Oncology — MCQs

Oncology Indian Medical PG Practice Questions and MCQs

Question 101: NNK, NNN, and polonium 210 are carcinogens specific for which type of cancer?

A. Tobacco-related oral cancer (Correct Answer)
B. Tobacco-related bronchogenic carcinoma
C. Prostatic carcinoma
D. Hepatocellular carcinoma

Explanation: ### Explanation The correct answer is **A. Tobacco-related oral cancer.** **Understanding the Concept:** Tobacco contains over 60 known carcinogens. Among these, **Tobacco-Specific Nitrosamines (TSNAs)** are the most potent. * **NNK** [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] and **NNN** (N-nitrosonornicotine) are formed by the nitrosation of nicotine during the curing and processing of tobacco [2]. * **Polonium-210** is a radioactive alpha-emitter absorbed by tobacco leaves from phosphate fertilizers. While these are found in cigarette smoke, they are uniquely concentrated in **smokeless tobacco (chewing tobacco/snuff)**. NNN and NNK undergo metabolic activation to form DNA adducts, leading to mutations in the oral mucosa, making them the primary drivers for **oral cavity cancers**. **Analysis of Incorrect Options:** * **B. Bronchogenic Carcinoma:** While NNK is a systemic carcinogen that can cause lung cancer, the primary drivers for lung cancer in smokers are **Polycyclic Aromatic Hydrocarbons (PAHs)** like Benzo[a]pyrene [1]. * **C. Prostatic Carcinoma:** This is primarily linked to age, genetics (BRCA2), and hormonal factors (androgens), rather than specific tobacco nitrosamines. * **D. Hepatocellular Carcinoma:** The major risk factors are Chronic Hepatitis B/C, Alcohol, and **Aflatoxin B1** (produced by *Aspergillus*) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most potent TSNA:** NNK is considered the most carcinogenic. * **Benzo[a]pyrene:** The classic "high-yield" carcinogen associated with cigarette smoke and lung cancer (induces *TP53* mutations). * **Vinyl Chloride:** Associated with Angiosarcoma of the liver. * **Beta-naphthylamine:** Associated with Transitional Cell Carcinoma (TCC) of the bladder in dye industry workers [1].

Question 102: All of the following are examples of cardiotoxic drugs except?

A. Cyclophosphamide
B. 5-FU
C. Adriamycin
D. Cisplatin (Correct Answer)

Explanation: **Explanation:** The correct answer is **Cisplatin**. While Cisplatin is associated with significant nephrotoxicity and ototoxicity, it is not traditionally classified as a primary cardiotoxic agent. **1. Why Cisplatin is the correct answer:** Cisplatin’s dose-limiting toxicities are **nephrotoxicity** (prevented by aggressive hydration and amifostine) and **ototoxicity**. While it may rarely cause electrolyte imbalances that lead to secondary arrhythmias, it does not have a direct, predictable toxic effect on the myocardium compared to the other drugs listed. **2. Why the other options are wrong:** * **Adriamycin (Doxorubicin):** The classic example of cardiotoxicity. It causes dose-dependent, irreversible dilated cardiomyopathy via **oxygen free radical formation** and lipid peroxidation. The lifetime cumulative dose is limited to <450–550 mg/m². * **5-Fluorouracil (5-FU):** Known for causing **coronary vasospasm**, which can manifest as angina or even myocardial infarction. This is a unique form of cardiotoxicity unrelated to pump failure. * **Cyclophosphamide:** High doses (usually in bone marrow transplant settings) can cause **acute hemorrhagic myocarditis** and pericardial effusion. **Clinical Pearls for NEET-PG:** * **Anthracyclines (Adriamycin):** Monitor with ECHO/MUGA scans; look for a drop in Left Ventricular Ejection Fraction (LVEF). **Dexrazoxane** is the antidote used to prevent damage. * **Trastuzumab (Herceptin):** Also causes cardiotoxicity, but unlike Adriamycin, it is **not dose-dependent** and is usually **reversible** upon discontinuation. * **Taxanes (Paclitaxel):** Frequently cause asymptomatic documentation.

Question 103: Kaposi sarcoma is commonly seen in which part of the body?

