Neoplasia — MCQs
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Which of the following genetic changes is commonly observed in cancers?
What is the most common lymphoma associated with Sicca syndrome?
Which of the following is described as a unicentric, non-functional, anatomically benign, and clinically persistent tumor?
Which electrolyte imbalance is characteristic of tumor lysis syndrome?
All of the following predispose to squamous cell carcinoma, EXCEPT?
A 60-year-old woman presents with a large breast mass that she first detected 3 months ago. Mammography reveals a well-circumscribed mass measuring 8 cm in diameter. A breast biopsy shows loose fibroconnective tissue with a sarcomatous stroma, abundant mitoses, and nodules and ridges lined by cuboidal epithelial cells. What is the most likely diagnosis?
Overexpression of BCL-2 proteins occurs in which of the following conditions?
What is the most important prognostic indicator for Wilms tumor?
A 48-year-old woman presents with new-onset seizures and behavioral changes that began approximately 6 months ago. Advanced imaging reveals multiple round metastatic lesions in her brain. Her past medical history is remarkable for a black lesion on her toe that was excised 20 years prior. A thorough workup and multiple additional imaging studies reveal no primary malignancy. A lesion on the arm is noted and shown. Which of the following most likely characterizes this type of malignancy?
Which of the following is not a tumor marker?
Neoplasia Indian Medical PG Practice Questions and MCQs
Question 231: Which of the following genetic changes is commonly observed in cancers?
- A. Hypomethylation of oncogenes
- B. Methylation of tumor suppressor genes (Correct Answer)
- C. Loss of heterozygosity
- D. Mutation of introns
Explanation: **Explanation:** The correct answer is **B. Methylation of tumor suppressor genes.** This process is a key epigenetic mechanism in carcinogenesis [1][3]. In many cancers, the promoter regions of tumor suppressor genes (TSGs) undergo **hypermethylation**. This leads to transcriptional silencing (gene "switching off"), preventing the production of proteins that normally inhibit cell proliferation or repair DNA (e.g., *p16/INK4a*, *BRCA1*, and *VHL*) [1][3][4]. Unlike mutations, epigenetic changes do not alter the DNA sequence but significantly impact gene expression. **Analysis of Incorrect Options:** * **A. Hypomethylation of oncogenes:** While global DNA hypomethylation is seen in cancer (leading to genomic instability) [2], oncogenes are typically activated by **amplification or point mutations**, not specifically by hypomethylation. * **C. Loss of Heterozygosity (LOH):** While LOH is a common mechanism for losing the second allele of a TSG (Knudson’s Two-Hit Hypothesis), it refers to a **structural chromosomal change** (deletion) rather than a purely chemical modification like methylation. * **D. Mutation of introns:** Introns are non-coding regions. While mutations at splice sites can be pathogenic, most cancer-driving mutations occur in **exons** (coding regions) or **promoter sequences** that directly affect protein structure or quantity. **High-Yield Clinical Pearls for NEET-PG:** * **Knudson’s Two-Hit Hypothesis:** TSGs usually require both alleles to be inactivated to promote cancer. The "first hit" is often a mutation, while the "second hit" can be methylation or LOH. * **Hypermethylation Examples:** *MLH1* hypermethylation is a classic cause of sporadic Microsatellite Instability (MSI) in colorectal cancer. * **Epigenetic Therapy:** Drugs like **5-azacytidine** (DNA methyltransferase inhibitors) are used in Myelodysplastic Syndrome (MDS) to "reactivate" silenced genes. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 230-231. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 327-328. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 213-214. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 305-306.
Question 232: What is the most common lymphoma associated with Sicca syndrome?
