Principles of Chemotherapy, Immunotherapy and Targeted Therapy — MCQs
Antigen presented on MHC class I molecules activates which of the following cells?
Match the following drugs with the targets of their actions: Drugs: A. Trastuzumab B. Infliximab C. Sirolimus D. Imatinib Targets: 1. BCR-ABL tyrosine kinase 2. mTOR 3. TNF alpha 4. HER2/neu
Cells are most sensitive to ionizing radiation during which phase?
What is true about HER2/neu overexpression in cancer?
Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-
Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
Therapeutic exposure is a core technique primarily used in which type of therapy?
Which of the following drugs is associated with untoward side effect of renal tubular damage?
What is the treatment for HER-2 positive trastuzumab resistant breast cancer?
Transition from G2 to M phase of the cell cycle is controlled by which?
Principles of Chemotherapy, Immunotherapy and Targeted Therapy Indian Medical PG Practice Questions and MCQs
Question 1: Antigen presented on MHC class I molecules activates which of the following cells?
- A. NK cells
- B. Helper cells
- C. B cells
- D. Cytotoxic T cells (Correct Answer)
Explanation: ***Cytotoxic T cells*** - **MHC class I** molecules present **intracellular antigens** (e.g., viral or tumor antigens) to **CD8+ T cells** (cytotoxic T cells). - This binding activates the cytotoxic T cells, leading to the destruction of the **infected** or **abnormal host cell**. *NK cells* - **Natural Killer (NK) cells** recognize and kill target cells that have **reduced or absent MHC class I** expression, which often occurs in virally infected or tumor cells, not cells presenting antigens on MHC class I. - They are part of the **innate immune system** and do not require prior sensitization or MHC-peptide presentation for activation. *Helper cells* - **Helper T cells** (CD4+ T cells) recognize antigens presented on **MHC class II** molecules, typically expressed by **antigen-presenting cells** (APCs) like macrophages, B cells, and dendritic cells. - Their primary role is to **orchestrate immune responses** by releasing cytokines. *B cells* - **B cells** are primarily involved in **humoral immunity**, producing antibodies after recognizing specific antigens directly via their B cell receptors or with T cell help. - While they can present antigens on **MHC class II** to helper T cells, direct antigen binding to **MHC class I** does not activate B cells.
Question 2: Match the following drugs with the targets of their actions: Drugs: A. Trastuzumab B. Infliximab C. Sirolimus D. Imatinib Targets: 1. BCR-ABL tyrosine kinase 2. mTOR 3. TNF alpha 4. HER2/neu
- A. A-2, B-3, C-1, D-4
- B. A-3, B-4, C-2, D-1
- C. A-4, B-3, C-1, D-2
- D. A-4, B-3, C-2, D-1 (Correct Answer)
Explanation: ***Correct Answer: A-4, B-3, C-2, D-1*** - **Trastuzumab** (Herceptin) is a **monoclonal antibody** that targets the **HER2/neu receptor (4)** [1], [2], commonly overexpressed in certain breast cancers and gastric cancers. - **Infliximab** is another **monoclonal antibody** that specifically targets and neutralizes **TNF-alpha (3)**, an inflammatory cytokine, making it useful in treating autoimmune diseases like rheumatoid arthritis and Crohn's disease. - **Sirolimus** is an **immunosuppressant** drug that inhibits the mammalian target of rapamycin (**mTOR (2)**), a protein kinase involved in cell growth and proliferation, used in transplant medicine and as an anticancer agent. - **Imatinib** is a **tyrosine kinase inhibitor** that primarily targets the **BCR-ABL fusion protein (1)** [1], [2], which is characteristic of chronic myeloid leukemia. *Incorrect: A-2, B-3, C-1, D-4* - This option incorrectly matches Trastuzumab with mTOR and Sirolimus with BCR-ABL, which are not their primary targets. - Trastuzumab targets HER2/neu [1], [2], and Sirolimus targets mTOR. *Incorrect: A-3, B-4, C-2, D-1* - This option incorrectly matches Trastuzumab with TNF-alpha and Infliximab with HER2/neu. - Infliximab targets TNF-alpha, and Trastuzumab targets HER2/neu [1], [2]. *Incorrect: A-4, B-3, C-1, D-2* - This option incorrectly matches Sirolimus with BCR-ABL and Imatinib with mTOR. - Sirolimus inhibits mTOR, and Imatinib inhibits BCR-ABL [1], [2].