A. Upper limbs
B. Lower limbs (Correct Answer)
C. Head and neck
D. Trunk

Explanation: **Explanation:** Kaposi Sarcoma (KS) is a multicentric vascular neoplasm caused by **Human Herpesvirus 8 (HHV-8)** [1]. It is most frequently associated with HIV/AIDS (Epidemic KS) and elderly men of Mediterranean or Eastern European descent (Classic KS). **Why Lower Limbs is Correct:** In the **Classic (Sporadic) form** of Kaposi Sarcoma, the lesions typically manifest as purple, red, or brown macules, plaques, or nodules. These lesions have a strong predilection for the **lower extremities**, particularly the distal portions like the feet and ankles. This is attributed to venous stasis and lymphedema, which are thought to promote the local proliferation of spindle cells and inflammatory cytokines. **Analysis of Incorrect Options:** * **Upper Limbs:** While KS can involve the arms, it is rarely the primary or most common site of presentation compared to the legs. * **Head and Neck:** In HIV-associated (Epidemic) KS, lesions frequently appear on the face (especially the nose) and the oral cavity (hard palate) [1]. However, across all clinical subtypes, the lower limbs remain the most characteristic site for initial cutaneous manifestation. * **Trunk:** Truncal involvement is usually seen in advanced, disseminated stages of the disease rather than as the primary site of presentation. **NEET-PG High-Yield Pearls:** * **Pathogenesis:** Proliferation of spindle cells (endothelial origin) infected with **HHV-8**. * **Histology:** Characterized by **slit-like vascular spaces** containing extravasated red blood cells and hemosiderin staining. * **Clinical Variants:** Classic (Elderly), Endemic (African), Iatrogenic (Transplant-related), and Epidemic (AIDS-related) [1]. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) is the first-line treatment for AIDS-related KS; localized lesions may be treated with cryotherapy or radiation.

Question 104: Lutetium dotatate was approved by FDA in 2018 for which of the following conditions?

A. Tuberculosis
B. Neuroendocrine tumours (Correct Answer)
C. Crohn's disease
D. Peptic ulcer

Explanation: **Explanation:** **Lutetium-177 (177Lu) dotatate** (commercially known as Lutathera) represents a breakthrough in **Peptide Receptor Radionuclide Therapy (PRRT)**. Its approval by the FDA in 2018 marked a significant shift in the management of somatostatin receptor-positive **Neuroendocrine Tumors (NETs)**, specifically those affecting the gastroenteropancreatic system (GEP-NETs) [2]. **Why the correct answer is right:** The mechanism of action involves a "search and destroy" approach. Lutetium-177 is a beta-emitting radionuclide conjugated to **DOTATATE**, a somatostatin analog. Most NETs overexpress **Somatostatin Receptors (SSTR)**, particularly subtype 2 [3]. The DOTATATE molecule binds specifically to these receptors, allowing the Lutetium-177 to be internalized into the tumor cell. Once inside, the beta radiation causes localized DNA damage, leading to tumor cell death while sparing surrounding healthy tissue. **Why incorrect options are wrong:** * **Tuberculosis (A):** An infectious disease caused by *M. tuberculosis*; treated with multidrug antitubercular therapy (ATT), not radiopharmaceuticals. * **Crohn’s Disease (C):** An inflammatory bowel disease (IBD) managed with immunosuppressants, steroids, and biologics (e.g., Infliximab) [4]. * **Peptic Ulcer (D):** A mucosal break caused by *H. pylori* or NSAIDs; treated with Proton Pump Inhibitors (PPIs) and antibiotics [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Specifically approved for adult patients with SSTR-positive GEP-NETs (including foregut, midgut, and hindgut tumors) [2]. * **Diagnostic Pairing:** Before treatment, a **Ga-68 DOTATATE PET/CT** (Theranostics) is usually performed to confirm SSTR expression. * **Side Effects:** The most critical dose-limiting toxicity is **nephrotoxicity** and bone marrow suppression. Amino acid infusions (Lysine/Arginine) are administered concurrently to protect the kidneys. * **Radiation Type:** Lutetium-177 is primarily a **Beta emitter** (for therapy) but also emits low-energy **Gamma rays**, which allows for post-therapy imaging (scintigraphy).

Question 105: Which of the following conditions is associated with hypercalcemia?