- A. MALToma (Correct Answer)
- B. Burkitt lymphoma
- C. Diffuse large B-cell lymphoma (DLBCL)
- D. Lymphoplasmacytic lymphoma
Explanation: **Explanation:** **Sicca syndrome** (primary Sjögren syndrome) is a chronic autoimmune disorder characterized by lymphocytic infiltration of the exocrine glands (lacrimal and salivary). Patients with Sjögren syndrome have a **40-fold increased risk** [1] of developing non-Hodgkin lymphoma compared to the general population. **1. Why MALToma is correct:** The chronic antigenic stimulation by the autoimmune process leads to the development of **Extranodal Marginal Zone B-cell Lymphoma**, also known as **MALToma** [1]. In the context of Sicca syndrome, this typically arises within the **parotid gland**. The transition from benign lymphoepithelial lesions to malignant lymphoma is a classic progression in these patients. **2. Why the other options are incorrect:** * **Burkitt lymphoma:** This is a high-grade B-cell lymphoma associated with EBV infection and the c-MYC translocation; it is not linked to chronic autoimmune sialadenitis. * **Diffuse large B-cell lymphoma (DLBCL):** While DLBCL can occur as a secondary transformation of a MALToma, it is not the *most common* primary lymphoma associated with Sicca syndrome. * **Lymphoplasmacytic lymphoma:** This is associated with Waldenström macroglobulinemia and typically involves the bone marrow and spleen, not the exocrine glands. **Clinical Pearls for NEET-PG:** * **Most common site:** Parotid gland (look for unilateral swelling in a Sjögren patient). * **Key Marker:** A sudden decrease in serum rheumatoid factor or the development of hypogammaglobulinemia in a Sjögren patient may signal the onset of lymphoma. * **Other MALToma associations:** *H. pylori* (Stomach - most common overall), *Chlamydophila psittaci* (Ocular adnexa), and *Borrelia burgdorferi* (Skin). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 235-236.
Question 233: Which of the following is described as a unicentric, non-functional, anatomically benign, and clinically persistent tumor?
- A. CEOT
- B. Enameloma
- C. Odontorna
- D. Ameloblastoma (Correct Answer)
Explanation: **Explanation:** The question describes the classic definition of **Ameloblastoma** as proposed by Robinson. 1. **Why Ameloblastoma is correct:** Ameloblastoma is a true neoplasm of odontogenic epithelium. It is characterized as: * **Unicentric:** It originates from a single center (though it can be multicentric in rare cases). * **Non-functional:** It does not produce hard tooth structures (enamel or dentin). * **Anatomically Benign:** Histologically, it lacks features of malignancy (like anaplasia or rapid metastasis). * **Clinically Persistent:** It is locally invasive, has a high recurrence rate, and can cause significant bone destruction, making it "locally malignant" in behavior. 2. **Analysis of Incorrect Options:** * **CEOT (Pindborg Tumor):** While it is a neoplasm, it is characterized by the production of amyloid-like material and calcifications (Liesegang rings), which differentiates its "functional" nature from Ameloblastoma. * **Enameloma (Enamel Pearl):** This is a developmental anomaly (ectopic enamel), not a true persistent neoplasm. * **Odontoma:** These are considered **hamartomas** rather than true neoplasms. They are "functional" as they produce mature enamel, dentin, and cementum. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Mandible (80%), specifically the molar-ramus area. * **Radiological appearance:** Classically described as a **"Soap bubble"** or **"Honeycombed"** multilocular radiolucency. * **Histopathology:** Shows "Vickers-Gorlin" features—palisading basal cells with **reverse polarity** and subnuclear vacuolization. * **Most common variant:** Follicular type. * **Unicystic Ameloblastoma:** Often associated with an impacted third molar, mimicking a dentigerous cyst.
Question 234: Which electrolyte imbalance is characteristic of tumor lysis syndrome?
- A. Hyperkalemia (Correct Answer)
- B. Hypercalcemia
- C. Hypokalemia
- D. Increased serum sodium
Explanation: **Explanation:** **Tumor Lysis Syndrome (TLS)** is an oncologic emergency caused by the rapid destruction of a large number of metabolically active tumor cells (most commonly in high-grade lymphomas and leukemias) following chemotherapy [1]. When these cells rupture, they release their intracellular contents into the systemic circulation. **Why Hyperkalemia is Correct:** Potassium is the primary intracellular cation. The massive lysis of tumor cells leads to an immediate release of potassium into the bloodstream, resulting in **Hyperkalemia**. This is the most dangerous component of TLS as it can lead to lethal cardiac arrhythmias. **Analysis of Incorrect Options:** * **Hypercalcemia:** In TLS, **Hypocalcemia** occurs, not hypercalcemia. This happens because the release of intracellular phosphorus leads to hyperphosphatemia; the excess phosphate binds to serum calcium, causing it to precipitate as calcium phosphate crystals. * **Hypokalemia:** This is the opposite of what occurs in TLS. Potassium levels rise due to cellular rupture. * **Increased serum sodium:** Sodium is primarily an extracellular ion; its levels are not characteristically elevated by the release of intracellular contents in TLS. **High-Yield Clinical Pearls for NEET-PG:** * **The Metabolic Tetrad of TLS:** 1. **Hyperkalemia** (Risk of arrhythmias) 2. **Hyperphosphatemia** (From breakdown of intracellular proteins) 3. **Hyperuricemia** (From catabolism of purines/nucleic acids) [1] 4. **Hypocalcemia** (Secondary to hyperphosphatemia) * **Renal Failure:** Hyperuricemia and calcium phosphate crystals can lead to acute kidney injury (AKI) [1]. * **Prophylaxis:** Aggressive hydration and **Allopurinol** (xanthine oxidase inhibitor) or **Rasburicase** (recombinant urate oxidase) are used to manage uric acid levels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 941-942.
