Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 121: Which enzyme is used in the treatment of Leukemia?

A. Asparaginase (Correct Answer)
B. Lipase
C. Amylase
D. Transaminase

Explanation: **Explanation:** **L-Asparaginase** is a unique enzyme used primarily in the treatment of **Acute Lymphoblastic Leukemia (ALL)** [1]. **Mechanism of Action:** Normal cells can synthesize the amino acid **Asparagine** from aspartic acid using the enzyme *asparagine synthetase* [1]. However, certain leukemic cells lack this enzyme and are dependent on an exogenous supply of asparagine from the blood for protein synthesis and survival [1]. L-Asparaginase catalyzes the conversion of serum asparagine into aspartic acid and ammonia [1]. By depleting the extracellular supply of asparagine, the drug "starves" the leukemic cells, leading to inhibited protein synthesis and cell death (apoptosis) [1]. **Why Incorrect Options are Wrong:** * **B. Lipase:** An enzyme that breaks down dietary fats into fatty acids and glycerol; it has no role in oncology. * **C. Amylase:** An enzyme that hydrolyzes starch into sugars; it is a diagnostic marker for pancreatitis but not a therapeutic agent for cancer. * **D. Transaminase:** Enzymes (like ALT/AST) involved in amino acid metabolism; they are markers of liver injury rather than anticancer treatments. **High-Yield Clinical Pearls for NEET-PG:** * **Major Side Effect:** The most characteristic toxicity is **Hypersensitivity/Anaphylaxis** (as it is a foreign bacterial protein) [1]. * **Other Toxicities:** It can cause **Acute Pancreatitis**, decreased clotting factors (leading to **thrombosis or hemorrhage**), and hypoalbuminemia. * **Unique Feature:** Unlike most cytotoxic drugs, L-Asparaginase is **not bone marrow suppressant** (it is "bone marrow sparing").

Question 122: Which of the following conditions is treated with tyrosine kinase inhibitors?

A. Gastrointestinal stromal tumors (GIST) (Correct Answer)
B. Acute myeloid leukemia
C. Neurofibromatosis
D. Small cell carcinoma of the lung

Explanation: **Correct Option: A. Gastrointestinal stromal tumors (GIST)** Gastrointestinal stromal tumors (GIST) are characterized by the overexpression of the **c-KIT (CD117)** proto-oncogene, which encodes a transmembrane receptor tyrosine kinase. **Imatinib**, a first-generation tyrosine kinase inhibitor (TKI), specifically inhibits the BCR-ABL, c-KIT, and PDGF-R kinases. By blocking the ATP-binding site of the c-KIT enzyme, Imatinib inhibits the constitutive signaling that drives tumor cell proliferation. It is the first-line targeted therapy for unresectable or metastatic GIST [3]. **Analysis of Incorrect Options:** * **B. Acute myeloid leukemia (AML):** While some subtypes (like FLT3-mutated AML) use TKIs, the standard "7+3" induction regimen consists of Cytarabine and Anthracylines (Daunorubicin). TKIs are more classically associated with Chronic Myeloid Leukemia (CML) [2, 3]. * **C. Neurofibromatosis:** This is a genetic disorder caused by mutations in the NF1 or NF2 genes. While MEK inhibitors (like Selumetinib) are now used for plexiform neurofibromas, standard TKIs are not the primary treatment modality for the condition itself. * **D. Small cell carcinoma of the lung (SCLC):** SCLC is highly aggressive and primarily treated with chemotherapy (Etoposide + Cisplatin). TKIs (like Erlotinib or Gefitinib) are used for **Non-Small Cell Lung Cancer (NSCLC)** with EGFR mutations, not SCLC [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Imatinib** is the drug of choice for **CML** (targeting BCR-ABL/Philadelphia chromosome t(9;22)) [2, 3]. * **Adverse Effect:** A characteristic side effect of Imatinib is **periorbital edema**. * **Resistance:** Resistance to Imatinib in CML often occurs due to the **T315I mutation**, which is treated with **Ponatinib**. * **Sunitinib** is an alternative TKI used for Imatinib-resistant GIST.