A. Pancreatic cancer
B. Hepatocellular carcinoma (Correct Answer)
C. Gastric cancer
D. Gallbladder cancer

Explanation: **Explanation:** Hypercalcemia in malignancy is primarily driven by three mechanisms: secretion of **Parathyroid Hormone-related Protein (PTHrP)**, local osteolytic bone metastases, or excessive production of 1,25-dihydroxyvitamin D [1]. **Hepatocellular Carcinoma (HCC)** is a well-recognized cause of **Paraneoplastic Syndrome**, specifically through the secretion of PTHrP [1]. This protein mimics the action of PTH by binding to the same receptors in the bone and kidneys, leading to increased bone resorption and calcium reabsorption [3]. While not the most common malignancy associated with hypercalcemia (squamous cell carcinomas of the lung and head/neck are more frequent), HCC is the correct choice among the provided gastrointestinal/hepatobiliary options [1]. **Analysis of Incorrect Options:** * **Pancreatic, Gastric, and Gallbladder cancers:** While any advanced malignancy with extensive bone metastasis can theoretically cause hypercalcemia, these cancers are rarely associated with humoral hypercalcemia of malignancy (PTHrP secretion) [2]. They are much more likely to present with other paraneoplastic features (e.g., Trousseau sign in pancreatic cancer) or obstructive symptoms rather than metabolic hypercalcemia. **High-Yield NEET-PG Pearls:** * **Most common cause of hypercalcemia in hospitalized patients:** Malignancy. * **Most common mechanism:** Humoral hypercalcemia of malignancy (PTHrP) – accounts for ~80% of cases. * **Common PTHrP-secreting tumors:** Squamous cell carcinoma (Lung, Head/Neck), Renal Cell Carcinoma (RCC), Breast cancer, and HCC [1]. * **Treatment of choice:** Aggressive IV hydration with normal saline is the first step; Bisphosphonates (Zoledronic acid) are the mainstay for long-term management.

Question 106: Which of the following antineoplastic agents is used in the management of Hodgkin's lymphoma, non-Hodgkin's lymphoma, and small cell carcinoma of the lung?

A. Cisplatin (Correct Answer)
B. Bleomycin
C. Paclitaxel
D. Doxorubicin

Explanation: **Explanation:** The correct answer is **Cisplatin**. Cisplatin is a potent platinum-based alkylating-like agent that causes cross-linking of DNA strands, leading to apoptosis. It is a cornerstone of "combination chemotherapy" due to its broad-spectrum activity against both solid tumors and hematological malignancies. * **Why Cisplatin is correct:** It is a key component in salvage regimens for **Hodgkin’s Lymphoma** (e.g., DHAP: Dexamethasone, High-dose Ara-C, Cisplatin) and **Non-Hodgkin’s Lymphoma** (e.g., ESHAP) [1]. Furthermore, it is the gold-standard first-line treatment for **Small Cell Lung Cancer (SCLC)**, usually combined with Etoposide [1]. **Analysis of Incorrect Options:** * **Bleomycin:** While used in Hodgkin’s (ABVD regimen), it has no significant role in Small Cell Lung Cancer. Its main side effect is pulmonary fibrosis. * **Paclitaxel:** Primarily used in Non-Small Cell Lung Cancer (NSCLC), breast, and ovarian cancers. It is not a standard first-line agent for Hodgkin’s or SCLC. * **Doxorubicin:** Though a mainstay for Hodgkin’s (ABVD) and NHL (CHOP), it is rarely used for SCLC compared to the platinum-etoposide backbone. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Toxicity:** Characterized by the "3 Ns": **N**ephrotoxicity (prevented by aggressive hydration and Amifostine), **N**eurotoxicity (peripheral neuropathy), and severe **N**ausea/vomiting (highly emetogenic). It is also associated with **Ototoxicity**. * **Small Cell Lung Cancer:** Always remember the "Platinum + Etoposide" duo as the classic answer for management [1]. * **Vincristine vs. Vinblastine:** Remember **B**lastine for **B**one marrow suppression; **C**ristine for **C**onstipation and peripheral neuropathy.

Question 107: Which of the following is NOT true about Zollinger-Ellison syndrome?

A. Surgery is a treatment option.
B. It involves an exocrine tumor. (Correct Answer)
C. It is an endocrine disorder.
D. Secretory diarrhea is a common symptom.