Question 3: Cells are most sensitive to ionizing radiation during which phase?
- A. S phase
- B. G2M phase (Correct Answer)
- C. G0 phase
- D. G1 phase
Explanation: ***G2M phase*** - Cells are most sensitive to ionizing radiation during the **G2 phase** and **M phase** (mitosis) due to the highly condensed chromatin structure and active DNA repair mechanisms being less efficient [2], [3]. - During G2, DNA synthesis is complete, and the cell is preparing for division, making DNA damage particularly detrimental and harder to repair without compromising cell viability [2]. *S phase* - Cells in the **S phase** (DNA synthesis phase) are relatively radioresistant because of active **DNA replication** and associated repair mechanisms. - These repair pathways are highly efficient at correcting DNA damage during replication, making the cell less susceptible to radiation-induced lethality. *G1 phase* - Cells in the **G1 phase** (first gap phase) show intermediate radiosensitivity. - While less sensitive than G2/M phases, G1 cells are more vulnerable than those in late S phase due to active metabolic preparation for DNA synthesis [1]. *G0 phase* - Cells in the **G0 phase** (quiescent phase) are generally **radioresistant** because they are not actively dividing or synthesizing DNA [3]. - They have ample time for DNA repair before re-entering the cell cycle, and their DNA structure is less vulnerable than during active division [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 436-437.
Question 4: What is true about HER2/neu overexpression in cancer?
- A. Good prognosis
- B. Responds well to taxanes
- C. Responds well to monoclonal antibodies (Correct Answer)
- D. Seen in various cancers, including breast cancer
Explanation: ***Responds well to monoclonal antibodies*** - HER2/neu overexpression is targeted by **monoclonal antibodies** like trastuzumab (Herceptin), improving treatment outcomes [1]. - These therapies are specifically designed to **inhibit HER2-positive** tumors, leading to better overall prognosis compared to those without such therapies [1]. *Good prognosis* - HER2/neu overexpression is generally associated with a **poor prognosis** due to increased aggressiveness of the cancer. - It correlates with **higher rates of recurrence** and metastasis compared to HER2-negative breast cancers. *Responds well to taxanes* - While taxanes are commonly used in breast cancer treatment, HER2/neu positivity does not specifically imply a good response. - Response rates may not significantly differ based on HER2 status for taxane-based therapies alone. *Seen only in breast cancer* - HER2/neu overexpression can also occur in other cancers, such as **gastric and gastroesophageal junction cancers**. - It is not exclusive to breast cancer, though it is most commonly studied in this context [1].
Question 5: Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-
- A. Cyclophosphamide toxicity
- B. Doxorubicin toxicity
- C. Methotrexate toxicity (Correct Answer)
- D. Cisplatin toxicity
Explanation: ***Methotrexate toxicity*** - **Folinic acid (leucovorin)** is a reduced folate that bypasses the metabolic block caused by **methotrexate** on dihydrofolate reductase. - It replenishes the body's **folate stores** and protects healthy cells from methotrexate's cytotoxic effects, particularly in the bone marrow and gastrointestinal tract. *Cyclophosphamide toxicity* - **Cyclophosphamide** toxicity, primarily hemorrhagic cystitis, is prevented by **mesna** (2-mercaptoethane sulfonate). - Mesna inactivates the urotoxic metabolite **acrolein** in the urine, preventing bladder damage. *Doxorubicin toxicity* - **Doxorubicin** causes cardiotoxicity, which can be mitigated by the iron-chelating agent **dexrazoxane**. - Dexrazoxane reduces the formation of **free radicals** that contribute to doxorubicin-induced myocardial damage. *Cisplatin toxicity* - **Cisplatin** toxicity, especially nephrotoxicity, is largely prevented by **aggressive hydration** and administration of **diuretics**. - **Amifostine** is another agent that can reduce cisplatin-induced nephrotoxicity, neurotoxicity, and ototoxicity by acting as a cytoprotectant.
