Oncology — MCQs

A 74-year-old man presents with fatigue, shortness of breath on exertion, and back and rib pain worsened by movement. Investigations reveal anemia, elevated calcium, urea, and creatinine. X-rays show multiple lytic lesions in long bones and ribs, and protein electrophoresis is positive for an immunoglobulin G (IgG) paraprotein. What is the most likely mechanism for the renal injury?

Q56Easy

A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

Q57Easy

Which of the following are symptoms of carcinoid syndrome?

Q58Easy

What is the drug of choice for chronic myeloid leukemia?

Q59Medium

A 64-year-old man is admitted to the hospital for the assessment of hematuria after being involved in a motor vehicle accident. His physical examination is normal. A CT scan of the abdomen is shown in Figure below. Which of the following is the most likely diagnosis?

Q60Easy

A 62-year-old woman with a family history of breast cancer (her mother died of breast cancer at age 63) is concerned about her future risk. Which of the following features is a recognized risk factor for breast cancer?

Oncology Indian Medical PG Practice Questions and MCQs

Question 51: Tumor lysis syndrome is associated with all of the following laboratory features except?

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

Explanation: Explanation: Tumor Lysis Syndrome (TLS) is an oncologic emergency caused by the rapid lysis of malignant cells, usually following chemotherapy for high-grade hematologic malignancies (e.g., Burkitt lymphoma, ALL). When these cells rupture, they release their intracellular contents into the systemic circulation, leading to a predictable pattern of metabolic derangements. Why Hypercalcemia is the Correct Answer: TLS is characterized by Hypocalcemia, not hypercalcemia [1]. As intracellular phosphorus is released into the bloodstream (Hyperphosphatemia), it binds to circulating ionized calcium to form calcium-phosphate crystals. This precipitation leads to a secondary decrease in serum calcium levels, which can cause tetany or arrhythmias. Analysis of Incorrect Options: * Hyperkalemia (A): Potassium is the primary intracellular cation. Rapid cell lysis floods the extracellular space with potassium, which is the most immediate life-threatening complication of TLS due to the risk of cardiac arrest. * Hyperuricemia (C): The breakdown of intracellular nucleic acids releases purines, which are metabolized by the liver into uric acid. Excessive uric acid can crystallize in the renal tubules, leading to acute kidney injury (AKI). * Hyperphosphatemia (D): Malignant cells contain significantly higher concentrations of phosphorus than normal cells. Their destruction leads to a massive release of phosphate into the blood. NEET-PG High-Yield Pearls: * Cairo-Bishop Definition: Clinical TLS is diagnosed when laboratory TLS is present along with increased creatinine, seizures, or cardiac arrhythmias. * Prophylaxis/Treatment: Aggressive hydration is the mainstay. Allopurinol (xanthine oxidase inhibitor) prevents new uric acid formation, while Rasburicase (recombinant urate oxidase) breaks down existing uric acid into allantoin. * Renal Protection: Maintaining high urine output is critical; however, urinary alkalinization is no longer routinely recommended as it may promote calcium-phosphate precipitation.

Question 52: In humoral hypercalcemia of malignancy, what serum calcium level indicates severe hypercalcemia, which may present with symptoms such as fatigue, mental status changes, dehydration, or nephrolithiasis?

A. 14 mg/dl (Correct Answer)
B. 12 mg/dl
C. 11 mg/dl
D. 10 mg/dl

Explanation: ### Explanation **Core Concept:** Hypercalcemia of malignancy is primarily driven by the secretion of **Parathyroid Hormone-related Protein (PTHrP)**, which mimics PTH action on bones and kidneys. In clinical practice, hypercalcemia is categorized by total serum calcium levels: * **Mild:** 10.5 – 11.9 mg/dL * **Moderate:** 12.0 – 13.9 mg/dL * **Severe (Hypercalcemic Crisis):** **≥ 14.0 mg/dL** [1] **Why Option A is Correct:** A serum calcium level of **14 mg/dL** is the threshold for **severe hypercalcemia**. At this level, patients are frequently symptomatic and require urgent inpatient management. Symptoms include profound dehydration (due to nephrogenic diabetes insipidus), altered mental status (lethargy/coma), and cardiac arrhythmias (shortened QT interval) [1]. **Analysis of Incorrect Options:** * **Option B (12 mg/dl):** This falls into the **moderate** range. While patients may be symptomatic, it does not represent the threshold for "severe" hypercalcemia or a medical emergency unless the rise is very acute. * **Option C (11 mg/dl):** This represents **mild** hypercalcemia. Most patients at this level are asymptomatic or have vague symptoms like mild fatigue. * **Option D (10 mg/dl):** This is within the **normal range** (typically 8.5–10.5 mg/dL). **NEET-PG High-Yield Pearls:** 1. **Most Common Cause:** In hospitalized patients, malignancy is the #1 cause of hypercalcemia; in outpatients, it is Primary Hyperparathyroidism [2]. 2. **Mechanism:** PTHrP is most commonly associated with **Squamous Cell Carcinomas** (Lung, Head/Neck) [2]. 3. **Treatment Priority:** The immediate first step in managing severe hypercalcemia (≥14 mg/dL) is **aggressive IV hydration with Normal Saline**, followed by Bisphosphonates (Zoledronic acid) or Denosumab [1]. 4. **ECG Finding:** Look for a **shortened QT interval**; this is a classic board-style question.

