Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 431: Which of the following anticancer drugs exhibits dose-dependent least neurotoxicity?

A. Cisplatin
B. Bleomycin (Correct Answer)
C. Doxorubicin
D. Vinblastine

Explanation: **Explanation:** The correct answer is **Bleomycin**. In the context of the options provided, Bleomycin is unique because its dose-limiting toxicity is **pulmonary fibrosis**, not neurotoxicity. It has virtually no significant penetration into the central nervous system and does not typically cause peripheral neuropathy, making it the drug with the least neurotoxicity among the choices. **Why the other options are incorrect:** * **Cisplatin:** This platinum-based agent is notorious for significant **dose-dependent neurotoxicity**, primarily manifesting as peripheral sensory neuropathy (stocking-glove pattern) and ototoxicity (high-frequency hearing loss). * **Vinblastine:** As a microtubule inhibitor (Vinca alkaloid), it interferes with axonal transport. While Vinblastine is more associated with bone marrow suppression than Vincristine, it still carries a significant risk of peripheral neuropathy and autonomic dysfunction. * **Doxorubicin:** While its primary dose-limiting toxicity is **cardiotoxicity**, it can contribute to "chemo-brain" (cognitive impairment) and, in high doses or specific formulations, exhibits more neurological interference than Bleomycin. **High-Yield Clinical Pearls for NEET-PG:** 1. **Bleomycin Specifics:** It acts by inducing free radical formation, causing DNA strand breaks. It is "cell cycle specific" for the **G2 phase**. 2. **The "B" Rule:** Remember **B**leomycin for **B**low (Pulmonary Fibrosis) and **B**one marrow sparing (it is one of the few anticancer drugs that does not cause significant myelosuppression). 3. **Cisplatin Triad of Toxicity:** Nephrotoxicity (prevented by Amifostine/hydration), Ototoxicity, and Peripheral Neuropathy. 4. **Vincristine vs. Vinblastine:** Vincristine is dose-limited by **Neurotoxicity**; Vinblastine is dose-limited by **Bone marrow suppression** ("Blast" = Bone marrow).

Question 432: Following a myocardial infarct, a patient is stabilized on warfarin, with the dose adjusted to give a prothrombin time of 22 seconds. Which one of the following statements regarding potential drug interactions in this patient is accurate?

A. Cholestyramine will increase prothrombin time.
B. Cimetidine is likely to decrease prothrombin time.
C. Antibacterial sulfonamides may enhance the effects of warfarin. (Correct Answer)
D. Vitamin K would restore prothrombin time to normal within 30 minutes.

Explanation: ### Explanation **Correct Option: C (Antibacterial sulfonamides may enhance the effects of warfarin)** Warfarin is a narrow-therapeutic-index drug metabolized primarily by the hepatic CYP450 system (specifically CYP2C9). **Sulfonamides** enhance the effects of warfarin through two mechanisms: 1. **Enzyme Inhibition:** They inhibit CYP2C9, reducing warfarin metabolism and increasing its plasma concentration. 2. **Protein Displacement:** They are highly protein-bound and can displace warfarin from albumin, increasing the "free" active fraction of the drug. This leads to an increased Prothrombin Time (PT) and International Normalized Ratio (INR), raising the risk of bleeding. **Analysis of Incorrect Options:** * **A. Cholestyramine:** This is a bile acid sequestrant that binds to drugs in the gastrointestinal tract. It **decreases** the absorption of warfarin, thereby **decreasing** PT/INR, not increasing it. * **B. Cimetidine:** Cimetidine is a potent CYP450 enzyme **inhibitor**. By slowing down the metabolism of warfarin, it would **increase** the PT/INR, not decrease it. * **D. Vitamin K:** While Vitamin K is the specific antidote for warfarin, it acts by promoting the hepatic synthesis of clotting factors (II, VII, IX, X). This process requires protein synthesis and takes **6 to 24 hours** to significantly alter PT. It cannot restore PT to normal within 30 minutes (for immediate reversal, Fresh Frozen Plasma or Prothrombin Complex Concentrate is required). **High-Yield Clinical Pearls for NEET-PG:** * **CYP450 Inducers (Decrease Warfarin effect):** Rifampicin, Phenytoin, Carbamazepine, Griseofulvin, Chronic Alcoholism. * **CYP450 Inhibitors (Increase Warfarin effect):** Erythromycin, Ketoconazole, Cimetidine, Valproate, Amiodarone, Acute Alcoholism. * **Broad-spectrum antibiotics** can also enhance warfarin's effect by killing gut flora that synthesize Vitamin K. * **Monitoring:** Warfarin is monitored by **PT/INR** (Extrinsic pathway), whereas Heparin is monitored by **aPTT** (Intrinsic pathway).