Question 6: Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
- A. Cyclophosphamide
- B. Methotrexate
- C. Cisplatin (Correct Answer)
- D. Dacarbazine
Explanation: ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug that forms **DNA cross-links**, inhibiting DNA synthesis and leading to the death of rapidly dividing cells, making it highly effective against **ovarian carcinoma**. - It is a cornerstone of chemotherapy regimens for ovarian cancer, often used in combination with other agents such as paclitaxel. *Methotrexate* - **Methotrexate** is an **antimetabolite** that inhibits dihydrofolate reductase, thereby interfering with DNA synthesis. - While it is used in various cancers like leukemia, lymphoma, and some solid tumors (e.g., breast cancer, gestational trophoblastic disease), it is **not a primary recommended drug for ovarian carcinoma**. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that causes DNA damage, leading to cell death. - It is used in many cancers, including lymphoma, breast cancer, and some leukemias, but it is **not a first-line or primary agent for ovarian carcinoma** in contemporary treatment guidelines. *Dacarbazine* - **Dacarbazine** is an **alkylating agent** primarily used in the treatment of **malignant melanoma** and Hodgkin lymphoma. - It is **not indicated for the treatment of ovarian carcinoma**.
Question 7: Therapeutic exposure is a core technique primarily used in which type of therapy?
- A. Behavior therapy with exposure techniques (Correct Answer)
- B. Cognitive therapy modifying thought patterns
- C. Supportive therapy providing emotional support
- D. Psychoanalysis focusing on unconscious conflicts
Explanation: ***Behavior therapy with exposure techniques*** - **Exposure therapy** is a core component of **behavior therapy**, specifically designed to address **anxiety disorders** and phobias by gradually exposing individuals to feared stimuli. - The goal is to reduce fear and avoidance behaviors by helping the individual learn that the feared object or situation is harmless and that their anxiety will naturally decrease over time (habituation). *Cognitive therapy modifying thought patterns* - **Cognitive therapy** focuses on identifying and changing **maladaptive thought patterns** and beliefs that contribute to psychological distress. - While it may be combined with behavioral techniques, **exposure** itself is not its primary methodology but rather a behavioral intervention. *Supportive therapy providing emotional support* - **Supportive therapy** aims to reduce distress by offering **emotional support**, encouragement, and practical advice, helping patients cope with current stressors. - It does not typically involve structured techniques like exposure to modify specific behaviors or thought patterns, but rather a more empathetic and less directive approach. *Psychoanalysis focusing on unconscious conflicts* - **Psychoanalysis** is a long-term, intensive therapy that explores **unconscious conflicts**, repressed memories, and past experiences to bring them to conscious awareness. - Its techniques include **free association**, dream analysis, and transference interpretation, rather than direct exposure to feared stimuli.
Question 8: Which of the following drugs is associated with untoward side effect of renal tubular damage?