Explanation: **Explanation:** Zollinger-Ellison Syndrome (ZES) is characterized by the development of a **gastrinoma**, a neuroendocrine tumor that secretes excessive amounts of gastrin [1]. **1. Why Option B is the correct answer (The "NOT true" statement):** ZES involves an **endocrine** tumor, not an exocrine one. Gastrinomas arise from the G-cells (neuroendocrine cells) typically located in the "gastrinoma triangle" (duodenum, pancreas, or lymph nodes) [1]. Exocrine tumors of the pancreas (like adenocarcinoma) arise from ductal cells and do not secrete hormones into the bloodstream. **2. Analysis of other options:** * **Option A (Surgery):** Surgery is a definitive treatment option, especially for localized tumors without metastasis, to prevent malignancy and control hormonal excess. * **Option C (Endocrine disorder):** This is true. ZES is a classic endocrine pathology where ectopic hormone production (gastrin) leads to systemic effects (hyperchlorhydria) [1]. * **Option D (Secretory diarrhea):** This is a hallmark symptom. The massive acid production inactivates pancreatic enzymes and damages the intestinal mucosa, leading to malabsorption and secretory diarrhea. **Clinical Pearls for NEET-PG:** * **The Triad:** Gastric acid hypersecretion, severe peptic ulceration, and non-beta cell islet tumor (gastrinoma). * **Association:** Approximately 25% of ZES cases are associated with **Multiple Endocrine Neoplasia Type 1 (MEN1)**. * **Diagnosis:** Best initial test is **fasting serum gastrin levels** (>1000 pg/mL is diagnostic). The most specific provocative test is the **Secretin Stimulation Test** (paradoxical rise in gastrin) [1]. * **Location:** Most gastrinomas are found in the **Gastrinoma Triangle** (Passaro's Triangle).

Question 108: A 64-year-old man receiving chemotherapy for squamous cell cancer of the lung develops erythema, induration, thickening, and eventual peeling of the skin on his fingers, palms, and soles of his feet. What is the most likely chemotherapeutic agent causing this adverse reaction?

A. methotrexate
B. cytarabine
C. 5-fluorouracil (5-FU)
D. bleomycin (Correct Answer)

Explanation: ### **Explanation** The clinical presentation described—erythema, induration, thickening, and peeling of the skin on the palms and soles—is characteristic of **Hand-Foot Syndrome (Palmar-Plantar Erythrodysesthesia)** or localized dermatological toxicity. **Why Bleomycin is the Correct Answer:** Bleomycin is unique among chemotherapeutic agents because it is inactivated by the enzyme **bleomycin hydrolase**. This enzyme is found in high concentrations in most tissues but is notably **deficient in the skin and the lungs**. Consequently, bleomycin accumulates in these organs, leading to its hallmark toxicities: pulmonary fibrosis and dermatological reactions [1]. Specific skin findings include hyperpigmentation (often "flagellate" streaks), hyperkeratosis, and the induration/peeling described in the question. These features of symmetrical thickening, tightening, and induration (sclerodactyly) reflect the drug's specialized skin toxicity [2]. **Why Other Options are Incorrect:** * **Methotrexate:** Primarily causes mucosal toxicity (mucositis/stomatitis), myelosuppression, and hepatotoxicity. While it can cause photosensitivity, it does not typically present with this specific induration/peeling pattern. * **Cytarabine:** Known for causing "Ara-C syndrome" (fever, rash, conjunctivitis) and cerebellar toxicity at high doses. * **5-Fluorouracil (5-FU):** While 5-FU and its prodrug Capecitabine are classic causes of Hand-Foot Syndrome, in the context of **Squamous Cell Carcinoma (SCC) of the lung**, Bleomycin is a more historically relevant and frequently tested association for specific scleroderma-like skin changes and induration. **NEET-PG High-Yield Pearls:** 1. **Flagellate Hyperpigmentation:** A pathognomonic sign for Bleomycin toxicity (linear streaks on the trunk). 2. **Pulmonary Toxicity:** Bleomycin causes interstitial fibrosis; monitor with DLCO (Diffusion Capacity of Lung). 3. **Cell Cycle:** Bleomycin is **G2 phase-specific** and works by inducing free radical formation, causing DNA strand breaks. 4. **Hand-Foot Syndrome (General):** Most commonly associated with **Capecitabine, 5-FU, and Cytarabine**. However, when "induration and thickening" are emphasized in a patient with SCC, think of Bleomycin’s scleroderma-like effects [2].