Question 123: Which of the following statements about cyclophosphamide is incorrect?

A. Causes immunosuppression
B. Causes local irritation (Correct Answer)
C. Well absorbed orally
D. Alkylating agent

Explanation: **Explanation:** **Cyclophosphamide** is a nitrogen mustard derivative and a prototype **alkylating agent**. The key to understanding this question lies in its pharmacokinetics: it is a **prodrug**. **Why "Causes local irritation" is Incorrect (The Correct Answer):** Unlike many other alkylating agents (like Mechlorethamine), cyclophosphamide is **not a vesicant**. It is inactive in its original form and must be activated in the liver by cytochrome P450 enzymes (specifically CYP2B6) into active metabolites like phosphoramide mustard and acrolein. Because it is inactive at the site of administration, it does **not cause local tissue irritation** or cellulitis if extravasation occurs. **Analysis of Other Options:** * **A. Causes immunosuppression:** Cyclophosphamide is a potent immunosuppressant. It suppresses both B-cell and T-cell functions and is frequently used in autoimmune diseases like SLE and Wegener’s granulomatosis. * **C. Well absorbed orally:** It has high oral bioavailability (nearly 100%), making it one of the few anticancer drugs that can be administered both orally and intravenously. * **D. Alkylating agent:** It acts by attaching an alkyl group to the guanine base of DNA (at the N-7 position), leading to cross-linking and inhibition of DNA replication. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Bone marrow suppression. * **Specific Toxicity:** **Hemorrhagic Cystitis**, caused by the metabolite **Acrolein**. * **Prevention:** Aggressive hydration and administration of **MESNA** (2-Mercaptoethane sulfonate Na), which neutralizes acrolein in the bladder. * **Other Side Effects:** SIADH (dilutional hyponatremia), alopecia, and secondary malignancies (bladder cancer).

Question 124: Rituximab is used in the treatment of which of the following conditions?

A. Hodgkin's disease
B. Acute myeloid leukemia
C. Non–Hodgkin lymphoma (Correct Answer)
D. Multiple myeloma

Explanation: **Explanation:** **Rituximab** is a chimeric monoclonal antibody directed against the **CD20 antigen**, which is primarily expressed on the surface of normal and malignant **B-lymphocytes**. 1. **Why Non-Hodgkin Lymphoma (NHL) is correct:** Rituximab binds to CD20, inducing B-cell lysis through complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis. It is a cornerstone of therapy for B-cell NHLs, such as Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma (often used in the R-CHOP regimen). 2. **Why the other options are incorrect:** * **Hodgkin’s Disease:** Classic Hodgkin lymphoma is characterized by Reed-Sternberg cells which are typically **CD20 negative** (they are CD15+ and CD30+). The drug of choice here is often Brentuximab vedotin (anti-CD30). * **Acute Myeloid Leukemia (AML):** AML involves myeloid precursors, not B-cells. Common targets in AML include CD33 (Gemtuzumab ozogamicin) or FLT3. * **Multiple Myeloma:** This is a malignancy of plasma cells. Mature plasma cells usually **lose CD20 expression**. Treatment involves proteasome inhibitors (Bortezomib) or anti-CD38 antibodies (Daratumumab). **High-Yield Clinical Pearls for NEET-PG:** * **Other Indications:** Rheumatoid Arthritis (refractory to TNF-inhibitors), Wegener’s Granulomatosis (GPA), and Pemphigus Vulgaris. * **Adverse Effects:** The most significant side effect is an **infusion-related reaction** (cytokine release syndrome). Pre-medication with paracetamol and antihistamines is required. * **Black Box Warning:** Reactivation of **Hepatitis B virus (HBV)**; screening is mandatory before starting therapy. * **Target:** It does not target stem cells or plasma cells (as they lack CD20), allowing for B-cell regeneration after treatment.

Question 125: Bortezomib is used for the treatment of which cancer?