- A. Streptozotocin
- B. Methysergide
- C. Cyclophosphamide
- D. Cisplatin (Correct Answer)
Explanation: ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug well-known for its dose-limiting nephrotoxicity, primarily causing **renal tubular damage**. - Its mechanism involves direct DNA damage within renal tubular cells, leading to **acute tubular necrosis** if not managed with aggressive hydration and other protective measures. *Streptozotocin* - **Streptozotocin** is an alkylating agent primarily used in treating **pancreatic neuroendocrine tumors**; its main toxicity is typically to pancreatic beta cells (leading to hypoglycemia) and to the liver. - While it can be nephrotoxic, its predominant and most recognized untoward side effect is not renal tubular damage, but rather **pancreatic beta-cell destruction**. *Methysergide* - **Methysergide** is an ergot alkaloid used for **migraine prophylaxis** but is largely discontinued due to severe side effects like **retroperitoneal fibrosis**. - Renal damage in the context of methysergide is typically due to this fibrosis compressing the ureters, rather than direct tubular toxicity. *Cyclophosphamide* - **Cyclophosphamide** is an alkylating agent known for its immunosuppressive and chemotherapeutic effects; its major side effects include **hemorrhagic cystitis** and myelosuppression. - While high doses can cause nephrotoxicity, its primary and most feared renal-related toxicity is hemorrhagic cystitis, not direct tubular damage as seen with cisplatin.
Question 9: What is the treatment for HER-2 positive trastuzumab resistant breast cancer?
- A. Sorafenib
- B. Lapatinib (Correct Answer)
- C. Vemurafenib
- D. Erlotinib
Explanation: ***Lapatinib*** - Lapatinib is a **dual tyrosine kinase inhibitor** that targets both **HER-2** and **epidermal growth factor receptor (EGFR)**, acting as a **small molecule inhibitor** that binds to the intracellular domain of these receptors. - Unlike trastuzumab (a monoclonal antibody targeting the extracellular domain), Lapatinib's **intracellular mechanism of action** allows it to overcome common mechanisms of trastuzumab resistance, such as receptor truncation or masking of the extracellular epitope. - It is specifically approved for the treatment of **HER-2 positive metastatic breast cancer** in combination with capecitabine after progression on trastuzumab-containing regimens. *Sorafenib* - Sorafenib is a **multi-kinase inhibitor** primarily targeting RAF, VEGFR, and PDGFR, and is used in renal cell carcinoma and hepatocellular carcinoma. - It does not specifically target HER-2 and is **not indicated** for HER-2 positive trastuzumab-resistant breast cancer. *Vemurafenib* - Vemurafenib is a **BRAF inhibitor** used for treating BRAF V600E mutation-positive melanoma. - This drug has no direct indications or demonstrated efficacy for **HER-2 positive breast cancer** and does not address trastuzumab resistance mechanisms. *Erlotinib* - Erlotinib is an **EGFR tyrosine kinase inhibitor** primarily used for non-small cell lung cancer with activating EGFR mutations. - While it targets EGFR, it does **not effectively target HER-2** and lacks the dual inhibition necessary to overcome trastuzumab resistance in HER-2 positive breast cancer.
Question 10: Transition from G2 to M phase of the cell cycle is controlled by which?
- A. Retinoblastoma gene product
- B. p53 protein
- C. Cyclin E
- D. Cyclin B (Correct Answer)
Explanation: ***Cyclin B*** - The transition from G2 to M phase is primarily controlled by the **maturation-promoting factor (MPF)**, which is a complex of **cyclin B** and **CDK1 (cyclin-dependent kinase 1)**. - **Cyclin B** levels rise during G2 and peak at M phase, activating CDK1 to initiate mitosis. *Retinoblastoma gene product* - The **retinoblastoma (Rb) protein** primarily regulates the G1/S transition by inhibiting the E2F transcription factor. - It acts as a **tumor suppressor**, preventing uncontrolled cell proliferation. *p53 protein* - The **p53 protein** is a critical **tumor suppressor** that monitors DNA integrity at various cell cycle checkpoints, particularly G1/S and G2/M. - If DNA damage is detected, p53 can induce cell cycle arrest and/or apoptosis, but it is not directly responsible for initiating M phase. *Cyclin E* - **Cyclin E** is essential for the **G1/S transition**, forming a complex with CDK2 to initiate DNA replication. - Its activity peaks during late G1 and early S phase, not during the G2/M transition.
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