Question 109: Which paraneoplastic syndrome is NOT seen in renal cell carcinoma?

A. Acanthosis nigricans
B. Amyloidosis
C. Polycythemia (Correct Answer)
D. Systemic Lupus Erythematosus (SLE)

Explanation: Renal Cell Carcinoma (RCC) is famously known as the **"Internist’s Tumor"** because it presents with a wide array of paraneoplastic syndromes (PNS) due to the ectopic secretion of hormones and cytokines [1]. **Explanation of the Correct Answer:** The question asks which syndrome is **NOT** seen in RCC. However, there appears to be a discrepancy in the provided key: **Polycythemia is actually a classic paraneoplastic manifestation of RCC**, occurring in 1-5% of patients due to the ectopic production of **Erythropoietin (EPO)** [1]. In the context of standard medical examinations, **Systemic Lupus Erythematosus (SLE)** (Option D) is the correct answer for "NOT seen." While RCC can cause various autoimmune-like phenomena, it does not typically cause SLE. If the provided key insists on Polycythemia, it contradicts standard medical literature (Harrison’s Principles of Internal Medicine). **Analysis of Options:** * **Polycythemia:** A classic PNS of RCC caused by inappropriate EPO production [1]. * **Amyloidosis:** Secondary (AA) amyloidosis occurs in ~3-5% of RCC cases due to chronic inflammation and elevated Serum Amyloid A. * **Acanthosis Nigricans:** While more common in gastric cancer, it is a recognized (though rare) cutaneous paraneoplastic manifestation of various visceral malignancies, including RCC. * **SLE:** This is a primary autoimmune disease and is not recognized as a paraneoplastic syndrome of RCC. **High-Yield Clinical Pearls for NEET-PG:** * **Most common PNS in RCC:** Hypercalcemia (due to PTHrP) [1]. * **Stauffer’s Syndrome:** Reversible hepatic dysfunction (elevated LFTs) in the absence of liver metastases. * **Other common PNS:** Hypertension (Renin), Cushing’s syndrome (ACTH), and Galactorrhea (Prolactin). * **Classic Triad (only in 10%):** Hematuria, Flank pain, and Palpable mass [2].

Question 110: What is the recommended screening method for hepatocellular carcinoma (HCC) in patients with chronic liver disease?

A. Serial Ultrasound (USG) and Alpha-fetoprotein (AFP) (Correct Answer)
B. Serial Liver Function Tests (LFT) and AFP
C. Serial LFT and CT scan
D. Serial USG and serial LFT

Explanation: **Explanation:** The primary goal of screening for Hepatocellular Carcinoma (HCC) is early detection in high-risk individuals (primarily those with cirrhosis or chronic Hepatitis B/C) [1] to allow for curative interventions. **Why Option A is Correct:** The current standard of care, supported by AASLD and EASL guidelines, is the combination of **Abdominal Ultrasound (USG) and Serum Alpha-fetoprotein (AFP)** performed every **6 months**. * **USG** is the preferred imaging modality due to its non-invasive nature, cost-effectiveness, and high specificity [1]. * **AFP** is a tumor marker that increases the sensitivity of screening when used alongside USG, as USG alone may miss small lesions in a nodular cirrhotic liver [1]. **Why Other Options are Incorrect:** * **Options B & D (LFTs):** Liver Function Tests (ALT, AST, Bilirubin) reflect the degree of liver inflammation or synthetic dysfunction but are not diagnostic or predictive of malignancy. * **Option C (CT Scan):** While Triple-phase CT is the gold standard for *diagnosis* [1], it is not used for *screening* due to high costs, radiation exposure, and the risk of contrast-induced nephropathy [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Interval:** 6 months (based on the doubling time of HCC). * **Diagnostic Gold Standard:** Contrast-enhanced CT or MRI showing **"Wash-in"** (arterial enhancement) and **"Wash-out"** (venous/delayed phase) is diagnostic of HCC in cirrhotic patients [1]; a biopsy is often unnecessary. * **AFP Cut-off:** While >20 ng/mL is often used for screening, values >400 ng/mL are highly suggestive of HCC. * **Target Population:** All cirrhotic patients (Child-Pugh A and B) and specific non-cirrhotic HBV carriers.

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