A. Multiple myeloma (Correct Answer)
B. Breast cancer
C. Tyrosine kinase inhibitor
D. Janus kinase inhibitor

Explanation: **Explanation:** **Bortezomib** [1] is a first-in-class **proteasome inhibitor** [2]. Its primary clinical indication is the treatment of **Multiple Myeloma** [1], [2] and Mantle Cell Lymphoma [2]. 1. **Mechanism of Action (Why A is correct):** Bortezomib reversibly inhibits the **26S proteasome** [2], a multi-enzyme complex responsible for degrading intracellular proteins [1]. By blocking this "garbage disposal" system, it leads to the accumulation of pro-apoptotic proteins and inhibits **NF-̴̴̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̨̱̱̤̹̖̥̥̥̥̥̥̤̲̥̥̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̤̥̥̹̹̤̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̤̱̱̥̥̥̥̥̥̥̥̥̥̥̥̥̥̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̱̀́͂̀̂̅̑̀̔́̃̅́̀̔̂̑̂̔̅̂̀̔̂̔̂̔̑̔̔̑͂̔̑̅̂̑̅̅́́́́́́́́́́́́́́̔̔̔̔̔̔̔̔̂̂̂̂̂̂̂̂̂̔̂̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̔̑̓̑̂̑̓̂̑̓̂̑̓̑̑̑̑̂̔̂̔̂̔̓̑̂̑̂̂̂̂̂̂̑̂̀̔̑̑̀̔̀̔̀̔̀̔̔̔̔̔̔̔̑̑̑̂̔̂̔̂̔̂̔̂̔̂̔̂̂̂̑̑̑̑̑̑̑̑̂̔̂̔̂̔̑̑̂̔̂̔̑̓̑̂̔̂̔̔̂̔́̀̔́̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̂̔̂̔̂̔̂̔̂̔̂̔̂̔̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̅̅̅̓̓̑̆́̀̔̂̑̂́̀̔̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̓̑̂̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̂̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̕̕̕ᄑ̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑̑

Question 126: Chemotherapy used after surgery or radiotherapy for cancer is termed as:

A. Combination chemotherapy
B. Adjuvant chemotherapy (Correct Answer)
C. Neoadjuvant chemotherapy
D. Concomitant chemotherapy

Explanation: ### Explanation **Correct Option: B. Adjuvant chemotherapy** **Concept:** Adjuvant chemotherapy refers to the administration of anticancer drugs **after** the primary treatment (usually surgery or radiotherapy). The primary goal is to eliminate "micrometastases"—small clusters of cancer cells that may have spread from the original site but are undetectable by imaging. By targeting these residual cells, adjuvant therapy reduces the risk of local recurrence and distant metastasis, thereby improving overall survival. **Analysis of Incorrect Options:** * **C. Neoadjuvant chemotherapy:** This is chemotherapy given **before** the primary treatment (surgery/radiotherapy). It is used to shrink large tumors to make them operable or to allow for organ-preserving surgeries (e.g., in breast cancer). * **D. Concomitant (Concurrent) chemotherapy:** This involves giving chemotherapy **simultaneously** with radiotherapy. The drugs often act as "radiosensitizers," enhancing the lethal effect of radiation on tumor cells (e.g., Cisplatin in cervical cancer). * **A. Combination chemotherapy:** This refers to the use of **multiple drugs** with different mechanisms of action and non-overlapping toxicities (e.g., the CHOP regimen) to prevent drug resistance and increase the "log kill" of cancer cells. It does not specify the timing relative to surgery. **High-Yield Clinical Pearls for NEET-PG:** * **Palliative Chemotherapy:** Given in advanced, metastatic stages where the goal is not a cure, but to improve quality of life and prolong survival. * **Maintenance Chemotherapy:** Low-dose, long-term treatment given after a patient has achieved complete remission to delay regrowth (common in Leukemias). * **Recruitment:** A strategy where cell-cycle specific drugs are used after cell-cycle non-specific drugs to "recruit" resting cells into the active cycle for better killing.

Question 127: Which of the following drugs can cause non-ischaemic chest pain?