Question 235: All of the following predispose to squamous cell carcinoma, EXCEPT?
- A. Lichen planus of mouth (Correct Answer)
- B. Bowen's disease
- C. Inverted papilloma of nose
- D. Chronic irritation of oral mucosa by jagged teeth
Explanation: **Explanation:** The correct answer is **A. Lichen planus of mouth**. While Oral Lichen Planus (OLP) is historically listed as a "potentially malignant disorder," its actual rate of transformation into Squamous Cell Carcinoma (SCC) is extremely low (often cited <1%). In the context of competitive exams like NEET-PG, it is generally considered a chronic inflammatory condition rather than a definitive premalignant lesion [1], especially when compared to the other high-risk options provided. **Analysis of Options:** * **Bowen’s Disease:** This is essentially **SCC in situ** of the skin or mucous membranes [4]. It has a high risk of progressing to invasive squamous cell carcinoma if left untreated. * **Inverted Papilloma of the Nose:** This is a benign but locally aggressive sinonasal tumor. It is notorious for its high recurrence rate and a significant association with synchronous or metachronous **SCC (approx. 5-15% of cases)**. * **Chronic Irritation (Jagged Teeth):** Persistent mechanical trauma from sharp teeth or ill-fitting dentures causes chronic inflammation and cellular atypia [5], which is a well-recognized risk factor for oral SCC [3]. **Clinical Pearls for NEET-PG:** * **Pre-malignant lesions of the Oral Cavity:** Erythroplakia (highest risk), Leukoplakia (speckled variety is high risk) [2], and Oral Submucous Fibrosis (OSMF) [3]. * **Marjolin’s Ulcer:** A specific type of SCC arising in chronic scars or non-healing burn wounds. * **Schistosomiasis:** Predisposes to SCC of the urinary bladder (unlike the usual transitional cell carcinoma). * **Plummer-Vinson Syndrome:** Triad of iron deficiency anemia, esophageal webs, and glossitis; predisposes to post-cricoid SCC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1168-1170. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 344-345. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 738-739. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 209-210. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-644.
Question 236: A 60-year-old woman presents with a large breast mass that she first detected 3 months ago. Mammography reveals a well-circumscribed mass measuring 8 cm in diameter. A breast biopsy shows loose fibroconnective tissue with a sarcomatous stroma, abundant mitoses, and nodules and ridges lined by cuboidal epithelial cells. What is the most likely diagnosis?
- A. Fibroadenoma
- B. Medullary carcinoma
- C. Paget disease
- D. Phyllodes tumor (Correct Answer)
Explanation: **Explanation:** The clinical and histopathological features described are characteristic of a **Phyllodes tumor**. [1] **1. Why the correct answer is right:** Phyllodes tumors are fibroepithelial neoplasms that typically present in older women (40–60 years) as large, rapidly growing, well-circumscribed masses. [1] * **Histology:** They are defined by a "leaf-like" architecture (nodules and ridges) created by an exaggerated growth of the **stromal component**. [1] * **Key features:** Unlike fibroadenomas, Phyllodes tumors exhibit high stromal cellularity, a **sarcomatous/hypercellular stroma**, and increased mitotic figures. [1] The presence of cuboidal epithelial-lined spaces confirms its fibroepithelial nature. **2. Why other options are incorrect:** * **Fibroadenoma:** Usually occurs in younger women (20–30s). While also fibroepithelial, the stroma is delicate and hypocellular without the sarcomatous features or high mitotic rate seen here. [3] * **Medullary Carcinoma:** A subtype of invasive ductal carcinoma characterized by a lymphoid infiltrate and sheets of pleomorphic cells. [2] It lacks the biphasic (epithelial + stromal) leaf-like pattern. * **Paget Disease:** Presents clinically as an eczematous crusting of the nipple/areola due to the intraepidermal spread of malignant cells (usually from an underlying DCIS or invasive cancer). It does not present as a large, well-circumscribed stromal mass. **3. NEET-PG High-Yield Pearls:** * **Grading:** Phyllodes tumors are graded as Benign, Borderline, or Malignant based on stromal cellularity, atypia, mitotic activity, and border circumscription. [1] * **Metastasis:** Malignant Phyllodes tumors spread via the **hematogenous route** (most commonly to the lungs), rather than lymphatics. [1] * **Treatment:** Wide local excision with a 1 cm margin is required because of the high risk of local recurrence. Axillary lymph node dissection is usually not necessary. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1072-1074. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 448-449.
