Anticancer Drugs Practice Questions

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

Bleomycin. **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).

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

Kaposi sarcoma. **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.

Q: Anastrazole belongs to which class of drug?

Aromatase inhibitors. **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.

Q: Gemtuzumab ozogamycin is a monoclonal antibody against which target?

CD 33. **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).

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

Gastrointestinal toxicity. **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.

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

It does not cause hyperuricemia.. **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.

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

Etoposide. **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.

Question 1

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

Accepted Answer

Bleomycin

Answer

Cisplatin

Answer

Doxorubicin

Answer

Vinblastine

Question 2

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?

Accepted Answer

Antibacterial sulfonamides may enhance the effects of warfarin.

Answer

Cholestyramine will increase prothrombin time.

Answer

Cimetidine is likely to decrease prothrombin time.

Answer

Vitamin K would restore prothrombin time to normal within 30 minutes.

Question 3

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?

Accepted Answer

Actinomycin

Answer

Bleomycin

Answer

Mitomycin

Answer

Busulfan

Question 4

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

Accepted Answer

Bone marrow suppression

Answer

Gastrointestinal toxicity

Answer

Neurotoxicity

Answer

Nephrotoxicity

Question 5

Steroids are used in all of the following conditions except?

Accepted Answer

Kaposi sarcoma

Answer

Chronic lymphoid leukemia

Answer

Hodgkin's lymphoma

Answer

Multiple myeloma

Question 6

Anastrazole belongs to which class of drug?

Accepted Answer

Aromatase inhibitors

Answer

Estrogen receptor down regulators (SERDs)

Answer

Selective estrogen receptor modulators (SERMs)

Answer

Selective tissue estrogenic activity regulator (STEAR)

Question 7

Gemtuzumab ozogamycin is a monoclonal antibody against which target?

Accepted Answer

CD 33

Answer

CD 30

Answer

CD 45

Answer

CD 79a

Question 8

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

Accepted Answer

Gastrointestinal toxicity

Answer

Bone marrow depression

Answer

Cardiotoxicity

Answer

Neurotoxicity

Question 9

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

Accepted Answer

It does not cause hyperuricemia.

Answer

It is metabolized by xanthine oxidase.

Answer

Its dose should be reduced when allopurinol is given concurrently.

Answer

It is an active metabolite of azathioprine.

Question 10

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

Accepted Answer

Etoposide

Answer

High dose methotrexate

Answer

Bleomycin, Cyclophosphamide, Doxorubicin (BCD)

Answer

Vincristine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?