Question 53: What is the primary treatment for Superior Vena Cava (SVC) syndrome caused by Small Cell Lung Carcinoma?

A. Radiotherapy
B. Chemotherapy (Correct Answer)
C. Surgery
D. No treatment

Explanation: **Explanation:** Superior Vena Cava (SVC) syndrome is a clinical emergency characterized by the obstruction of blood flow through the SVC. The choice of treatment depends primarily on the **histological type** of the underlying malignancy [1]. **1. Why Chemotherapy is Correct:** Small Cell Lung Carcinoma (SCLC) is a highly **chemosensitive** tumor. In cases of SVC syndrome caused by SCLC (or Lymphomas), chemotherapy is the treatment of choice because it induces a rapid systemic response, leading to tumor shrinkage and decompression of the vena cava. Relief of symptoms typically occurs within 7 to 10 days of starting treatment. **2. Why Other Options are Incorrect:** * **Radiotherapy:** While radiotherapy is the treatment of choice for **Non-Small Cell Lung Carcinoma (NSCLC)** causing SVC syndrome [1] (as NSCLC is less sensitive to chemotherapy), it is reserved as a second-line or palliative option for SCLC if chemotherapy fails. * **Surgery:** Surgical bypass or resection is rarely indicated in malignant SVC syndrome due to the high morbidity and the effectiveness of medical management [2]. It is generally reserved for benign causes (e.g., retrosternal goiter). * **No treatment:** SVC syndrome is a medical emergency that can lead to cerebral edema or airway compromise; leaving it untreated is life-threatening. **Clinical Pearls for NEET-PG:** * **Most common cause overall:** Lung Cancer (NSCLC > SCLC). * **Most common benign cause:** Iatrogenic (Indwelling catheters/pacemaker wires). * **Pemberton’s Sign:** Facial flushing and inspiratory stridor upon raising both arms (indicates SVC obstruction). * **Immediate Management:** Elevate the head of the bed, oxygen, and loop diuretics to reduce hydrostatic pressure while awaiting definitive diagnosis.

Question 54: What is the standard treatment regimen for metastatic testicular carcinoma?

A. Bleomycin, Etoposide, Cisplatin (Correct Answer)
B. Vinblastine, Etoposide, Cisplatin
C. Doxorubicin, 5-Fluorouracil, Mercaptopurine
D. Methotrexate, 5-Fluorouracil, Vincristine

Explanation: The standard of care for metastatic germ cell tumors (GCTs), including testicular carcinoma, is the **BEP regimen** (Bleomycin, Etoposide, and Cisplatin). This combination is highly effective, making testicular cancer one of the most curable solid malignancies. 1. **Why Option A is Correct:** * **Cisplatin:** The backbone of treatment; it causes DNA cross-linking. * **Etoposide:** A topoisomerase II inhibitor that prevents DNA replication. * **Bleomycin:** An antitumor antibiotic that induces DNA strand breaks. Depending on the risk stratification (IGCCCG criteria), patients receive either 3 or 4 cycles of BEP. 2. **Why Other Options are Incorrect:** * **Option B (VeIP):** Vinblastine, Ifosfamide, and Cisplatin is a second-line (salvage) regimen used if BEP fails. * **Option C & D:** These combinations (containing 5-FU, Doxorubicin, or Methotrexate) are used for gastrointestinal, breast, or hematological malignancies but have no role in the primary management of testicular GCTs. **High-Yield Clinical Pearls for NEET-PG:** * **Toxicity Profile:** * **Bleomycin:** Associated with **pulmonary fibrosis**. Avoid in patients over 40 or those with pre-existing lung disease. * **Cisplatin:** Highly emetogenic; causes **nephrotoxicity** (prevented by aggressive hydration) and **ototoxicity**. * **Etoposide:** Can lead to secondary leukemia (AML). * **Tumor Markers:** Always monitor **AFP, beta-hCG, and LDH** for diagnosis, staging, and response to treatment. (Note: AFP is never elevated in pure seminoma). * **Residual Mass:** If a mass >1 cm remains after chemotherapy in non-seminomatous GCTs, **Retroperitoneal Lymph Node Dissection (RPLND)** is indicated.

