Anticancer Drugs Practice Questions

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.

Q: The provided figure illustrates the mechanism of action of which of the following drugs?

Vinblastine. ***Vinblastine*** - **Binds to tubulin** and prevents **microtubule polymerization**, disrupting the mitotic spindle formation. - Causes **metaphase arrest** by blocking chromosome separation, leading to cancer cell death. *Cisplatin* - Works by forming **DNA cross-links** between and within DNA strands, not by affecting microtubules. - Mechanism involves **alkylation** of DNA bases, particularly guanine, leading to DNA damage and apoptosis. *Imatinib* - Acts as a **tyrosine kinase inhibitor**, specifically targeting **BCR-ABL** fusion protein in chronic myeloid leukemia. - Does not interact with **microtubules** but rather blocks abnormal protein kinase signaling pathways. *Trastuzumab* - A **monoclonal antibody** that targets **HER2 receptors** on breast cancer cells overexpressing this protein. - Works through **antibody-dependent cellular cytotoxicity** and receptor blockade, not microtubule disruption.

Q: Which anticancer drug is known to cause nephrotoxicity?

Cisplatin. **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. Its dose-limiting toxicity is **nephrotoxicity**, specifically causing acute tubular necrosis (ATN) in the proximal convoluted tubules. This occurs because cisplatin accumulates in the renal tubular cells, leading to oxidative stress and apoptosis. To prevent this, patients are managed with **aggressive pre- and post-treatment hydration** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **Analysis of Incorrect Options:** * **A. Imatinib:** A tyrosine kinase inhibitor (BCR-ABL) used in CML. Its hallmark side effect is **periorbital edema** and fluid retention, not primary nephrotoxicity. * **B. Irinotecan:** A Topoisomerase I inhibitor used in colorectal cancer. Its signature toxicity is **severe diarrhea** (early phase due to cholinergic crisis; late phase due to SN-38 metabolite). * **C. Fosfestrol:** A synthetic estrogen (prodrug of diethylstilbestrol) used in prostate cancer. Common side effects include gynecomastia and thromboembolic complications. **NEET-PG High-Yield Pearls:** * **Cisplatin Toxicities:** Remember the "3 Os": **O**totoxicity (high-frequency hearing loss), **O**liguria (Nephrotoxicity), and severe **O**mesis (highly emetogenic). * **Electrolyte Imbalance:** Cisplatin frequently causes **hypomagnesemia** due to renal wasting. * **Drug of Choice:** While Cisplatin is nephrotoxic, **Carboplatin** (its analog) is more associated with **myelosuppression** (thrombocytopenia) but has significantly less renal and ototoxicity.

Q: Alkylating agents are known to cause which of the following conditions?

Both bladder cancer and acute myelocytic leukemia. **Explanation:** Alkylating agents (e.g., Cyclophosphamide, Busulfan, Melphalan) are cell-cycle non-specific drugs that act by forming covalent bonds with DNA, leading to cross-linking and strand breaks. While they are effective in treating malignancies, they are inherently **mutagenic and carcinogenic** due to their permanent alteration of DNA structure. 1. **Acute Myelocytic Leukemia (AML):** This is a well-documented long-term complication of alkylating agent therapy. These drugs induce chromosomal aberrations (often involving chromosomes 5 and 7) in hematopoietic stem cells. This "therapy-related AML" typically occurs 3–10 years after treatment. 2. **Bladder Cancer:** Specifically associated with **Cyclophosphamide** and **Ifosfamide**. These drugs are metabolized into **Acrolein**, a toxic metabolite that causes hemorrhagic cystitis. Chronic irritation and DNA damage to the urothelium by acrolein significantly increase the risk of transitional cell carcinoma of the bladder. **Analysis of Options:** * **Option A & B:** Both are correct, but incomplete individually. * **Option D:** There is no established causal link between alkylating agents and the development of prostate cancer. **High-Yield Clinical Pearls for NEET-PG:** * **Mesna** (2-Mercaptoethane sulfonate Na) is administered with Cyclophosphamide to neutralize acrolein and prevent hemorrhagic cystitis. * **Busulfan** is notorious for causing **Pulmonary Fibrosis** ("Busulfan lung") and hyperpigmentation. * **Nitrosoureas** (Lomustine, Carmustine) are highly lipid-soluble and are the drugs of choice for **Brain tumors** (Glial tumors). * **Secondary Malignancy:** Alkylating agents are the most common class of anticancer drugs to cause secondary cancers.