A. Bleomycin (Correct Answer)
B. Vincristine
C. Cyclophosphamide
D. Cisplatin

Explanation: **Explanation:** **Bleomycin** is a glycopeptide antibiotic used in cancer chemotherapy (e.g., Hodgkin lymphoma, germ cell tumors). While its most notorious side effect is pulmonary fibrosis, it is also uniquely associated with **acute chest pain syndrome**. This is a **non-ischaemic** phenomenon, often occurring during or shortly after infusion. It is characterized by retrosternal pain that mimics pleurisy or pericarditis but occurs without evidence of myocardial ischemia or EKG changes. The exact mechanism is thought to be related to acute inflammation or irritation of the pleura or mediastinal structures. **Analysis of Incorrect Options:** * **Vincristine:** Primarily known for **peripheral neuropathy** (stocking-glove pattern) and autonomic dysfunction (paralytic ileus). While it can rarely cause vasospastic angina, it is not the classic cause of non-ischaemic chest pain. * **Cyclophosphamide:** Its dose-limiting toxicity is **hemorrhagic cystitis** (prevented by Mesna). At very high doses, it can cause acute cardiotoxicity (myocarditis), but this is typically ischaemic or congestive in nature, not simple non-ischaemic chest pain. * **Cisplatin:** Highly **nephrotoxic** and **emetogenic**. It is associated with electrolyte imbalances and ototoxicity, but not specifically with non-ischaemic chest pain. **High-Yield Clinical Pearls for NEET-PG:** * **Bleomycin:** Remember the "Pulmonary-Skin-Pain" triad: Pulmonary fibrosis, skin hyperpigmentation (flagellate dermatosis), and non-ischaemic chest pain. * **Oxygen Caution:** Patients previously treated with Bleomycin are at high risk of fatal pulmonary toxicity if given high concentrations of inspired oxygen (FiO2) during surgery. * **Cell Cycle:** Bleomycin acts on the **G2 phase** by inducing free radical-mediated DNA strand breaks.

Question 128: What is the mechanism of action of Rituximab?

A. Targets CD 20 antigen (Correct Answer)
B. Targets CD 52 antigen
C. Targets CD 22 antigen
D. Targets CD 38 antigen

Explanation: **Explanation:** **1. Why Option A is Correct:** Rituximab is a chimeric monoclonal antibody that specifically targets the **CD20 antigen** [1]. CD20 is a transmembrane protein expressed primarily on the surface of pre-B and mature B-lymphocytes, but not on hematopoietic stem cells or plasma cells. When Rituximab binds to CD20, it triggers B-cell lysis through three main mechanisms: Antibody-Dependent Cellular Cytotoxicity (ADCC), Complement-Dependent Cytotoxicity (CDC), and induction of apoptosis. It is a cornerstone therapy for B-cell non-Hodgkin lymphomas (like Diffuse Large B-cell Lymphoma) and Chronic Lymphocytic Leukemia (CLL) [1]. **2. Why the Other Options are Incorrect:** * **Option B (CD52):** This is the target for **Alemtuzumab**. It is used in B-CLL and Multiple Sclerosis. * **Option C (CD22):** This is the target for **Epratuzumab** and **Inotuzumab ozogamicin**. CD22 is also found on B-cells but is distinct from CD20. * **Option D (CD38):** This is the target for **Daratumumab**, which is primarily used in the treatment of Multiple Myeloma. **3. High-Yield Clinical Pearls for NEET-PG:** * **Non-Oncology Uses:** Rituximab is also used in autoimmune conditions like Rheumatoid Arthritis (refractory cases), Wegener’s Granulomatosis (GPA), and Pemphigus Vulgaris. * **Side Effects:** The most significant risk is **Infusion-related reactions** (often managed with antihistamines and steroids) [1]. * **Black Box Warning:** It can cause **Reactivation of Hepatitis B**; therefore, screening for HBV is mandatory before starting therapy [1]. It is also associated with Progressive Multifocal Leukoencephalopathy (PML) [1].

Question 129: Peripheral neuropathy may occur with the use of all the following anticancer agents except?