Question 433: A patient with breast carcinoma underwent radiation therapy for three months, followed by chemotherapy. Within days of starting chemotherapy, the patient developed rashes over the previously irradiated areas. Which of the following chemotherapeutic agents is most likely to cause this condition?

A. Actinomycin (Correct Answer)
B. Bleomycin
C. Mitomycin
D. Busulfan

Explanation: ### Explanation The clinical phenomenon described is **Radiation Recall Dermatitis (RRD)**. This is an inflammatory skin reaction that occurs in a previously irradiated area triggered by the administration of certain cytotoxic drugs, even months after the radiation therapy has concluded [1]. **1. Why Actinomycin D is the Correct Answer:** **Actinomycin D (Dactinomycin)** is one of the most notorious triggers for radiation recall. It is an antitumor antibiotic that intercalates into DNA [1]. The underlying mechanism involves the drug "recalling" the latent cellular damage caused by radiation, leading to an acute inflammatory response (erythema, edema, or vesiculation) strictly localized to the previous radiation field. **2. Why the Other Options are Incorrect:** * **Bleomycin:** While it is an antitumor antibiotic, its classic cutaneous side effect is **flagellate hyperpigmentation** (whip-like streaks) [1]. It is more commonly associated with pulmonary fibrosis than radiation recall [1]. * **Mitomycin C:** Known primarily for causing delayed myelosuppression and **Hemolytic Uremic Syndrome (HUS)** [1]. While it can rarely cause skin toxicity, it is not the classic agent associated with radiation recall in a NEET-PG context. * **Busulfan:** An alkylating agent primarily used in CML and bone marrow transplants. Its hallmark side effects are **pulmonary fibrosis** ("Busulfan lung") and **generalized hyperpigmentation** (Addisonian-like pigmentation), not localized radiation recall. **3. High-Yield Clinical Pearls for NEET-PG:** * **Common Triggers of RRD:** Actinomycin D (most common), Doxorubicin (and other Anthracyclines), Taxanes (Paclitaxel), and Gemcitabine. * **Actinomycin D Uses:** It is the drug of choice for **Wilms’ tumor**, Rhabdomyosarcoma, and Choriocarcinoma. * **Management:** The primary treatment for Radiation Recall Dermatitis is the temporary discontinuation of the offending drug and the use of topical or systemic corticosteroids.

Question 434: What is the most important dose-limiting toxicity of cancer chemotherapy?

A. Gastrointestinal toxicity
B. Neurotoxicity
C. Bone marrow suppression (Correct Answer)
D. Nephrotoxicity

Explanation: ### Explanation **1. Why Bone Marrow Suppression is Correct:** Bone marrow suppression (myelosuppression) is the most common and clinically significant **dose-limiting toxicity (DLT)** for the majority of cytotoxic anticancer drugs. Most chemotherapy agents target rapidly dividing cells by interfering with DNA synthesis or mitosis. Since hematopoietic stem cells in the bone marrow have a high turnover rate, they are highly susceptible to these drugs. This leads to leukopenia (increasing infection risk), thrombocytopenia (increasing bleeding risk), and anemia. If the blood counts drop below a critical threshold (the "nadir"), the treatment must be delayed or the dose reduced to allow for marrow recovery, directly limiting the intensity of therapy. **2. Why Other Options are Incorrect:** * **Gastrointestinal Toxicity:** While nausea, vomiting, and mucositis are very common side effects, they are usually manageable with antiemetics (like Ondansetron) or mucosal coating agents and rarely necessitate stopping the entire treatment regimen. * **Neurotoxicity:** This is a specific DLT for certain drugs like **Vincristine** (peripheral neuropathy) or **Cisplatin** (ototoxicity), but it is not the most common DLT across the entire class of chemotherapy. * **Nephrotoxicity:** This is a major DLT specifically for **Cisplatin** and **Methotrexate**, but it is not a universal dose-limiting factor for most other agents. **3. High-Yield Clinical Pearls for NEET-PG:** * **Exceptions:** Not all drugs cause myelosuppression. Notable exceptions include **Vincristine, Bleomycin, Cisplatin, and L-Asparaginase**. * **Nadir:** The point of lowest blood cell count, typically occurring **7–14 days** after chemotherapy administration. * **Rescue Agents:** To mitigate DLTs, specific "rescue" agents are used: * **Filgrastim (G-CSF):** For neutropenia. * **Amifostine:** To reduce Cisplatin-induced nephrotoxicity. * **Mesna:** To prevent Cyclophosphamide-induced hemorrhagic cystitis. * **Dexrazoxane:** To prevent Doxorubicin-induced cardiotoxicity.

