Anticancer Drugs Practice Questions

Q: Which of the following is a cardiotoxic anticancer drug?

Doxorubicin. **Explanation:** **Doxorubicin** is the correct answer because it belongs to the **Anthracycline** class of antibiotics, which are notorious for their dose-dependent **cardiotoxicity** [1]. The underlying mechanism involves the generation of **superoxide free radicals** and iron-dependent lipid peroxidation, which damages the myocardial cells (which have low levels of protective catalase) [2]. This toxicity manifests in two forms: 1. **Acute:** Transient ECG changes and arrhythmias [1]. 2. **Chronic:** Cumulative dose-related **Dilated Cardiomyopathy (DCM)** and congestive heart failure [1]. **Analysis of Incorrect Options:** * **A. Bleomycin:** Primarily known for **Pulmonary Fibrosis** (interstitial pneumonitis). It lacks significant cardiac side effects but can cause skin hyperpigmentation. * **C. 5-Fluorouracil:** An antimetabolite primarily associated with GI toxicity, hand-foot syndrome, and rarely, coronary vasospasm (angina) [4], but it is not the classic "cardiotoxic" drug compared to Doxorubicin. * **D. Dactinomycin:** An antitumor antibiotic used in pediatric tumors (Wilms tumor) [3]; its dose-limiting toxicity is primarily bone marrow suppression and GI distress. **High-Yield Clinical Pearls for NEET-PG:** * **Antidote:** **Dexrazoxane** (an iron chelator) is used to prevent/reduce Doxorubicin-induced cardiotoxicity [2]. * **Monitoring:** Periodic **ECHO/MUGA scans** to monitor Left Ventricular Ejection Fraction (LVEF) are mandatory [1]. * **Cumulative Dose:** The risk of heart failure increases significantly when the cumulative dose of Doxorubicin exceeds **450–550 mg/m²** [1]. * **Liposomal Doxorubicin:** This formulation is used to reduce cardiotoxicity by altering drug distribution.

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 active metabolite of azathioprine?

6-mercaptopurine. **Explanation:** **Azathioprine** is a prodrug belonging to the class of purine antimetabolites (immunosuppressants). After administration, it undergoes non-enzymatic cleavage by glutathione in the liver and red blood cells to release its active form, **6-mercaptopurine (6-MP)** [1], [4]. 6-MP is further metabolized into thio-inosinic acid, which inhibits the synthesis of adenine and guanine nucleotides, thereby suppressing T-cell and B-cell proliferation [1]. This makes it highly effective in preventing organ transplant rejection [2] and managing autoimmune conditions like SLE and Crohn’s disease [4]. **Analysis of Options:** * **Option A (6-thioguanine):** This is a separate purine analog used primarily in acute myeloid leukemia [1]. While 6-MP can eventually be converted into thioguanine nucleotides (TGNs) downstream, 6-MP is the immediate active metabolite of azathioprine [1]. * **Option B (6-thiouracil):** This is not a metabolite of azathioprine; it is structurally related to pyrimidines and antithyroid drugs (like Propylthiouracil). * **Option D (6-mercaptoguanine):** This is an incorrect chemical name in this metabolic context. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug Interaction:** 6-MP is metabolized by the enzyme **Xanthine Oxidase** [3]. **Allopurinol** (a xanthine oxidase inhibitor) significantly increases the levels of 6-MP, leading to life-threatening bone marrow suppression [3]. The dose of azathioprine must be reduced by 75% if given with allopurinol. 2. **Pharmacogenomics:** Patients with a genetic deficiency of the enzyme **TPMT (Thiopurine Methyltransferase)** are at a high risk of severe toxicity (pancytopenia) when taking azathioprine. 3. **Side Effects:** The most common dose-limiting toxicity is **bone marrow suppression** (leukopenia) [2].

Q: Leucovorin rescue is related to which of the following?