A. Vincristine
B. Cisplatin
C. L-Asparaginase (Correct Answer)
D. Procarbazine

Explanation: **Explanation:** The correct answer is **L-Asparaginase**. **1. Why L-Asparaginase is the correct answer:** L-Asparaginase is an enzyme used primarily in Acute Lymphoblastic Leukemia (ALL). Its mechanism involves depleting circulating asparagine, which leukemic cells cannot synthesize. Unlike many other chemotherapeutic agents, it does not interfere with microtubule function or cause direct axonal damage. Its hallmark toxicities are related to protein synthesis inhibition, leading to **hypoalbuminemia, pancreatitis, and clotting factor deficiencies** (causing both thrombosis and hemorrhage). It is notably **not** associated with peripheral neuropathy. **2. Why the other options are incorrect:** * **Vincristine:** A microtubule inhibitor (Vinca alkaloid) that disrupts axonal transport. It is the most notorious cause of peripheral neuropathy among anticancer drugs, often presenting as "glove and stocking" anesthesia and foot drop. * **Cisplatin:** A platinum compound known for causing significant sensory neurotoxicity (ototoxicity and peripheral neuropathy) due to accumulation in the dorsal root ganglia. * **Procarbazine:** An alkylating agent that can cause a variety of CNS effects and peripheral neuropathy, especially when used in combination regimens like MOPP. **Clinical Pearls for NEET-PG:** * **Microtubule Inhibitors:** Both Vincas (Vincristine) and Taxanes (Paclitaxel) are high-yield causes of neuropathy. * **Cisplatin Toxicity Triad:** Nephrotoxicity, Ototoxicity, and Peripheral Neuropathy. (Amifostine is used to reduce nephrotoxicity). * **L-Asparaginase Unique Fact:** It is the only anticancer drug that acts as an enzyme and is known for causing **Acute Pancreatitis**. * **Thalidomide & Bortezomib:** Other important non-cytotoxic agents frequently tested for causing peripheral neuropathy.

Question 130: Which of the following statements about rituximab is FALSE?

A. It is a chimeric monoclonal antibody against CD-20.
B. It has dose-dependent kinetics. (Correct Answer)
C. It is used for the treatment of non-Hodgkin lymphoma.
D. Its most common adverse effect is infusion-related reactions.

Explanation: **Explanation** **Rituximab** is a cornerstone of immunotherapy in hematological malignancies and autoimmune disorders. Understanding its pharmacology is high-yield for NEET-PG. **1. Why Option B is the correct (False) statement:** Rituximab follows **non-linear (target-mediated) pharmacokinetics**, but it does **not** follow simple dose-dependent kinetics in the traditional sense. Its clearance decreases with repeated dosing because as the tumor burden (CD20+ cells) decreases, there are fewer targets for the drug to bind to, leading to a longer half-life over time. Therefore, its elimination is more dependent on the **target burden** rather than just the dose administered. **2. Analysis of Incorrect Options:** * **Option A (True):** Rituximab is a **chimeric** monoclonal antibody (indicated by the suffix *-ximab*). It specifically targets the **CD20 antigen** found on the surface of normal and malignant B-lymphocytes. * **Option C (True):** It is a first-line agent for **Non-Hodgkin Lymphoma (NHL)**, particularly Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma. It is also used in Chronic Lymphocytic Leukemia (CLL) and Rheumatoid Arthritis. * **Option D (True):** The **most common adverse effect** is **infusion-related reactions** (fever, chills, rigors), occurring typically during the first infusion due to cytokine release. **Clinical Pearls for NEET-PG:** * **Mechanism:** Causes B-cell lysis via Antibody-Dependent Cellular Cytotoxicity (ADCC) and Complement-Dependent Cytotoxicity (CDC). * **Black Box Warning:** Reactivation of **Hepatitis B virus (HBV)**; screening is mandatory before starting therapy. * **Rare Side Effect:** Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation. * **Target:** CD20 is expressed on pre-B and mature B cells but **not** on hematopoietic stem cells or plasma cells.

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

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Hormonal Agents

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Targeted Therapy

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Immunotherapy

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Management of Chemotherapy Side Effects

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