Question 435: Steroids are used in all of the following conditions except?

A. Chronic lymphoid leukemia
B. Hodgkin's lymphoma
C. Multiple myeloma
D. Kaposi sarcoma (Correct Answer)

Explanation: **Explanation:** **1. Why Kaposi Sarcoma is the Correct Answer:** Kaposi Sarcoma (KS) is a vascular neoplasm caused by **Human Herpesvirus-8 (HHV-8)**, most commonly seen in immunocompromised patients (e.g., HIV/AIDS). Glucocorticoids are strictly **contraindicated** in Kaposi Sarcoma because they can trigger a rapid, life-threatening progression of the disease. Steroids induce the expression of the HHV-8 receptor and promote the release of inflammatory cytokines (like IL-6), which act as growth factors for the tumor cells. **2. Why the other options are incorrect:** Glucocorticoids (like Prednisolone or Dexamethasone) are cornerstone therapies in hematological malignancies due to their **lympholytic** properties (they induce apoptosis of lymphocytes): * **Chronic Lymphoid Leukemia (CLL):** Steroids are used to manage autoimmune complications (AIHA/ITP) and as part of chemotherapy regimens to reduce the tumor burden of B-lymphocytes. * **Hodgkin’s Lymphoma:** Steroids are a vital component of standard protocols (e.g., **BEACOPP**) to induce remission. * **Multiple Myeloma:** Dexamethasone is a backbone of treatment (e.g., **VRd regimen**: Velcade, Revlimid, Dexamethasone) because it is directly toxic to malignant plasma cells. **Clinical Pearls for NEET-PG:** * **Steroid-induced Lysis:** In high-grade lymphomas, steroids can cause **Tumor Lysis Syndrome**; monitor uric acid and electrolytes. * **Pneumocystis jirovecii (PJP) Prophylaxis:** Always consider PJP prophylaxis when using long-term high-dose steroids in oncology. * **Other uses in Oncology:** Steroids are also used to manage **vasogenic brain edema** (Dexamethasone), chemotherapy-induced nausea/vomiting (CINV), and hypercalcemia of malignancy.

Question 436: Anastrazole belongs to which class of drug?

A. Estrogen receptor down regulators (SERDs)
B. Selective estrogen receptor modulators (SERMs)
C. Selective tissue estrogenic activity regulator (STEAR)
D. Aromatase inhibitors (Correct Answer)

Explanation: **Explanation:** **Anastrozole** is a potent and highly selective **non-steroidal aromatase inhibitor**. In postmenopausal women, the primary source of estrogen is the peripheral conversion of adrenal androgens (androstenedione and testosterone) into estrogens (estrone and estradiol). This process is catalyzed by the enzyme **aromatase** (CYP19). By inhibiting this enzyme, Anastrozole significantly reduces circulating estrogen levels, thereby depriving estrogen-dependent breast cancer cells of their growth stimulus. **Analysis of Incorrect Options:** * **Option A (SERDs):** Drugs like **Fulvestrant** work by binding to and degrading estrogen receptors, leading to their down-regulation. They do not inhibit estrogen synthesis. * **Option B (SERMs):** Drugs like **Tamoxifen** and **Raloxifene** act as competitive antagonists at estrogen receptors in the breast but may have agonistic effects in other tissues (e.g., bone or endometrium). * **Option C (STEAR):** **Tibolone** is the classic example. it has tissue-specific estrogenic, progestogenic, and androgenic effects, primarily used in hormone replacement therapy (HRT). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Anastrozole (and Letrozole) is the first-line adjuvant treatment for **postmenopausal** women with ER-positive breast cancer. * **Classification:** * *Type I (Irreversible/Steroidal):* Exemestane. * *Type II (Reversible/Non-steroidal):* Anastrozole, Letrozole. * **Side Effects:** Unlike Tamoxifen, aromatase inhibitors do **not** increase the risk of endometrial cancer or thromboembolism. However, they are associated with an increased risk of **osteoporosis** and joint pain (arthralgia) due to profound estrogen depletion.

