Oncology — MCQs

Oncology Indian Medical PG Practice Questions and MCQs

Question 31: Alpha-fetoprotein (AFP) is a marker for which of the following conditions?

A. Hepatoma
B. Seminoma
C. Neural tube defects
D. All of the above (Correct Answer)

Explanation: **Explanation:** Alpha-fetoprotein (AFP) is a glycoprotein normally produced by the fetal yolk sac and liver. In clinical practice, it serves as a crucial tumor marker and a screening tool for fetal anomalies. **Why "All of the above" is correct:** 1. **Hepatoma (Hepatocellular Carcinoma - HCC):** AFP is the primary tumor marker for HCC [1]. Levels >400 ng/mL in a patient with a liver mass are highly suggestive of malignancy. It is also used to monitor recurrence post-treatment. 2. **Seminoma (and Non-Seminomatous Germ Cell Tumors):** While **pure seminomas** typically do not produce AFP (they may secrete hCG), any elevation of AFP in a patient with a suspected seminoma indicates the presence of **yolk sac components** (mixed germ cell tumor) [2]. Therefore, AFP is a vital marker in the management and staging of testicular germ cell tumors. 3. **Neural Tube Defects (NTDs):** During pregnancy, maternal serum AFP (MSAFP) is used for screening. Elevated levels are associated with open NTDs (e.g., spina bifida, anencephaly) due to the leakage of fetal serum into the amniotic fluid. **High-Yield Clinical Pearls for NEET-PG:** * **Elevated AFP:** Seen in HCC, Yolk sac tumors (Endodermal sinus tumors), NTDs, and abdominal wall defects (Omphalocele/Gastroschisis). * **Rule of Thumb:** If a testicular biopsy says "Seminoma" but AFP is elevated, treat it as a **Non-Seminomatous Germ Cell Tumor (NSGCT)**. * **Other markers:** Remember that **hCG** is elevated in Choriocarcinoma and Seminoma [2], while **LDH** correlates with tumor burden in dysgerminomas.

Question 32: Maffucci syndrome is characterized by which of the following?

A. Enchondromas
B. Cavernous hemangiomas
C. Chondrosarcomas
D. Hamartomas (Correct Answer)

Explanation: **Explanation:** Maffucci syndrome is a rare genetic disorder characterized by the presence of multiple **enchondromas** (benign cartilage tumors) associated with multiple **soft tissue hemangiomas** (typically cavernous hemangiomas). In the context of pathology, both enchondromas and hemangiomas are classified as **hamartomas**—disorganized growths of mature cells indigenous to the particular site. Therefore, "Hamartomas" serves as the most encompassing pathological description for the lesions found in this syndrome. **Analysis of Options:** * **A. Enchondromas:** While these are a hallmark of Maffucci syndrome, they are only one component of the disease. The question asks for a characteristic that defines the nature of the lesions; enchondromas are themselves a type of cartilaginous hamartoma. * **B. Cavernous hemangiomas:** These are the classic vascular component of the syndrome, but like enchondromas, they represent only half of the clinical picture. * **C. Chondrosarcomas:** This is a common **malignant transformation** (occurring in up to 100% of cases over a lifetime) rather than the primary defining characteristic of the syndrome itself. * **D. Hamartomas (Correct):** This is the correct pathological classification for both the skeletal and vascular lesions seen in Maffucci syndrome. **NEET-PG High-Yield Pearls:** * **Genetics:** Most cases are sporadic and associated with somatic mutations in **IDH1 or IDH2** genes. * **Ollier Disease vs. Maffucci:** Ollier disease presents with multiple enchondromas only; Maffucci syndrome includes enchondromas **plus** hemangiomas. * **Malignancy Risk:** Maffucci has a significantly higher risk of secondary malignancies compared to Ollier disease, including chondrosarcoma, ovarian tumors, and pancreatic adenocarcinoma. * **Clinical Sign:** Look for "phleboliths" (calcified thrombi) on X-rays of the soft tissue hemangiomas.