Methotrexate toxicity. **Explanation:** **Leucovorin (Folinic Acid)** is a reduced form of folic acid. Its primary role in oncology is to bypass the metabolic block created by **Methotrexate (MTX)**. 1. **Why Methotrexate is the correct answer:** Methotrexate acts by inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**, which prevents the conversion of folic acid to its active form, Tetrahydrofolate (THF). This depletion of THF halts DNA synthesis, leading to cell death. Leucovorin does not require DHFR for activation; it provides a direct source of reduced folate to healthy cells, "rescuing" them from lethal toxicity. This is typically administered 24 hours after high-dose MTX to prevent bone marrow suppression and GI mucosal damage. 2. **Why other options are incorrect:** * **Cyclophosphamide:** Toxicity (Hemorrhagic Cystitis) is managed with **MESNA** and aggressive hydration. * **Oncovin (Vincristine):** Toxicity (Peripheral Neuropathy) is managed symptomatically; there is no specific "rescue" agent. * **Cisplatin:** Nephrotoxicity is managed with **Amifostine** and vigorous hydration with chloride diuresis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Leucovorin Potentiation":** While Leucovorin *rescues* cells from MTX, it actually *enhances* the activity of **5-Fluorouracil (5-FU)** by stabilizing the binding of 5-dUMP to thymidylate synthase. * **Glucarpidase:** An alternative for MTX toxicity in patients with renal failure; it enzymatically breaks down MTX. * **Mnemonic for MTX side effects:** **M**yelosuppression, **T**eratogenic, **X**-tra (Mucositis/Liver Cirrhosis).

Q: What enzyme is inhibited by etoposide?

Topoisomerase II. **Explanation:** **Correct Answer: B. Topoisomerase II** Etoposide (and its analog Teniposide) is a semi-synthetic derivative of podophyllotoxin. Its primary mechanism of action involves inhibiting **Topoisomerase II**. This enzyme is responsible for creating transient double-stranded breaks in DNA to relieve torsional strain during replication. Etoposide binds to the DNA-topoisomerase II complex, preventing the religation of these breaks. This leads to permanent DNA strand scission, triggering apoptosis. It is cell-cycle specific, acting primarily in the **late S and G2 phases**. **Analysis of Incorrect Options:** * **A. Topoisomerase I:** This enzyme creates single-stranded breaks. It is inhibited by the **Camptothecins** (e.g., Irinotecan and Topotecan). * **C. Dihydrofolate Reductase (DHFR):** This enzyme is inhibited by **Methotrexate**, which prevents the conversion of dihydrofolate to tetrahydrofolate, disrupting thymidylate synthesis. * **D. Dihydroorotate Oxidase:** This mitochondrial enzyme is involved in de novo pyrimidine synthesis and is inhibited by **Leflunomide** (used in Rheumatoid Arthritis). **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Etoposide is a cornerstone in treating Small Cell Lung Cancer (SCLC), testicular tumors (as part of the BEP regimen), and lymphomas. * **Adverse Effects:** Apart from myelosuppression, a high-yield side effect is **secondary leukemia** (specifically Acute Myeloid Leukemia with 11q23 translocation), which typically occurs 2–3 years after treatment. * **Mnemonic:** Remember "**E**-**T**-**O**-poside" inhibits Topoisomerase **TWO** (II).

Question 1

A 56-year-old female was prescribed trastuzumab. Which of the following statements regarding this drug is FALSE?

Accepted Answer

It is a chimeric antibody containing human and mouse components.

Answer

It is used for the treatment of HER2-positive breast carcinoma.

Answer

It can cause cardiac toxicity.

Answer

It is not effective orally.

Question 2

Which of the following is a cardiotoxic anticancer drug?

Accepted Answer

Doxorubicin

Answer

Bleomycin

Answer

5-Fluorouracil

Answer

Dactinomycin

Question 3

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

Accepted Answer

Bleomycin

Answer

Cisplatin

Answer

Doxorubicin

Answer

Vinblastine

Question 4

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 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 active metabolite of azathioprine?

Accepted Answer

6-mercaptopurine

Answer

6-thioguanine

Answer

6-thiouracil

Answer

6-mercaptoguanine

Question 9

Leucovorin rescue is related to which of the following?

Accepted Answer

Methotrexate toxicity

Answer

Cyclophosphamide toxicity

Answer

Oncovin toxicity

Answer

Cisplatin toxicity

Question 10

What enzyme is inhibited by etoposide?

Accepted Answer

Topoisomerase II

Answer

Topoisomerase I

Answer

Dihydrofolate reductase

Answer

Dihydroorotate oxidase

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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