Question 437: Gemtuzumab ozogamycin is a monoclonal antibody against which target?

A. CD 30
B. CD 33 (Correct Answer)
C. CD 45
D. CD 79a

Explanation: **Explanation:** **Gemtuzumab ozogamicin** is an antibody-drug conjugate (ADC) consisting of a recombinant humanized IgG4 monoclonal antibody covalently linked to a cytotoxic agent, **calicheamicin**. 1. **Why CD33 is correct:** The monoclonal antibody component of Gemtuzumab specifically targets the **CD33 antigen**. CD33 is a sialic acid-dependent cytoadhesion molecule expressed on the surface of leukemic blasts in approximately 90% of patients with **Acute Myeloid Leukemia (AML)**, as well as on normal myeloid progenitors, but it is absent from pluripotent hematopoietic stem cells. Upon binding, the conjugate is internalized, releasing calicheamicin to cause double-stranded DNA breaks, leading to cell death. 2. **Analysis of Incorrect Options:** * **CD30:** Targeted by **Brentuximab vedotin**, used in Hodgkin Lymphoma and Systemic Anaplastic Large Cell Lymphoma. * **CD45:** Known as the Leukocyte Common Antigen (LCA); while used in immunohistochemistry to identify hematopoietic cells, it is not a standard target for current therapeutic monoclonal antibodies like Gemtuzumab. * **CD79a:** A marker for B-cell lineage; it is often used in pathology to identify B-cell neoplasms but is not the target for Gemtuzumab. (Note: Polatuzumab vedotin targets CD79b). **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Specifically approved for CD33-positive **Acute Myeloid Leukemia (AML)**. * **Black Box Warning:** It is associated with **Hepatotoxicity**, specifically **Veno-occlusive disease (VOD)**, also known as Sinusoidal Obstruction Syndrome (SOS). * **Mechanism Tip:** Remember "33" for Gemtuzumab (G is the 7th letter, 7+3=10... or simply associate the 'm' in Gemtuzumab with Myeloid/CD33).

Question 438: What is the most common side effect of 5-Fluorouracil?

A. Gastrointestinal toxicity (Correct Answer)
B. Bone marrow depression
C. Cardiotoxicity
D. Neurotoxicity

Explanation: **Explanation:** **5-Fluorouracil (5-FU)** is a pyrimidine antimetabolite that acts as a "thymineless death" inducer by inhibiting the enzyme **thymidylate synthase**. 1. **Why Gastrointestinal (GI) Toxicity is the correct answer:** While 5-FU affects all rapidly dividing cells, its most frequent and dose-limiting clinical manifestation is **GI toxicity**. This typically presents as severe mucosal inflammation (mucositis), stomatitis, and life-threatening diarrhea. The drug causes extensive damage to the rapidly regenerating intestinal epithelium, leading to these symptoms more consistently than significant myelosuppression in standard regimens. 2. **Analysis of Incorrect Options:** * **Bone marrow depression:** While 5-FU does cause myelosuppression (leukopenia and thrombocytopenia), it is generally considered secondary to GI toxicity in terms of frequency and clinical prominence for this specific agent. * **Cardiotoxicity:** This is a rare but unique side effect of 5-FU, often manifesting as coronary vasospasm or angina-like chest pain. It is high-yield but not the *most common*. * **Neurotoxicity:** This is an uncommon side effect, usually presenting as acute cerebellar ataxia, more frequently seen with high doses or in patients with DPD deficiency. **Clinical Pearls for NEET-PG:** * **Hand-Foot Syndrome (Palmar-Plantar Erythrodysesthesia):** A very characteristic side effect of 5-FU (and its prodrug Capecitabine), presenting as redness, swelling, and pain in the palms and soles. * **DPD Deficiency:** Patients deficient in **Dihydropyrimidine dehydrogenase (DPD)**—the enzyme that metabolizes 5-FU—are at risk for severe, fatal toxicity. * **Leucovorin Rescue? No:** Unlike Methotrexate, Leucovorin is given with 5-FU to **enhance** its efficacy (it stabilizes the binding of 5-FU to thymidylate synthase), not to reduce toxicity.

