Anticancer Drugs Practice Questions

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).

Q: Which tyrosine kinase inhibitor has HER2/NEU receptor inhibition activity?

Lapatinib. **Explanation:** **Lapatinib** is a dual tyrosine kinase inhibitor (TKI) that targets both the **Epidermal Growth Factor Receptor (EGFR/ErbB1)** and the **Human Epidermal Growth Factor Receptor 2 (HER2/neu/ErbB2)**. Unlike monoclonal antibodies like Trastuzumab which bind to the extracellular domain, Lapatinib acts intracellularly to inhibit the ATP-binding domain of these receptors. It is primarily used in the treatment of HER2-positive advanced or metastatic breast cancer. **Analysis of Incorrect Options:** * **Imatinib:** The first-line TKI for Chronic Myeloid Leukemia (CML). It targets **BCR-ABL**, c-KIT, and PDGFR. It has no activity against HER2. * **Nilotinib:** A second-generation TKI designed to overcome Imatinib resistance in CML. Like Imatinib, its primary target is the **BCR-ABL** tyrosine kinase. * **Sunitinib:** A multi-targeted TKI that primarily inhibits **VEGFR** and PDGFR. It is used in Renal Cell Carcinoma (RCC) and Gastrointestinal Stromal Tumors (GIST) due to its potent anti-angiogenic properties. **High-Yield Clinical Pearls for NEET-PG:** * **Lapatinib vs. Trastuzumab:** Lapatinib is small enough to cross the **blood-brain barrier**, making it useful for CNS metastases in HER2+ breast cancer, where Trastuzumab (a large antibody) has limited penetration. * **Side Effects:** A common side effect of Lapatinib is a skin rash (common to EGFR inhibitors) and diarrhea. * **Other HER2 Inhibitors:** **Neratinib** and **Afatinib** are irreversible ErbB family blockers. * **Drug of Choice:** Imatinib remains the DOC for CML and GIST (c-KIT positive).

Q: Temozolomide is used in the treatment of which of the following conditions?

Brain tumor. **Explanation:** **Temozolomide** is an oral alkylating agent belonging to the **triazene class**. Its primary clinical utility stems from its unique ability to cross the **blood-brain barrier (BBB)** effectively. 1. **Why Brain Tumor is Correct:** Temozolomide is a prodrug that undergoes rapid non-enzymatic conversion at physiological pH to its active metabolite, **MTIC** (monomethyl triazenoimidazole carboxamide). It exerts its cytotoxic effect by alkylating DNA at the **O6 and N7 positions of guanine**, leading to DNA damage and apoptosis. It is the standard-of-care (first-line) treatment for **Glioblastoma Multiforme (GBM)** and is also used for Anaplastic Astrocytoma. 2. **Why Other Options are Incorrect:** * **Epilepsy:** Treated with anti-seizure medications (e.g., Levetiracetam, Phenytoin) that modulate ion channels or neurotransmitters, not cytotoxic alkylating agents. * **Stroke:** Managed with thrombolytics (Alteplase) or antiplatelets/anticoagulants. * **Multiple Sclerosis:** Managed with disease-modifying therapies (DMTs) like Interferon-beta, Glatiramer, or monoclonal antibodies (Ocrelizumab). **High-Yield Clinical Pearls for NEET-PG:** * **Route:** It is highly bioavailable when taken **orally**. * **Radiosensitizer:** It is often used concurrently with radiotherapy (Stupp Protocol) because it sensitizes tumor cells to radiation. * **Resistance:** High levels of the DNA repair enzyme **MGMT** (O6-methylguanine-DNA methyltransferase) can cause resistance to Temozolomide. Patients with a *methylated* MGMT promoter respond better to treatment. * **Side Effects:** Myelosuppression (thrombocytopenia and leukopenia) is the dose-limiting toxicity.