Question 33: A 72-year-old woman presented with skin changes over her left breast. She had a history of breast cancer 5 years earlier and was treated with a lumpectomy and radiation therapy. What is the diagnosis?

A. Inflammatory breast cancer
B. Mastitis
C. Radiation-induced angiosarcoma (Correct Answer)
D. Fat necrosis

Explanation: ***Radiation-induced angiosarcoma*** - Develops **5-10 years** after radiation therapy for breast cancer, with skin changes in the previously irradiated field being highly suggestive of this rare but serious complication. - Presents as **purple, bruise-like lesions** or nodules on the skin, often mistaken for benign conditions but requiring urgent biopsy and aggressive treatment. *Inflammatory breast cancer* - Characterized by **rapid onset** of breast erythema, warmth, and **peau d'orange** appearance, typically occurring in previously untreated breast tissue. - Usually presents with **lymphatic invasion** and aggressive clinical course, not typically associated with prior radiation therapy. *Mastitis* - Commonly occurs in **lactating women** with symptoms of breast pain, fever, and systemic illness from bacterial infection. - Responds well to **antibiotics** and is not associated with skin changes following radiation therapy years later. *Fat necrosis* - Presents as **firm, painless masses** following trauma or surgery, often with characteristic **oil cysts** on imaging. - Typically occurs **immediately** or within months of radiation, not years later, and lacks the vascular skin changes seen in angiosarcoma.

Question 34: What is the most common cause of ectopic ACTH production?

A. Renal cell carcinoma
B. Hepatocellular carcinoma
C. Small cell carcinoma of the lung (Correct Answer)
D. Pheochromocytoma

Explanation: **Explanation:** **Ectopic ACTH Syndrome** occurs when a non-pituitary tumor secretes adrenocorticotropic hormone, leading to ACTH-dependent Cushing syndrome [1]. 1. **Why Small Cell Carcinoma of the Lung (SCLC) is correct:** SCLC is a neuroendocrine tumor and is the **most common cause** of ectopic ACTH production, accounting for approximately 50% of cases [2]. These tumors possess the cellular machinery to express the *POMC* gene, the precursor to ACTH. Clinically, these patients often present with rapid-onset hypertension, profound hypokalemia, and metabolic alkalosis, rather than the classic "cushingoid" physical features (like buffalo hump), due to the aggressive nature of the underlying malignancy. 2. **Why the other options are incorrect:** * **Renal cell carcinoma:** While RCC is known for various paraneoplastic syndromes (like EPO production leading to polycythemia or PTHrP leading to hypercalcemia), it is a very rare cause of ectopic ACTH [2]. * **Hepatocellular carcinoma:** Similar to RCC, HCC can cause paraneoplastic hypoglycemia or erythrocytosis, but it is not a classic source of ACTH [2]. * **Pheochromocytoma:** While pheochromocytomas are neuroendocrine tumors and *can* secrete ACTH, they are much rarer causes compared to SCLC. **NEET-PG High-Yield Pearls:** * **Most common cause of Ectopic ACTH:** Small cell carcinoma of the lung [2]. * **Second most common cause:** Carcinoid tumors (especially bronchial carcinoids). * **Diagnostic clue:** High ACTH levels that are **not suppressed** by high-dose dexamethasone (8mg), unlike Pituitary Cushing’s (Cushing Disease). * **Classic Lab Finding:** Severe hypokalemia is a hallmark of ectopic ACTH due to the mineralocorticoid effects of high cortisol levels.

Question 35: What is true about malignant melanoma?