Q: All are true regarding selective estrogen receptor downregulator (SERD), Fulvestrant, except?

Is slower, short-acting, and less safe than SERMs.. **Explanation** **Fulvestrant** is a unique hormonal agent classified as a **Selective Estrogen Receptor Downregulator (SERD)** [1]. Unlike SERMs (e.g., Tamoxifen), which have agonist effects in some tissues and antagonist effects in others, Fulvestrant is a **pure estrogen antagonist** with no agonist activity [3]. **Why Option C is the correct (False) statement:** Fulvestrant is actually **longer-acting** and has a **better safety profile** compared to many SERMs. It has a long half-life (approx. 40 days), allowing for infrequent dosing [1]. Furthermore, because it lacks the partial agonist activity of Tamoxifen, it does **not** increase the risk of endometrial cancer or venous thromboembolism, making it safer in those specific regards [2]. **Analysis of other options:** * **Option A:** It is FDA-approved for the treatment of hormone receptor-positive (HR+) **advanced or metastatic breast cancer**, particularly in postmenopausal women who have progressed on other anti-estrogen therapies [3]. * **Option B:** It binds to estrogen receptors (ER) with high affinity, blocking estrogen binding and triggering the **degradation (downregulation)** of the receptor protein [1]. Thus, it acts as a pure antagonist. * **Option D:** Due to its pharmacokinetic profile, it is administered as a **500 mg intramuscular (IM) injection** once monthly (after an initial loading dose) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** "Bind, Block, Degrade." It leads to a total reduction in the number of estrogen receptors in the cell [1]. * **Indication:** Second-line therapy for metastatic breast cancer after Tamoxifen or Aromatase Inhibitor failure [3]. * **Side Effects:** Most common are injection site pain, hot flashes, and nausea. * **Comparison:** Unlike Tamoxifen (SERM), Fulvestrant does **not** carry a risk of uterine (endometrial) hyperplasia [2].

Q: Tretinoin is useful in the treatment of which type of leukemia?

M3. **Explanation:** **Tretinoin (All-Trans Retinoic Acid or ATRA)** is the standard of care for **Acute Promyelocytic Leukemia (APL)**, which is classified as **M3** under the French-American-British (FAB) system. **Why M3 is correct:** APL (M3) is characterized by a specific chromosomal translocation **t(15;17)**. This translocation fuses the Retinoic Acid Receptor alpha (RARα) gene on chromosome 17 with the Promyelocytic Leukemia (PML) gene on chromosome 15. The resulting **PML-RARα fusion protein** blocks myeloid differentiation at the promyelocyte stage. Tretinoin works by binding to this abnormal receptor, inducing the **differentiation** of leukemic promyelocytes into mature neutrophils, thereby inducing remission. **Why other options are incorrect:** * **M2 (Acute Myeloblastic Leukemia with maturation):** Commonly associated with t(8;21). It does not involve the RARα mutation and does not respond to differentiation therapy with ATRA. * **M5 (Acute Monocytic Leukemia):** Characterized by monocytic lineage; often associated with gum hypertrophy and skin involvement. It is treated with standard induction chemotherapy (7+3 regimen). * **M7 (Acute Megakaryoblastic Leukemia):** Associated with Down Syndrome (in children <5 years) and extensive marrow fibrosis. It does not respond to ATRA. **High-Yield Clinical Pearls for NEET-PG:** * **Differentiation Syndrome:** A life-threatening side effect of ATRA characterized by fever, dyspnea, and pulmonary infiltrates. It is managed with **Dexamethasone**. * **DIC Risk:** M3 is highly associated with **Disseminated Intravascular Coagulation (DIC)** due to the release of procoagulants from promyelocyte granules. * **Arsenic Trioxide:** Also used in M3 to degrade the PML-RARα protein, often in combination with ATRA.

