFR exon 19 deletion. He is started on osimertinib as first-line therapy. What is the specific pharmacological advantage of osimertinib over first-generation EGFR TKIs (erlotinib, gefitinib) for EGFR-mutant NSCLC?
92. Imatinib (Gleevec) was the first targeted kinase inhibitor approved for CML. Primary resistance to imatinib most commonly occurs due to:
93. Trastuzumab (Herceptin) targets HER2 (ErbB2) overexpressed in ~15–20% of breast cancers. Beyond blocking ligand-independent dimerisation, trastuzumab's additional anti-tumour mechanisms include:
94. Imatinib (a first-generation TKI) is used in CML. Its mechanism and the basis of resistance via T315I mutation are:
95. Rituximab is a monoclonal antibody used in CD20-positive B-cell lymphomas. Its mechanisms of B-cell killing include all EXCEPT:
96. Trastuzumab (Herceptin) is used in HER2-positive breast cancer. Its pharmacological mechanisms include:
97. Pembrolizumab (anti-PD-1) and ipilimumab (anti-CTLA-4) are checkpoint inhibitors. The distinct immune regulation site of each is:
98. Imatinib revolutionised the treatment of CML. Its primary mechanism involves:
99. Rituximab targets CD20 on B-lymphocytes. CD20 is absent on plasma cells; this explains why rituximab:
100. Checkpoint inhibitors like pembrolizumab act on the immune system rather than directly on tumor cells. Its target, PD-1, when ligated by PD-L1 expressed on tumors, causes:
101. Cyclophosphamide is an alkylating agent that requires hepatic activation. The metabolite responsible for its antineoplastic effect and its dose-limiting hemorrhagic cystitis is:
102. Bevacizumab is used in metastatic colorectal cancer. It exerts its antitumour effect by: