Neoplasia — MCQs

A patient presents with bilateral proptosis. Biopsy from the orbital region shows spindle cells arranged in compact fascicles with nuclear palisading forming Verocay bodies (Antoni A pattern), alternating with loose hypocellular myxoid areas (Antoni B pattern). Immunohistochemistry shows strong S-100 positivity. What is the most likely diagnosis?

Q558Medium

Which of the following is NOT a common childhood tumor?

Q559Easy

Carcinoembryonic antigen (CEA) is elevated in all conditions except which one?

Q560Easy

All of the following are markers of melanoma except?

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 551: Immunohistochemistry of a sample shows HMB-45. What malignancy does this marker indicate?

A. Sarcoma
B. Melanoma (Correct Answer)
C. Carcinoma
D. None of the above

Explanation: **Explanation:** **Correct Answer: B. Melanoma** HMB-45 (Human Melanoma Black-45) is a highly specific monoclonal antibody that reacts with **gp100**, a glycophosphoprotein found in the **pre-melanosomes** of melanocytes [1]. In pathology, it is a gold-standard immunohistochemical (IHC) marker used to confirm the diagnosis of malignant melanoma. While its sensitivity can be lower than S100 (which is very sensitive but less specific), HMB-45 is excellent for distinguishing melanoma from other poorly differentiated tumors [1]. **Why other options are incorrect:** * **A. Sarcoma:** These are tumors of mesenchymal origin. The characteristic IHC marker for most sarcomas is **Vimentin**. Specific sarcomas have their own markers (e.g., Desmin for rhabdomyosarcoma). * **C. Carcinoma:** These are tumors of epithelial origin. The primary IHC marker for carcinomas is **Cytokeratin (CK)**. * **D. None of the above:** Incorrect, as HMB-45 is a well-established marker for melanocytic lineage. **High-Yield Clinical Pearls for NEET-PG:** * **S100:** The most sensitive marker for melanoma (also positive in Schwann cells and Langerhans cells). * **Melan-A (MART-1):** Another highly specific and sensitive marker for melanocytic differentiation. * **SOX10:** A nuclear marker increasingly used for its high sensitivity in both primary and metastatic melanoma. * **HMB-45 Exception:** It is also positive in **Angiomyolipoma (AML)**, a benign tumor often associated with Tuberous Sclerosis, as AML contains "perivascular epithelioid cells" (PEComas) that express melanocytic markers. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1151-1152.

Question 552: Erythropoietin is increased in all of the following conditions except:

A. Hepatocellular carcinoma
B. Renal cell carcinoma
C. Cerebellar hemangioblastoma
D. Pancreatic carcinoma (Correct Answer)

Explanation: This question tests your knowledge of **Paraneoplastic Syndromes**, specifically the ectopic production of Erythropoietin (EPO), which leads to secondary polycythemia [1]. ### **Explanation** Ectopic EPO production is a classic paraneoplastic manifestation associated with specific tumors. While many tumors secrete hormones, **Pancreatic carcinoma** is typically associated with Trousseau syndrome (migratory thrombophlebitis) and non-bacterial thrombotic endocarditis [3], but **not** with increased EPO production. ### **Analysis of Options** * **Renal Cell Carcinoma (RCC):** This is the most common tumor associated with ectopic EPO production. It occurs in approximately 1-5% of cases. * **Hepatocellular Carcinoma (HCC):** Liver tumors are a well-documented source of ectopic EPO, leading to erythrocytosis in a subset of patients. * **Cerebellar Hemangioblastoma:** This benign vascular tumor is a high-yield association for EPO production, often seen in the context of Von Hippel-Lindau (VHL) syndrome. ### **High-Yield Clinical Pearls for NEET-PG** To remember the tumors associated with **Ectopic EPO production**, use the mnemonic **"Potentially High Hematocrit Reverses My Life"**: 1. **P**heochromocytoma 2. **H**epatocellular Carcinoma 3. **H**emangioblastoma (Cerebellar) 4. **R**enal Cell Carcinoma 5. **M**yoma (Uterine Leiomyoma) 6. **L**eukemia (Rarely) **Key Distinction:** In these conditions, the polycythemia is **secondary** (high EPO, normal/low oxygen saturation) [1]. This is distinct from **Polycythemia Vera**, which is a primary myeloproliferative neoplasm characterized by a *low* serum EPO level due to feedback inhibition [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 522-523.

Question 553: In which of the following types of carcinoma of the breast is a comedo growth pattern seen?

A. Ductal carcinoma in situ (Correct Answer)
B. Medullary carcinoma
C. Lobular carcinoma in situ
D. Infiltrating lobular carcinoma

Explanation: **Ductal Carcinoma In Situ (DCIS)** is the correct answer because the **comedo pattern** is a specific high-grade subtype of DCIS [1], [2]. It is characterized by solid sheets of pleomorphic cells with high-grade nuclei and **central areas of necrosis** [1]. The term "comedo" refers to the toothpaste-like necrotic material that can be extruded from the ducts when the tissue is squeezed during gross examination. On histology, these necrotic centers often undergo calcification, which is frequently detected as microcalcifications on mammography [1], [2]. **Why other options are incorrect:** * **Medullary Carcinoma:** Characterized by a well-circumscribed mass, syncytial growth patterns, and a dense lymphoplasmacytic infiltrate. It does not show comedo necrosis. * **Lobular Carcinoma In Situ (LCIS):** Characterized by a monomorphic population of small, loosely cohesive cells (due to loss of E-cadherin) filling the acini. It typically lacks the high-grade necrosis seen in comedo DCIS. * **Infiltrating Lobular Carcinoma:** Known for the "Indian file" pattern where cells invade the stroma in single-file rows [3]. **High-Yield Clinical Pearls for NEET-PG:** * **E-cadherin:** Positive in DCIS/Ductal CA; Negative in LCIS/Lobular CA (due to mutation in *CDH1* gene). * **Mammography:** DCIS most commonly presents as microcalcifications [1]; LCIS is usually an incidental finding and rarely shows calcifications. * **Paget’s Disease of the Nipple:** Almost always associated with an underlying DCIS or invasive ductal carcinoma [4]. * **Most common type of breast cancer:** Invasive Ductal Carcinoma (NOS). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 452-453. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1062. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 454-455. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1062-1064.

Question 554: Which histological feature characterizes an adenomatoid odontogenic tumour?

A. Polyhedral epithelial cells
B. Tubular or duct-like cells (Correct Answer)
C. Stellate shaped cells
D. Stratified squamous epithelial cells

Explanation: **Adenomatoid Odontogenic Tumour (AOT)**, often referred to as the "Two-Thirds Tumor," is a benign odontogenic neoplasm. The hallmark histological feature of AOT is the presence of **tubular or duct-like structures** (Option B). These structures are formed by cuboidal or columnar epithelial cells arranged in a circular pattern, with nuclei polarized away from the central lumen. This lumen often contains eosinophilic material or pre-dentin. It is important to note that these are not true glandular ducts but rather a specific pattern of odontogenic epithelium. **Analysis of Incorrect Options:** * **Option A (Polyhedral epithelial cells):** These are characteristic of **Pindborg Tumors** (Calcifying Epithelial Odontogenic Tumor), which feature sheets of polyhedral cells with distinct intercellular bridges and amyloid-like deposits. * **Option C (Stellate shaped cells):** Stellate reticulum-like cells are the classic feature of **Ameloblastoma**. While AOT can have spindle cells, the "star-shaped" arrangement is specific to the central portion of Ameloblastoma follicles. * **Option D (Stratified squamous epithelial cells):** These are found in **Squamous Odontogenic Tumors** or odontogenic cysts (like Keratocystic Odontogenic Tumors), but are not a defining feature of AOT. **NEET-PG High-Yield Pearls:** * **The "Two-Thirds" Rule:** 2/3rd occur in the **maxilla**, 2/3rd in **young females** (teens), and 2/3rd are associated with an **impacted canine** [1]. * **Radiology:** Appears as a well-defined radiolucency surrounding an unerupted tooth (follicular type), often containing "snowflake" calcifications. * **Treatment:** Conservative enucleation; recurrence is extremely rare. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Question 555: What is true about multiple papillomatosis?

A. Herpes Simplex Virus is the causative agent.
B. Radiotherapy is the treatment of choice.
C. It is a premalignant condition. (Correct Answer)
D. It is more common in individuals aged 15 to 33 years.

Explanation: **Explanation:** **Multiple Papillomatosis** (specifically Juvenile Laryngeal Papillomatosis) refers to the development of multiple benign squamous papillomas in the respiratory tract [1]. **1. Why Option C is Correct:** While individual papillomas are benign, multiple papillomatosis is considered a **premalignant condition**. Although the risk of spontaneous malignant transformation into squamous cell carcinoma is low (approx. 1–3%), it is a well-documented complication, especially in cases with long-standing disease or those exposed to co-carcinogens [1]. **2. Why the other options are incorrect:** * **Option A:** The causative agent is the **Human Papillomavirus (HPV)**, specifically genotypes **6 and 11**, not Herpes Simplex Virus. * **Option B:** **Radiotherapy is contraindicated.** It is not the treatment of choice because it significantly increases the risk of malignant transformation into an aggressive squamous cell carcinoma. The standard treatment is surgical debulking (CO2 laser or microdebrider). * **Option D:** Multiple papillomatosis is most common in **children (under age 5)** [1], often acquired during childbirth via an infected birth canal. A second peak occurs in adulthood (20–40 years), but the "multiple" juvenile form is classically a pediatric diagnosis. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of symptoms:** Hoarseness of voice, chronic cough, and stridor. * **Histology:** Finger-like projections of non-keratinized stratified squamous epithelium with a central fibrovascular core and characteristic **koilocytic changes** [1]. * **Adjuvant therapy:** Cidofovir (antiviral) or Interferon-alpha may be used in refractory cases. * **Prevention:** The HPV vaccine (Gardasil) is effective in reducing the incidence of maternal transmission. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 745-746.

Question 556: What is the most common virus implicated in lymphoproliferative cancer in a child post-kidney transplant?

A. Cytomegalovirus (CMV)
B. Varicella-zoster virus
C. Human papillomavirus (HPV)
D. Epstein-Barr virus (EBV) (Correct Answer)

Explanation: ### Explanation The correct answer is **Epstein-Barr virus (EBV)**. **Why it is correct:** The condition described is **Post-Transplant Lymphoproliferative Disorder (PTLD)**. In patients undergoing solid organ transplantation (like a kidney transplant), chronic immunosuppression is required to prevent graft rejection [1]. This suppresses T-cell surveillance, which normally keeps B-cell proliferation in check [2]. EBV, a member of the Herpesvirus family, infects B-cells and drives their uncontrolled proliferation via the expression of oncogenic proteins like **LMP-1** (Latent Membrane Protein 1) [3]. In children, who are often EBV-naive before transplant, the risk of primary EBV infection and subsequent PTLD is significantly higher [1]. **Why the other options are incorrect:** * **Cytomegalovirus (CMV):** While CMV is the most common viral infection post-transplant and can cause systemic disease (pneumonitis, colitis), it is not typically oncogenic or a primary cause of lymphoproliferative disorders. * **Varicella-zoster virus (VZV):** VZV causes chickenpox and shingles. While it can cause severe disseminated disease in immunocompromised hosts, it does not lead to malignancy. * **Human papillomavirus (HPV):** HPV is associated with squamous cell carcinomas (cervical, oropharyngeal, and skin cancers), not lymphoid malignancies [4]. **High-Yield Clinical Pearls for NEET-PG:** * **PTLD Spectrum:** Ranges from benign polyclonal B-cell hyperplasia to aggressive monoclonal B-cell lymphomas (e.g., Diffuse Large B-cell Lymphoma) [1]. * **EBV Association:** EBV is also linked to Burkitt Lymphoma (starry-sky appearance), Nasopharyngeal Carcinoma, and Hodgkin Lymphoma [4]. * **Diagnosis:** Monitoring **EBV DNA PCR** levels in the blood is a standard screening tool for high-risk transplant recipients. * **Management:** The first step in managing PTLD is often the **reduction of immunosuppressive therapy** to allow the host's immune system to recover and target the EBV-infected cells. **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. 181-182. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336. [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. 219-220.

Question 557: A patient presents with bilateral proptosis. Biopsy from the orbital region shows spindle cells arranged in compact fascicles with nuclear palisading forming Verocay bodies (Antoni A pattern), alternating with loose hypocellular myxoid areas (Antoni B pattern). Immunohistochemistry shows strong S-100 positivity. What is the most likely diagnosis?

A. Leiomyoma
B. Schwannoma (Correct Answer)
C. Rhabdomyosarcoma
D. Fibromatosis

Explanation: ***Schwannoma*** - Bilateral proptosis with **Antoni A and B patterns** and **Verocay bodies** on biopsy are pathognomonic for schwannoma, particularly in the orbital region. - **S-100 positive** staining confirms neural origin, and orbital schwannomas commonly present with gradual **proptosis** and visual disturbances. *Leiomyoma* - Shows **smooth muscle differentiation** with spindle cells arranged in fascicles, positive for **smooth muscle actin (SMA)**. - Lacks the characteristic **Antoni patterns** and **Verocay bodies** seen in neural tumors like schwannoma. *Rhabdomyosarcoma* - Most common **primary orbital malignancy** in children, showing **cross-striations** and positive **desmin** staining. - Presents with **rapid onset proptosis** and is highly aggressive, unlike the benign nature suggested by typical schwannoma biopsy findings. *Fibromatosis* - Characterized by **proliferating fibroblasts** in a collagenous stroma without the **biphasic Antoni A/B pattern**. - Shows **beta-catenin positivity** and lacks **S-100 expression** and **Verocay bodies** diagnostic of schwannoma.

Question 558: Which of the following is NOT a common childhood tumor?

A. Wilm's tumor
B. Neuroblastoma
C. Embryonal rhabdomyoma
D. Pleomorphic rhabdomyosarcoma (Correct Answer)

Explanation: **Explanation:** The correct answer is **Pleomorphic rhabdomyosarcoma**. In pediatric pathology, childhood tumors are typically **"small round blue cell tumors"** or embryonal in origin, often ending with the suffix "-blastoma." [2] 1. **Why Pleomorphic Rhabdomyosarcoma is the correct answer:** While rhabdomyosarcoma is the most common soft tissue sarcoma in children, it has distinct histological subtypes [3]. The **Pleomorphic** variant is characterized by large, atypical, and bizarre cells; it occurs almost exclusively in **adults** (usually >45 years old) and is rarely seen in children [1]. 2. **Analysis of Incorrect Options:** * **Wilms Tumor (Nephroblastoma):** The most common primary renal tumor of childhood, typically presenting between ages 2 and 5. It is derived from the mesonephric blastema [2, 3]. * **Neuroblastoma:** The most common extracranial solid tumor of childhood. It arises from neural crest cells in the adrenal medulla or sympathetic chain [2, 3]. * **Embryonal Rhabdomyosarcoma:** This is the most common subtype of rhabdomyosarcoma in children (accounting for ~60% of cases), typically affecting children under age 10 [1]. A classic variant is *Sarcoma Botryoides* (grape-like masses in the vagina or bladder) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common childhood malignancy:** Leukemia (specifically ALL) [3]. * **Most common childhood solid tumor:** CNS tumors [3]. * **Small Round Blue Cell Tumors (Differential):** Remember the mnemonic **"WENCH"** — **W**ilms, **E**wing’s sarcoma, **N**euroblastoma, **C**arcinoma (small cell), **H**odgkin’s/Non-Hodgkin’s Lymphoma. * **Rhabdomyosarcoma Subtypes:** Embryonal and Alveolar are for **kids**; Pleomorphic is for **adults** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225. [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. 211-212. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-484.

Question 559: Carcinoembryonic antigen (CEA) is elevated in all conditions except which one?

A. Alcoholic Cirrhosis
B. Carcinoma of the Colon
C. Ulcerative Colitis
D. Emphysema (Correct Answer)

Explanation: **Explanation:** Carcinoembryonic Antigen (CEA) is a high-molecular-weight glycoprotein normally produced during fetal development by the gastrointestinal tract and liver [2]. In adults, it is typically present in very low levels. It serves as a **non-specific oncofetal antigen** and is primarily used as a tumor marker for monitoring recurrence rather than for primary diagnosis [2]. **Why Emphysema is the correct answer:** While CEA levels can be elevated in chronic smokers and certain chronic inflammatory lung conditions, **Emphysema** (a subtype of COPD) is not typically associated with significant elevations of CEA [1]. The other options involve tissues (colon and liver) where CEA expression is either pathologically upregulated or its clearance is impaired. **Analysis of Incorrect Options:** * **Carcinoma of the Colon:** This is the most classic association. CEA is highly elevated in colorectal cancer and is the gold-standard marker for monitoring treatment response and detecting recurrence [2]. * **Alcoholic Cirrhosis:** CEA is metabolized by the liver. In cirrhosis, impaired hepatic function leads to decreased clearance of CEA, resulting in elevated serum levels. * **Ulcerative Colitis:** Inflammatory Bowel Diseases (IBD) cause rapid cell turnover and inflammation of the intestinal mucosa, which can lead to transient or persistent elevations of CEA [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Use:** CEA is **not** used for screening (due to low specificity) but is excellent for **monitoring recurrence** of colorectal carcinoma after surgical resection [2]. * **Other Malignancies:** CEA can also be elevated in pancreatic, gastric, breast, and medullary thyroid carcinomas [2]. * **Benign Elevations:** Apart from cirrhosis and IBD, CEA can be elevated in heavy smokers, pancreatitis, and peptic ulcer disease. * **Prognostic Value:** Pre-operative CEA levels correlate with the stage of the tumor; very high levels often suggest metastasis (especially to the liver). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685. [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. 213-214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 807-809.

Question 560: All of the following are markers of melanoma except?

A. S-100
B. Cytokeratin-20 (Correct Answer)
C. HMB-45
D. Vimentin

Explanation: **Explanation:** The diagnosis of malignant melanoma relies heavily on Immunohistochemistry (IHC) because it can mimic various carcinomas and sarcomas histologically. **Why Cytokeratin-20 (CK20) is the correct answer:** Melanoma is a tumor of neuroectodermal origin (melanocytes), not epithelial origin. **Cytokeratins** are intermediate filaments found in epithelial cells; therefore, melanoma is characteristically **Cytokeratin negative**. CK20, specifically, is a marker for gastrointestinal carcinomas, transitional cell carcinomas, and Merkel cell carcinoma. Its absence helps rule out epithelial malignancies. **Analysis of Incorrect Options:** * **S-100:** This is the **most sensitive** marker for melanoma. While it lacks specificity (also positive in nerve sheath tumors, Langerhans cells, and cartilage), a negative S-100 almost always rules out melanoma. [1] * **HMB-45:** This is a highly **specific** marker for melanoma. It reacts against gp100, a protein found in stage II melanosomes. It is excellent for confirming the diagnosis but may be negative in desmoplastic variants. * **Vimentin:** As melanocytes are derived from the neural crest, they express vimentin (an intermediate filament of mesenchymal cells). Almost all melanomas are Vimentin positive. **High-Yield Clinical Pearls for NEET-PG:** * **Melan-A (MART-1):** Another highly specific and sensitive marker frequently used alongside HMB-45. * **SOX10:** A nuclear marker that is gaining popularity for its high sensitivity in both conventional and desmoplastic melanomas. * **The "Melanoma IHC Panel":** Typically includes S-100, HMB-45, and Melan-A. * **Rule of Thumb:** Melanoma is **S-100 (+), Vimentin (+), but Cytokeratin (-).** [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1150-1153.

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Neoplasia — MCQs

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