Q: A patient was incidentally diagnosed with a lump during a routine health checkup. Following ultrasound and guided biopsy, histopathological examination revealed a diagnosis. The patient was initiated on chemotherapy that included a drug obtained from a specific plant. What is the site of action of this drug?

Tubulin (mitotic inhibitor). ***Tubulin (mitotic inhibitor)*** - Plant-derived chemotherapeutic agents like **vinca alkaloids** (vincristine, vinblastine from *Vinca rosea*) and **taxanes** (paclitaxel from *Taxus brevifolia*) target **tubulin** and disrupt **microtubule** formation. - These drugs prevent proper **mitotic spindle** formation, leading to cell cycle arrest in **M-phase** and subsequent **apoptosis** in rapidly dividing cancer cells. *DNA alkylation* - **Alkylating agents** like **cyclophosphamide** and **nitrogen mustards** form **covalent bonds** with DNA bases, causing cross-linking. - These are not typically plant-derived drugs and work through direct **DNA damage** rather than affecting cellular structures. *Topoisomerase II inhibition* - **Etoposide** and **doxorubicin** inhibit **topoisomerase II**, preventing DNA **supercoiling** and causing DNA breaks. - While some topoisomerase inhibitors are plant-derived, the question specifically hints at drugs affecting **cellular division machinery** rather than DNA enzymes. *DNA intercalation* - **Intercalating agents** like **actinomycin D** insert between **DNA base pairs**, distorting the double helix structure. - These drugs primarily affect **transcription** and **replication** processes rather than the **mitotic apparatus** targeted by plant-derived anti-mitotic agents.

Question 1

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

Accepted Answer

Lapatinib

Answer

Imatinib

Answer

Nilotinib

Answer

Sunitinib

Question 2

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

Accepted Answer

Brain tumor

Answer

Epilepsy

Answer

Stroke

Answer

Multiple sclerosis

Question 3

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

Question 4

The provided figure illustrates the mechanism of action of which of the following drugs?

Accepted Answer

Vinblastine

Answer

Cisplatin

Answer

Imatinib

Answer

Trastuzumab

Question 5

Cetuximab (an EGFR antagonist) can be used in which of the following conditions?

Accepted Answer

Palliation in head and neck cancer

Answer

Anal canal carcinoma

Answer

Gastric carcinoma

Answer

Lung carcinoma

Question 6

Which anticancer drug is known to cause nephrotoxicity?

Accepted Answer

Cisplatin

Answer

Imitanib

Answer

Irinotecan

Answer

Fosfestrol

Question 7

Alkylating agents are known to cause which of the following conditions?

Accepted Answer

Both bladder cancer and acute myelocytic leukemia

Answer

Bladder cancer

Answer

Acute myelocytic leukemia

Answer

Prostate cancer

Question 8

All are true regarding selective estrogen receptor downregulator (SERD), Fulvestrant, except?

Accepted Answer

Is slower, short-acting, and less safe than SERMs.

Answer

Used for the treatment of advanced breast cancer.

Answer

Is a selective estrogen antagonist.

Answer

Administered as a once-monthly intramuscular dose.

Question 9

Tretinoin is useful in the treatment of which type of leukemia?

Accepted Answer

M3

Answer

M2

Answer

M5

Answer

M7

Question 10

A patient was incidentally diagnosed with a lump during a routine health checkup. Following ultrasound and guided biopsy, histopathological examination revealed a diagnosis. The patient was initiated on chemotherapy that included a drug obtained from a specific plant. What is the site of action of this drug?

Accepted Answer

Tubulin (mitotic inhibitor)

Answer

DNA alkylation

Answer

Topoisomerase II inhibition

Answer

DNA intercalation

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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