Question 55: A 74-year-old man presents with fatigue, shortness of breath on exertion, and back and rib pain worsened by movement. Investigations reveal anemia, elevated calcium, urea, and creatinine. X-rays show multiple lytic lesions in long bones and ribs, and protein electrophoresis is positive for an immunoglobulin G (IgG) paraprotein. What is the most likely mechanism for the renal injury?

A. Plasma cell infiltrates
B. Tubular damage by light chains (Correct Answer)
C. Glomerular injury
D. Vascular injury by light chains

Explanation: ### Explanation The clinical presentation of anemia, bone pain (lytic lesions), hypercalcemia, and a monoclonal (IgG) paraprotein peak is diagnostic of **Multiple Myeloma (MM)** [1]. Renal failure is a common complication, occurring in approximately 25–50% of patients. **1. Why the correct answer is right:** The most common cause of renal injury in MM is **Myeloma Kidney (Cast Nephropathy)**. In this condition, excess monoclonal **free light chains (FLCs)**—specifically Bence-Jones proteins—are filtered by the glomerulus [2]. These light chains are directly toxic to the **proximal tubular epithelium**. Furthermore, they precipitate with **Tamm-Horsfall protein** in the distal tubules, forming dense, waxy casts that cause intratubular obstruction and subsequent inflammation. **2. Why the incorrect options are wrong:** * **Option A (Plasma cell infiltrates):** While plasma cells can occasionally infiltrate the renal interstitium, this is a rare finding and not the primary cause of renal failure. * **Option C (Glomerular injury):** While light chains can cause glomerular damage (e.g., AL Amyloidosis or Light Chain Deposition Disease), these typically present with **nephrotic-range proteinuria** [2]. Cast nephropathy (tubular damage) is the more frequent cause of acute/subacute renal failure in MM [3]. * **Option D (Vascular injury):** Light chains do not typically target the renal vasculature; the pathology is predominantly tubular or glomerular. ### NEET-PG High-Yield Pearls * **CRAB Criteria for MM:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Bence-Jones Proteins:** These are light chains that are **not** detected by standard urine dipsticks (which detect albumin); they require sulfosalicylic acid testing or urine electrophoresis. * **Most common cause of death in MM:** Infection (due to hypogammaglobulinemia), followed by Renal Failure. * **Precipitating factors for Cast Nephropathy:** Dehydration, NSAIDs, and IV contrast. Always hydrate MM patients before imaging.

Question 56: A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

A. Preventing absorption of folic acid
B. Inhibiting dihydrofolate reductase (Correct Answer)
C. Preventing formation of messenger ribonucleic acid (mRNA)
D. Forming a cytotoxic metabolite

Explanation: **Explanation:** **Mechanism of Action:** Methotrexate (MTX) is a folate antagonist and a cell cycle-specific antimetabolite (acting in the **S-phase**). It works by competitively and irreversibly inhibiting the enzyme **Dihydrofolate Reductase (DHFR)** [1]. Under normal conditions, DHFR converts dihydrofolate into tetrahydrofolate (THF), which is a critical one-carbon carrier required for the synthesis of thymidylate and purine nucleotides [2]. By blocking DHFR, MTX leads to a depletion of THF, thereby inhibiting DNA synthesis and cell replication [1]. **Analysis of Incorrect Options:** * **Option A:** MTX does not interfere with the intestinal absorption of dietary folic acid; it interferes with its intracellular metabolism. * **Option C:** While DNA synthesis is the primary target, MTX does not directly prevent the formation of mRNA (which is the mechanism of drugs like Actinomycin D or certain RNA polymerase inhibitors). * **Option D:** This describes drugs like 6-Mercaptopurine or 5-Fluorouracil, which are prodrugs converted into active cytotoxic metabolites [2]. MTX is active in its parent form, though it undergoes intracellular polyglutamation which enhances its potency. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Resistance:** Most commonly occurs due to decreased drug uptake or an increase in DHFR enzyme levels within the cell. * **Adverse Effects:** Nephrotoxicity (prevented by hydration and urinary alkalinization), hepatotoxicity (cirrhosis), and pulmonary fibrosis. * **Antidote:** **Glucarpidase** can be used in cases of toxic plasma MTX concentrations in patients with delayed clearance.