Q: A young male was diagnosed with acute myeloid leukemia and received induction chemotherapy with a doxorubicin-based regimen, which was successful. Two months later, he presents with swelling of both feet and dyspnea on exertion, along with paroxysmal nocturnal dyspnea. Which of the following is most likely responsible for this patient's symptoms?

Dilated cardiomyopathy. **Explanation:** The patient is presenting with classic signs of **congestive heart failure (CHF)**—peripheral edema, dyspnea on exertion, and paroxysmal nocturnal dyspnea (PND)—following chemotherapy with **Doxorubicin** (an Anthracycline). **Why Dilated Cardiomyopathy is correct:** Anthracyclines like Doxorubicin and Daunorubicin cause dose-dependent cardiotoxicity. The underlying mechanism involves the generation of **iron-dependent free radicals** (superoxide anions) and the inhibition of **Topoisomerase IIβ** in cardiomyocytes. This leads to oxidative stress, mitochondrial dysfunction, and myofibrillar loss, ultimately resulting in **Dilated Cardiomyopathy (DCM)**. This toxic effect is often irreversible and leads to systolic dysfunction (reduced ejection fraction). **Why other options are incorrect:** * **Restrictive Cardiomyopathy:** Typically caused by infiltrative diseases (e.g., amyloidosis, sarcoidosis) or radiation therapy, not anthracyclines. * **Hypertrophic Cardiomyopathy:** Usually a genetic condition (mutations in sarcomere proteins) or a result of chronic hypertension; it is not a side effect of chemotherapy. * **Pericardial Fibrosis:** While radiation to the chest can cause constrictive pericarditis/fibrosis, Doxorubicin specifically targets the myocardium, not the pericardium. **High-Yield Clinical Pearls for NEET-PG:** * **Dose Limit:** The risk of heart failure increases significantly when the cumulative dose of Doxorubicin exceeds **450–550 mg/m²**. * **Prevention:** **Dexrazoxane**, an iron-chelating agent, is administered to reduce free radical formation and protect the heart. * **Monitoring:** Periodic **Echocardiography** or **MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF). * **Early vs. Late Toxicity:** Acute toxicity (arrhythmias) is usually reversible; delayed toxicity (DCM) is chronic and often progressive.

Question 1

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 2

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 3

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 4

Gemtuzumab ozogamycin is a monoclonal antibody against which target?

Accepted Answer

CD 33

Answer

CD 30

Answer

CD 45

Answer

CD 79a

Question 5

What is the active metabolite of azathioprine?

Accepted Answer

6-mercaptopurine

Answer

6-thioguanine

Answer

6-thiouracil

Answer

6-mercaptoguanine

Question 6

Leucovorin rescue is related to which of the following?

Accepted Answer

Methotrexate toxicity

Answer

Cyclophosphamide toxicity

Answer

Oncovin toxicity

Answer

Cisplatin toxicity

Question 7

What enzyme is inhibited by etoposide?

Accepted Answer

Topoisomerase II

Answer

Topoisomerase I

Answer

Dihydrofolate reductase

Answer

Dihydroorotate oxidase

Question 8

Which tyrosine kinase inhibitor has HER2/NEU receptor inhibition activity?

Accepted Answer

Lapatinib

Answer

Imatinib

Answer

Nilotinib

Answer

Sunitinib

Question 9

Temozolomide is used in the treatment of which of the following conditions?

Accepted Answer

Brain tumor

Answer

Epilepsy

Answer

Stroke

Answer

Multiple sclerosis

Question 10

A young male was diagnosed with acute myeloid leukemia and received induction chemotherapy with a doxorubicin-based regimen, which was successful. Two months later, he presents with swelling of both feet and dyspnea on exertion, along with paroxysmal nocturnal dyspnea. Which of the following is most likely responsible for this patient's symptoms?

Accepted Answer

Dilated cardiomyopathy

Answer

Restrictive cardiomyopathy

Answer

Hypertrophic cardiomyopathy

Answer

Pericardial fibrosis

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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