A. Lymphatic spread (Correct Answer)
B. Lymph node biopsy is always done
C. Biopsy is done when the sentinel node is involved
D. Microsatellitism is seen

Explanation: **Explanation:** **Malignant Melanoma** is a highly aggressive cutaneous malignancy arising from melanocytes [1]. Understanding its pattern of spread and staging is crucial for NEET-PG. **1. Why Option A is Correct:** The primary mode of initial metastasis for malignant melanoma is **lymphatic spread** to regional lymph nodes. This occurs via the lymphatic channels draining the primary site. The presence of regional lymph node involvement is the most important prognostic factor in patients with localized melanoma. **2. Why the other options are incorrect:** * **Option B:** Lymph node biopsy (or Sentinel Lymph Node Biopsy - SLNB) is **not always done**. It is generally indicated for intermediate-thickness melanomas (Breslow thickness 1 mm or more) or thinner lesions with high-risk features [1]. It is not indicated for very thin, low-risk lesions (Tis or T1a). * **Option C:** This is logically reversed. A **Sentinel Lymph Node Biopsy (SLNB)** is performed to *determine* if the node is involved [1]. If the sentinel node is positive, further management (like Completion Lymph Node Dissection or adjuvant therapy) is considered. * **Option D:** While **microsatellitosis** (microscopic nests of tumor cells >0.05 mm in diameter, separate from the primary tumor) can occur in melanoma, it is a specific pathological feature used for staging (N-category) rather than a universal defining characteristic or the "most true" general statement compared to the fundamental mechanism of lymphatic spread. **Clinical Pearls for NEET-PG:** * **Breslow Depth:** The most important prognostic factor (vertical thickness in mm) [1]. * **ABCDE Criteria:** Asymmetry, Border irregularity, Color variegation, Diameter >6mm, Evolving. * **Commonest Site:** Back (Men), Lower limbs (Women). * **Commonest Type:** Superficial Spreading Melanoma. * **Most Aggressive Type:** Nodular Melanoma. * **S-100 and HMB-45:** Key immunohistochemical markers.

Question 36: What are the commonly used criteria for response evaluation during cancer treatment?

A. RECIST (Correct Answer)
B. WHO pain score
C. Drug dose score
D. Ki67 score

Explanation: **Explanation:** The assessment of treatment efficacy in solid tumors is standardized using the **RECIST (Response Evaluation Criteria in Solid Tumors)**. Currently, version 1.1 is the gold standard used in clinical trials and practice. It relies on objective anatomical measurements (CT/MRI) of "target lesions" to categorize response into four groups: Complete Response (CR), Partial Response (PR), Stable Disease (SD), and Progressive Disease (PD). **Analysis of Options:** * **RECIST (Correct):** It provides a simplified, evidence-based method to quantify tumor burden changes. It uses the sum of the longest diameters (SLD) for non-nodal lesions and the short axis for lymph nodes. * **WHO Pain Score:** This is a tool for assessing pain intensity and guiding analgesic therapy (the WHO Analgesic Ladder), not for measuring tumor size or treatment response. * **Drug Dose Score:** This is not a standardized oncological metric for response evaluation; it may refer to pharmacovigilance or dosing protocols. * **Ki67 Score:** This is a cellular proliferation marker (immunohistochemistry) used for prognosis and grading [1], but it is not used to evaluate the overall clinical response to treatment. **High-Yield Clinical Pearls for NEET-PG:** * **RECIST 1.1 Criteria:** A **Partial Response (PR)** is defined as a **≥30% decrease** in the sum of diameters of target lesions. **Progressive Disease (PD)** is defined as a **≥20% increase** in the sum of diameters or the appearance of new lesions. * **iRECIST:** A modified version used specifically for **Immunotherapy**, accounting for "pseudoprogression" (initial increase in tumor size due to immune cell infiltration). * **Lugano Classification:** The standard for response evaluation in **Lymphoma**, which incorporates PET-CT (Deauville criteria) rather than just size.

Question 37: What is true about PEComa (perivascular epithelioid cell tumor)?