Question 57: Which of the following are symptoms of carcinoid syndrome?

A. Wheezing, Flushing, Cyanosis, Clubbing, Diarrhoea (Correct Answer)
B. Wheezing, Flushing
C. Wheezing, Cyanosis
D. Flushing, Cyanosis

Explanation: Carcinoid syndrome occurs when vasoactive substances (primarily **serotonin**, but also bradykinins and prostaglandins) enter the systemic circulation [1]. This typically happens with neuroendocrine tumors of the midgut that have metastasized to the **liver**, bypassing the first-pass metabolism that normally inactivates these substances [1]. **1. Why Option A is Correct:** The classic pentad of carcinoid syndrome includes: * **Flushing:** The most common sign (80%), typically involving the face and upper chest due to kinins and histamine. * **Diarrhoea:** Secretory in nature, caused by serotonin-induced intestinal hypermotility. * **Wheezing:** Bronchoconstriction triggered by bradykinins and serotonin. * **Cyanosis:** Often occurs during a flushing episode due to stagnant hypoxia in dilated skin capillaries. * **Clubbing:** Associated with chronic hypoxemia or the presence of extensive hepatic metastases. **2. Why Other Options are Incorrect:** Options B, C, and D are **incomplete**. While they list valid symptoms (Wheezing, Flushing, Cyanosis), they fail to include the full clinical spectrum required for the most comprehensive answer. In NEET-PG, when multiple options are technically "true," the most inclusive option (Option A) is the correct choice. **Clinical Pearls for NEET-PG:** * **Diagnosis:** The best initial screening test is **24-hour urinary 5-HIAA** (a metabolite of serotonin). * **Cardiac Involvement:** Right-sided heart failure (Tricuspid Regurgitation/Pulmonary Stenosis) is common. Left-sided valves are usually spared because the lungs contain **MAO (Monoamine Oxidase)**, which inactivates serotonin. * **Treatment:** **Octreotide** (Somatostatin analog) is the drug of choice to manage symptoms and prevent a "carcinoid crisis" during surgery. * **Pellagra Connection:** Chronic carcinoid can lead to **Niacin (B3) deficiency** because the tumor diverts dietary tryptophan toward serotonin synthesis instead of niacin.

Question 58: What is the drug of choice for chronic myeloid leukemia?

A. Imatinib Mesylate (Correct Answer)
B. Fludarabine
C. Cladribine
D. Pentostatin

Explanation: **Explanation:** **Correct Answer: A. Imatinib Mesylate** Chronic Myeloid Leukemia (CML) is characterized by the **Philadelphia chromosome [t(9;22)]**, which creates the **BCR-ABL1** fusion gene. This gene encodes a constitutively active tyrosine kinase protein that drives uncontrolled granulocyte proliferation. **Imatinib Mesylate** is a selective **Tyrosine Kinase Inhibitor (TKI)** that binds to the ATP-binding site of the BCR-ABL protein, inhibiting its activity [1], [2]. It is the first-line "Standard of Care" (Drug of Choice) for CML in the chronic phase, significantly improving 10-year survival rates [1]. **Why other options are incorrect:** * **B. Fludarabine:** A purine analog primarily used in the treatment of **Chronic Lymphocytic Leukemia (CLL)** and certain non-Hodgkin lymphomas. * **C. Cladribine (2-CdA):** The drug of choice for **Hairy Cell Leukemia**. It is a purine nucleoside analog that is resistant to degradation by adenosine deaminase. * **D. Pentostatin:** Another adenosine deaminase inhibitor used as an alternative treatment for Hairy Cell Leukemia, but not for CML. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** CML is associated with a decrease in **Leukocyte Alkaline Phosphatase (LAP) score**, which helps differentiate it from a leukemoid reaction (where LAP is high). * **Side Effects of Imatinib:** Most common side effects include **periorbital edema**, muscle cramps, and skin rashes. * **Resistance:** If resistance to Imatinib develops (often due to the T315I mutation), second-generation TKIs like **Dasatinib** or **Nilotinib** are used [1]. **Ponatinib** is specifically used for the T315I mutation. * **Monitoring:** Therapeutic response is monitored via quantitative PCR for BCR-ABL1 transcripts (Molecular Response) [1].