Question 237: Overexpression of BCL-2 proteins occurs in which of the following conditions?
- A. Burkitt's lymphoma
- B. Follicular lymphoma (Correct Answer)
- C. Diffuse large B-cell lymphoma
- D. Small lymphocytic lymphoma
Explanation: **Explanation:** **1. Why Follicular Lymphoma is Correct:** Follicular lymphoma is the classic example of a malignancy driven by the evasion of apoptosis [1]. The hallmark of this condition is the **t(14;18)(q32;q21) translocation** [2]. This translocation moves the **BCL-2 gene** from chromosome 18 to the **Immunoglobulin Heavy Chain (IgH)** locus on chromosome 14 [3]. Because the IgH promoter is highly active in B-cells, this results in the massive **overexpression of BCL-2 protein** [1], [2], [3]. BCL-2 is an anti-apoptotic protein that stabilizes the mitochondrial membrane; its excess prevents programmed cell death, leading to the accumulation of long-lived neoplastic B-cells. **2. Why Other Options are Incorrect:** * **Burkitt’s Lymphoma:** Characterized by **t(8;14)**, involving the **c-MYC** proto-oncogene [2]. This leads to increased cellular proliferation rather than the primary inhibition of apoptosis via BCL-2. * **Diffuse Large B-cell Lymphoma (DLBCL):** While some subtypes may show BCL-2 expression [4], it is not the defining pathognomonic feature. DLBCL is more heterogeneous, often involving mutations in BCL-6 [4]. * **Small Lymphocytic Lymphoma (SLL/CLL):** While SLL cells do express BCL-2, the mechanism is usually related to deletions (like 13q) or microRNA dysregulation rather than the classic t(14;18) translocation seen in Follicular Lymphoma. **3. High-Yield Facts for NEET-PG:** * **BCL-2 Function:** It acts by binding to and neutralizing pro-apoptotic proteins like BAX and BAK. * **Morphology:** Follicular lymphoma typically shows a "back-to-back" follicle pattern and lacks tingible body macrophages (which are present in reactive hyperplasia) [1]. * **Clinical Pearl:** Patients with Follicular Lymphoma are at risk of "Richter’s Transformation" into a more aggressive Diffuse Large B-cell Lymphoma. * **Treatment Note:** Venetoclax is a specific BCL-2 inhibitor used in hematological malignancies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564.
Question 238: What is the most important prognostic indicator for Wilms tumor?
- A. Nuclear grade
- B. Histological type (Correct Answer)
- C. Size
- D. Pathological staging
Explanation: In Wilms tumor (nephroblastoma), the **histological type** is the most significant prognostic factor. Histology is broadly categorized into **Favorable Histology (FH)** and **Unfavorable Histology (UH)**. * **Favorable Histology:** Characterized by the classic triphasic pattern (blastemal, stromal, and epithelial elements) [1]. It carries an excellent prognosis with survival rates exceeding 90%. * **Unfavorable Histology:** Defined by the presence of **Anaplasia** (diffuse or focal). Anaplasia—marked by enlarged, hyperchromatic nuclei and multipolar mitoses—is the single most important predictor of resistance to chemotherapy and poor clinical outcome. **Analysis of Incorrect Options:** * **Nuclear Grade:** While anaplasia involves nuclear changes, "nuclear grade" is not a standardized independent prognostic system for Wilms tumor; rather, it is subsumed under the histological classification. * **Size:** Tumor size/weight is considered during surgical planning, but it does not correlate as strongly with survival or treatment response as histology does [1]. * **Pathological Staging:** While staging (NWTS/SIOP systems) is crucial for determining the extent of treatment (surgery vs. radiation), the biological behavior and chemo-responsiveness dictated by the **histological subtype** remain the primary determinants of the overall prognosis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common primary renal tumor** in children. * **Genetic Association:** Deletion of the **WT1 gene** on chromosome **11p13** (WAGR syndrome, Denys-Drash syndrome) or **WT2** on **11p15** (Beckwith-Wiedemann syndrome) [2]. * **Microscopic Hallmark:** The "Triphasic" pattern (Blastema, Stroma, Tubules) [1]. * **Precursor Lesion:** Nephrogenic rests (important to identify in the contralateral kidney) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 488-490. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 487-488.