A. Melanin and HMB45 are markers (Correct Answer)
B. It is a malignant melanoma variant
C. It contains perivascular epithelioid cells
D. Angiomyolipoma (AML) is a subtype

Explanation: **Explanation:** **PEComas (Perivascular Epithelioid Cell Tumors)** are a unique family of mesenchymal tumors composed of histologically and immunohistochemically distinctive perivascular epithelioid cells. **Why Option A is correct:** The hallmark of PEComas is their **dual immunoreactivity**. They characteristically express both **myogenic markers** (like smooth muscle actin and desmin) and **melanocytic markers** (specifically **HMB-45**, Melan-A, and sometimes microphthalmia transcription factor/MITF). The presence of premelanosomes and melanin pigment is a defining feature that aids in diagnosis, making HMB-45 a highly specific marker for this group. **Analysis of Incorrect Options:** * **Option B:** While PEComas express melanocytic markers, they are **not** variants of malignant melanoma. They are distinct mesenchymal neoplasms arising from primitive cells, whereas melanomas arise from melanocytes. * **Option C:** This statement is technically true regarding the composition of the tumor; however, in the context of standard NEET-PG questioning, the **immunohistochemical profile (Option A)** is considered the most definitive "true" diagnostic feature used to distinguish it from other mimics. * **Option D:** This is a common point of confusion. **Angiomyolipoma (AML)**, along with Clear Cell Sugar Tumor (CCST) of the lung and Lymphangiomyomatosis (LAM), are actually members of the **PEComa family**, not subtypes of a single "PEComa" entity. **High-Yield Clinical Pearls for NEET-PG:** * **Association:** PEComas are strongly associated with **Tuberous Sclerosis Complex (TSC1/TSC2 mutations)**. * **Common Sites:** While they can occur anywhere, the most common sites are the uterus, kidney (AML), and lung (CCST). * **Treatment:** For malignant cases, **mTOR inhibitors** (like Sirolimus) are the targeted therapy of choice due to the activation of the mTOR pathway in these tumors.

Question 38: A patient with a Pancoast tumor develops a loss of voice after radiation. What is the most likely cause of this symptom?

A. Vocal cord infiltration with secondaries
B. Involvement of the recurrent laryngeal nerve (Correct Answer)
C. Direct irradiation to the vocal cords
D. Radiation stenosis of the larynx

Explanation: ### Explanation **Correct Option: B. Involvement of the recurrent laryngeal nerve** A Pancoast tumor (Superior Sulcus Tumor) is a bronchogenic carcinoma arising from the apex of the lung. The **Recurrent Laryngeal Nerve (RLN)**, particularly on the left side, loops around the arch of the aorta, while the right RLN loops around the subclavian artery. As a Pancoast tumor expands or causes local inflammatory changes/fibrosis following radiation, it can compress or infiltrate the RLN. This leads to **vocal cord paralysis**, typically presenting as hoarseness or a "bovine cough." [1] In the context of post-radiation, the symptom is often due to tumor progression or radiation-induced fibrosis affecting the nerve's path. **Why Incorrect Options are Wrong:** * **A. Vocal cord infiltration with secondaries:** While lung cancer metastasizes widely, direct secondary deposits on the vocal cords are extremely rare compared to the common mechanism of nerve compression. * **C. Direct irradiation to the vocal cords:** Pancoast tumors are apical; radiation fields are targeted at the lung apex and superior mediastinum. The larynx is generally superior to the treatment field, making direct radiation damage to the cords unlikely. * **D. Radiation stenosis of the larynx:** This is a late complication of head and neck cancers (e.g., laryngeal cancer) where the larynx is the primary target. It is not a standard complication of treating an apical lung tumor. **NEET-PG High-Yield Pearls:** * **Pancoast Syndrome Triad:** Ipsilateral Horner’s syndrome, shoulder pain radiating down the arm (C8-T2 distribution), and atrophy of hand intrinsic muscles. * **Horner’s Syndrome:** Caused by involvement of the **paravertebral sympathetic chain** (specifically the stellate ganglion). * **Most common histology:** Squamous cell carcinoma (though Adenocarcinoma is increasing in frequency). * **Phrenic Nerve involvement:** Can lead to hemidiaphragm paralysis (seen as an elevated dome on CXR). [2]

Question 39: Bilateral Renal cell carcinoma is seen in which of the following conditions?