Question 439: All of the following statements about 6-mercaptopurine are true EXCEPT:

A. It is metabolized by xanthine oxidase.
B. It does not cause hyperuricemia. (Correct Answer)
C. Its dose should be reduced when allopurinol is given concurrently.
D. It is an active metabolite of azathioprine.

Explanation: **Explanation:** **6-Mercaptopurine (6-MP)** is a purine analogue (antimetabolite) used primarily in the treatment of acute lymphoblastic leukemia (ALL) [2]. **Why Option B is the Correct Answer (The False Statement):** 6-Mercaptopurine **does** cause hyperuricemia. Like many cytotoxic drugs used in leukemia, 6-MP causes rapid lysis of tumor cells (Tumor Lysis Syndrome). This leads to the catabolism of nucleic acids into purines, which are eventually converted into uric acid [1]. Therefore, the statement that it does not cause hyperuricemia is incorrect. **Analysis of Other Options:** * **Option A:** 6-MP is metabolized by the enzyme **xanthine oxidase** into 6-thiouric acid (inactive) [1]. * **Option C:** Since **Allopurinol** is a xanthine oxidase inhibitor, it prevents the breakdown of 6-MP. This leads to toxic accumulation of 6-MP. Therefore, the dose of 6-MP must be reduced by **50-75%** when co-administered with allopurinol to avoid severe bone marrow suppression [1]. * **Option D:** **Azathioprine** is a prodrug that is non-enzymatically converted into 6-mercaptopurine in the body [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Pharmacogenomics:** 6-MP is also metabolized by **Thiopurine Methyltransferase (TPMT)**. Patients with genetic TPMT deficiency are at high risk of life-threatening myelosuppression and require significant dose reductions. * **Interaction:** While allopurinol interacts significantly with 6-MP, it does **not** interact with 6-Thioguanine (6-TG), as 6-TG is not primarily metabolized by xanthine oxidase [1]. * **Drug of Choice:** 6-MP is a mainstay for maintenance therapy in childhood ALL.

Question 440: The T-10 protocol for the treatment of osteosarcoma includes all of the following except?

A. High dose methotrexate
B. Bleomycin, Cyclophosphamide, Doxorubicin (BCD)
C. Vincristine
D. Etoposide (Correct Answer)

Explanation: **Explanation:** The **T-10 protocol**, developed by Gerald Rosen at Memorial Sloan Kettering Cancer Center, is a landmark multi-agent chemotherapy regimen used for the management of **Osteosarcoma**. It is characterized by the use of neoadjuvant (pre-operative) chemotherapy to assess histological response before definitive surgery. **1. Why Etoposide is the correct answer:** Etoposide is **not** a component of the classic T-10 protocol. While Etoposide is used in other bone tumor regimens (like the VDC/IE protocol for Ewing’s Sarcoma), the T-10 protocol specifically relies on a combination of High-Dose Methotrexate, Doxorubicin, and the BCD combination. **2. Analysis of Incorrect Options:** * **High-dose Methotrexate (HDMTX):** This is the cornerstone of the T-10 protocol, administered with Leucovorin rescue to minimize systemic toxicity. * **BCD (Bleomycin, Cyclophosphamide, Dactinomycin):** This triplet combination was historically used in the T-10 regimen to intensify treatment, particularly in patients showing poor initial response to Methotrexate. (Note: Doxorubicin is also a core component). * **Vincristine:** Often used in conjunction with High-dose Methotrexate in these cycles to enhance efficacy. **Clinical Pearls for NEET-PG:** * **Osteosarcoma Treatment:** The current standard of care (MAP regimen) includes **M**ethotrexate, **A**driamycin (Doxorubicin), and **P**latin (Cisplatin). * **Histological Response:** The most important prognostic factor in Osteosarcoma is the percentage of tumor necrosis following neoadjuvant chemotherapy (>90% necrosis indicates a good prognosis). * **Methotrexate Toxicity:** Always remember that **Leucovorin (Folinic acid)** is used to "rescue" normal cells from HDMTX by bypassing dihydrofolate reductase.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free