Question 239: A 48-year-old woman presents with new-onset seizures and behavioral changes that began approximately 6 months ago. Advanced imaging reveals multiple round metastatic lesions in her brain. Her past medical history is remarkable for a black lesion on her toe that was excised 20 years prior. A thorough workup and multiple additional imaging studies reveal no primary malignancy. A lesion on the arm is noted and shown. Which of the following most likely characterizes this type of malignancy?
- A. Originates from cells in the stratum basalis (Correct Answer)
- B. Negative staining for HMB45
- C. Prognosis typically determined by the amount of horizontal spread
- D. Signet ring cells are commonly seen on histology
Explanation: ***Originates from cells in the stratum basalis*** - **Melanoma** arises from **melanocytes** located in the **stratum basalis** (basal layer) of the epidermis, which produce melanin pigment. - The history of a **black lesion on the toe** 20 years prior with current **brain metastases** strongly suggests metastatic melanoma from the original site. *Negative staining for HMB45* - **HMB45** is a **positive marker** for melanoma, not negative, as it specifically stains melanocytes and melanoma cells. - **S-100 protein** and **Melan-A** are also characteristically **positive** in melanoma diagnosis. *Prognosis typically determined by the amount of horizontal spread* - Melanoma prognosis is determined by **Breslow thickness** (vertical depth of invasion), not horizontal spread. - **Clark's level** (anatomical depth) and **mitotic rate** are also important prognostic factors, but vertical invasion is key. *Signet ring cells are commonly seen on histology* - **Signet ring cells** are characteristic of **adenocarcinoma** (especially gastric), not melanoma. - Melanoma typically shows **epithelioid cells**, **spindle cells**, or **nevoid cells** with **melanin pigment** on histology.
Question 240: Which of the following is not a tumor marker?
- A. Carcinoembryonic antigen (CEA)
- B. Human Chorionic Gonadotropin (hCG)
- C. β2Microglobulin (Correct Answer)
- D. α Fetoprotein (AFP)
Explanation: **Explanation:** The correct answer is **C. β2-Microglobulin**. In the context of standard oncology, a **tumor marker** is a substance (produced by cancer cells or by the body in response to cancer) that can be measured in blood, urine, or tissues to screen for, diagnose, or monitor a specific malignancy [2]. * **Why β2-Microglobulin is the answer:** While β2-microglobulin levels are elevated in conditions like Multiple Myeloma, Chronic Lymphocytic Leukemia (CLL), and certain lymphomas, it is technically classified as a **prognostic marker** rather than a diagnostic tumor marker. It reflects the tumor burden and cell turnover but lacks the specificity to be used as a primary marker for "detecting" a specific tumor. In many standard pathology textbooks (like Robbins), it is categorized under "Other markers" or "Prognostic indicators" rather than classic tumor-associated antigens. **Analysis of Incorrect Options:** * **A. CEA:** A classic oncofetal antigen used primarily to monitor **Colorectal Carcinoma** [4]. It is also elevated in pancreatic, gastric, and breast cancers [3]. * **B. hCG:** A hormone marker produced by trophoblastic tissue. It is the gold standard for diagnosing and monitoring **Choriocarcinoma** and Hydatidiform moles, and is also elevated in some germ cell tumors [1]. * **D. AFP:** An oncofetal antigen used for the diagnosis of **Hepatocellular Carcinoma (HCC)** and **Yolk Sac Tumors** (Endodermal sinus tumors) [3]. **Clinical Pearls for NEET-PG:** * **Most specific marker for Pancreatic Cancer:** CA 19-9. * **Marker for Ovarian Cancer:** CA-125 (also elevated in endometriosis and PID). * **Marker for Medullary Carcinoma of Thyroid:** Calcitonin. * **Prostate Specific Antigen (PSA):** Organ-specific but not cancer-specific (elevated in BPH and prostatitis) [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 512-513. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 254-255. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 346. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 319-320.
Practice by Chapter
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Genetic Basis of Cancer
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Cancer Epidemiology and Prevention
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