A. Eagle Barrett syndrome
B. Beckwith-Wiedemann syndrome
C. Von Hippel-Lindau disease (Correct Answer)
D. Bilateral Angiomyolipoma

Explanation: Explanation: **Correct Answer: C. Von Hippel-Lindau (VHL) disease** Von Hippel-Lindau disease is an autosomal dominant multisystem neoplastic syndrome caused by a mutation in the **VHL gene on chromosome 3p25**. The VHL protein normally targets Hypoxia-Inducible Factor (HIF) for degradation. Its absence leads to increased angiogenesis and tumorigenesis. **Clear cell Renal Cell Carcinoma (RCC)** occurs in approximately 40-70% of VHL patients and is characteristically **bilateral and multicentric**, occurring at a much younger age than sporadic cases. [1] **Analysis of Incorrect Options:** * **A. Eagle-Barrett Syndrome (Prune Belly Syndrome):** Characterized by the triad of abdominal muscle deficiency, undescended testes, and urinary tract abnormalities (e.g., megaureter). It is not associated with a predisposition to RCC. * **B. Beckwith-Wiedemann Syndrome:** An overgrowth disorder (macrosomia, macroglossia, omphalocele). While it increases the risk of embryonal tumors, the classic renal association is **Wilms tumor**, not RCC. * **D. Bilateral Angiomyolipoma:** These are benign mesenchymal tumors composed of fat, blood vessels, and smooth muscle. They are strongly associated with **Tuberous Sclerosis**, not RCC. **High-Yield Clinical Pearls for NEET-PG:** * **VHL Manifestations (H-H-P-R):** **H**emangioblastomas (Retina/Cerebellum), **H**epatopancreatic cysts, **P**heochromocytoma, and **R**enal cell carcinoma (Clear cell type). * **Chromosome 3:** The "Rule of 3" applies—VHL gene is on Chromosome 3, and Clear cell RCC is associated with deletions of 3p. [1] * **Screening:** In VHL patients, annual abdominal imaging is recommended to detect RCC early.

Question 40: Tumor lysis syndrome causes all of the following EXCEPT:

A. Hypercalcemia (Correct Answer)
B. Hyperuricemia
C. Hypermagnesemia
D. Hyperkalemia

Explanation: **Explanation:** Tumor Lysis Syndrome (TLS) is an oncologic emergency caused by the rapid destruction of a large number of metabolically active tumor cells (usually following chemotherapy for high-grade lymphomas or leukemias). When these cells rupture, they release their intracellular contents into the systemic circulation. **Why Hypercalcemia is the correct answer:** TLS characteristically causes **Hypocalcemia**, not hypercalcemia. This occurs because the massive release of intracellular phosphorus leads to **Hyperphosphatemia**. The excess phosphate binds to ionized calcium, forming calcium-phosphate crystals that precipitate in soft tissues and the kidneys, thereby lowering serum calcium levels. **Analysis of other options:** * **Hyperuricemia (B):** Nucleic acids from the destroyed cell nuclei are catabolized into purines and then into uric acid by xanthine oxidase. This can lead to uric acid nephropathy. * **Hypermagnesemia (C):** Magnesium is primarily an intracellular cation. Rapid cell lysis releases magnesium into the blood. While less clinically emphasized than potassium, it is a recognized component of the electrolyte derangement in TLS. * **Hyperkalemia (D):** Potassium is the major intracellular cation. Its rapid release is the most immediate life-threatening complication of TLS, potentially causing fatal arrhythmias. **NEET-PG Clinical Pearls:** * **Cairo-Bishop Definition:** TLS is defined by derangements in four metabolic parameters: **↑ Uric acid, ↑ Potassium, ↑ Phosphate, and ↓ Calcium.** * **Prophylaxis:** Aggressive hydration is the most important step. * **Treatment:** **Rasburicase** (recombinant urate oxidase) is the drug of choice for established TLS as it converts uric acid to the highly soluble allantoin. **Allopurinol** is used for prophylaxis but does not reduce existing uric acid.

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Oncology — MCQs

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