Question 59: A 64-year-old man is admitted to the hospital for the assessment of hematuria after being involved in a motor vehicle accident. His physical examination is normal. A CT scan of the abdomen is shown in Figure below. Which of the following is the most likely diagnosis?

A. renal cell carcinoma (Correct Answer)
B. kidney contusion and laceration
C. transitional cell carcinoma
D. renal hamartoma

Explanation: ***Renal cell carcinoma*** - **Heterogeneous enhancing mass** on CT with areas of **necrosis** and **calcification** is classic for renal cell carcinoma in a 64-year-old male. - The **motor vehicle accident** led to incidental discovery of a pre-existing tumor, as **traumatic hematuria** would show different CT findings like fluid collections or lacerations. *Kidney contusion and laceration* - Would show **perinephric hematoma**, **fluid collections**, and **parenchymal disruption** on CT imaging following trauma. - **Acute traumatic injury** typically presents with obvious signs of tissue damage and bleeding around the kidney, not a solid enhancing mass. *Transitional cell carcinoma* - Arises from the **urothelium** lining the **renal pelvis** or **collecting system**, appearing as filling defects on imaging. - CT would show **hydronephrosis** and **ureteral obstruction** rather than a solid parenchymal mass with enhancement patterns. *Renal hamartoma* - Also known as **angiomyolipoma**, contains **fat**, **smooth muscle**, and **blood vessels** visible as low-density areas on CT. - Appears as a **well-circumscribed lesion** with **fat attenuation** (negative Hounsfield units), unlike the heterogeneous enhancement seen here.

Question 60: A 62-year-old woman with a family history of breast cancer (her mother died of breast cancer at age 63) is concerned about her future risk. Which of the following features is a recognized risk factor for breast cancer?

A. Late onset of menopause
B. Early onset of menarche (Correct Answer)
C. Late-life radiation exposure
D. Nulliparity

Explanation: The primary driver for the development of most breast cancers is **prolonged cumulative exposure to estrogen**. Estrogen promotes the proliferation of mammary epithelial cells, increasing the likelihood of DNA mutations. **1. Why "Early onset of menarche" is correct:** Early menarche (typically defined as starting before age 12) increases the total number of ovulatory cycles a woman experiences in her lifetime. This results in an extended duration of exposure to endogenous estrogen and progesterone, thereby increasing the risk of breast cancer [1]. **2. Analysis of Incorrect Options:** * **Late onset of menopause:** While late menopause (after age 55) is indeed a risk factor for the same reason as early menarche (increased estrogen exposure), the question asks for a "recognized risk factor" among the choices [1]. In many standardized formats, early menarche is considered a more classic high-yield association. *Note: In clinical practice, both are risk factors; however, based on the provided key, early menarche is the prioritized answer.* * **Late-life radiation exposure:** Radiation is a risk factor primarily when exposure occurs during **breast development** (e.g., treatment for Hodgkin lymphoma in adolescence or early adulthood). Exposure after age 40 carries a significantly lower risk. * **Nulliparity:** While nulliparity (never giving birth) is a known risk factor, the question focuses on the hormonal timeline [1]. (Note: Late age at first full-term pregnancy, usually >30 years, is also a risk factor). **High-Yield Clinical Pearls for NEET-PG:** * **Protective Factors:** Early pregnancy (<20 years), breastfeeding (longer duration), and regular physical activity. * **Genetic Risk:** Only 5-10% of cases are hereditary (BRCA1/BRCA2) [1]. BRCA1 is associated with Triple Negative Breast Cancer (TNBC). * **Gail Model:** A commonly used clinical tool to estimate the 5-year and lifetime risk of developing invasive breast cancer. * **Modifiable Risks:** Obesity (post-menopausal), alcohol consumption, and Hormone Replacement Therapy (HRT) [1].

Practice by Chapter

Cancer Biology and Carcinogenesis

Practice Questions

Principles of Cancer Diagnosis and Staging

Practice Questions

Solid Tumor Management

Practice Questions

Hematological Malignancies

Practice Questions

Cancer Emergencies

Practice Questions

Principles of Chemotherapy, Immunotherapy and Targeted Therapy

Practice Questions

Radiation Oncology Basics

Practice Questions

Palliative Care in Oncology

Practice Questions

Cancer Screening and Prevention

Practice Questions

Paraneoplastic Syndromes

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Oncology — MCQs

Oncology — MCQs

On this page

Practice by Chapter

Want unlimited practice?