Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 801: Which of the following is the most common epithelial tumor of the stomach?

A. Gastric adenocarcinoma (Correct Answer)
B. GIST
C. Sarcoma
D. Carcinoid tumor

Explanation: ***Gastric adenocarcinoma*** - This is the **most common** malignant epithelial tumor of the stomach, accounting for over 90% of all gastric cancers [1], [2]. - It arises from the **glandular epithelial cells** lining the stomach [1]. *GIST* - **Gastrointestinal Stromal Tumors (GISTs)** are mesenchymal tumors, originating from the interstitial cells of Cajal, not epithelial cells [2]. - While they are common **non-epithelial** tumors of the stomach, they are far less frequent than gastric adenocarcinoma [2]. *Sarcoma* - **Sarcomas** are rare **mesenchymal tumors** of the stomach, arising from connective tissues like muscle or fat, not epithelial cells. - They constitute a very small percentage of gastric malignancies. *Carcinoid tumor* - **Carcinoid tumors** are **neuroendocrine tumors** that originate from enterochromaffin-like cells in the stomach. - While they are epithelial in origin, they are much less common than gastric adenocarcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 354-355.

Question 802: Malignant peripheral nerve sheath tumour showing which of the following differentiation is termed as 'Triton tumour'?

A. Cartilaginous
B. Rhabdomyoblastic (Correct Answer)
C. Glandular
D. Osseous

Explanation: ***Rhabdomyoblastic*** - A **Triton tumour** is a specific subtype of **malignant peripheral nerve sheath tumour (MPNST)** characterized by the presence of **rhabdomyosarcomatous differentiation** [1]. - This differentiation means that the tumour cells express features of **skeletal muscle differentiation**, making it a challenging diagnosis due to its aggressive nature and mixed histological features [1], [2]. *Cartilaginous* - The presence of **cartilaginous differentiation** in an MPNST would lead to a diagnosis of an **MPNST with heterologous chondrosarcomatous differentiation**, not a Triton tumour. - While MPNSTs can show heterologous elements, cartilage is not the characteristic feature of a Triton tumour [1]. *Glandular* - If an MPNST exhibits **glandular differentiation**, it would be termed an **MPNST with heterologous glandular differentiation** [1]. - This is a distinct subtype and does not correspond to the definition of a Triton tumour. *Osseous* - An MPNST with **osseous differentiation** (bone formation) would be classified as an **MPNST with heterologous osteosarcomatous differentiation** [1]. - This is another example of heterologous differentiation but is not what defines a Triton tumour. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1250-1251. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225.

Question 803: Which of the following is true about prostate cancer?

A. Most common region involved is central zone
B. It is not a hormone dependent cancer
C. Most common type is squamous cell Carcinoma
D. Grading is based on Gleason score (Correct Answer)

Explanation: ***Grading is based on Gleason score*** - The **Gleason score** is a widely used system to grade the aggressiveness of prostate cancer based on its microscopic appearance [1]. - It assesses the architectural patterns of the tumor, assigning a grade from 1 to 5 to the two most prevalent patterns, which are then summed to yield a final score (ranging from 2-10), indicating the **prognosis** and guiding treatment [1]. *Most common region involved is central zone* - The most common region for prostate cancer to develop is the **peripheral zone**, accounting for about 70-80% of cases [1]. - The **central zone** accounts for less than 5% of prostate cancers. *It is not a hormone dependent cancer* - Prostate cancer is largely a **hormone-dependent cancer**, with its growth stimulated by androgens like testosterone [1]. - **Androgen deprivation therapy (ADT)** is a cornerstone of prostate cancer treatment, demonstrating its dependency on hormones [1]. *Most common type is squamous cell Carcinoma* - The most common type of prostate cancer is **adenocarcinoma**, which originates from the glandular cells of the prostate [1]. - **Squamous cell carcinoma** of the prostate is exceedingly rare, accounting for less than 1% of all prostate malignancies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 988-994.

Question 804: Most common genetic alteration in colorectal carcinoma?

A. BRAF mutation
B. KRAS mutation
C. p53 mutation
D. APC mutation (Correct Answer)

Explanation: ***APC mutation*** - **APC (adenomatous polyposis coli)** is a tumor suppressor gene, and its inactivation is the **earliest and most common genetic event** in colorectal carcinoma development [1]. - Mutations in APC lead to **uncontrolled cell proliferation** by disrupting the Wnt signaling pathway, which is crucial for colon crypt regeneration [1]. *BRAF mutation* - **BRAF mutations** are associated with a subset of colorectal cancers, particularly those with **microsatellite instability (MSI)** and poor prognosis, but are not the most common overall [2]. - They occur in approximately **5-10% of colorectal cancers** and are primarily found in the sporadic, right-sided tumors. *KRAS mutation* - **KRAS mutations** are found in about 30-50% of colorectal cancers and are important in predicting resistance to anti-EGFR therapies [1]. - While common, they typically occur **later** in the progression from adenoma to carcinoma than APC mutations [1]. *p53 mutation* - **p53 (TP53)** is a tumor suppressor gene, and mutations in p53 are very common in many cancers, including colorectal carcinoma. - However, p53 mutations usually occur in the **later stages** of colorectal cancer development, often associated with the transition from adenoma to carcinoma and metastasis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 819. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 373-374.

Question 805: Which immunohistochemical marker is specific for mesothelioma?

A. TTF-1
B. CK7
C. Calretinin (Correct Answer)
D. CEA

Explanation: ***Calretinin*** - **Calretinin** is a highly sensitive and relatively specific immunohistochemical marker used to distinguish **mesothelioma** from other pulmonary or pleural malignancies [1]. - It is a **calcium-binding protein** found in mesothelial cells, making its presence a strong indicator of mesothelial origin [1]. *TTF-1* - **Thyroid transcription factor 1 (TTF-1)** is a nuclear transcription factor primarily expressed in **lung adenocarcinomas** and thyroid carcinomas. - It is used to differentiate primary lung tumors from metastatic tumors, but its presence argues against a diagnosis of mesothelioma [1]. *CK7* - **Cytokeratin 7 (CK7)** is a type of intermediate filament expressed in many epithelial tissues, including pulmonary adenocarcinomas and mesotheliomas. - While typically positive in a significant percentage of mesotheliomas, it is **not specific** because it is also positive in many adenocarcinomas, thus not distinguishing between them. *CEA* - **Carcinoembryonic antigen (CEA)** is a glycoprotein commonly expressed in **adenocarcinomas** of various origins, including lung, colorectal, breast, and gastrointestinal tracts. - **Mesotheliomas are typically negative for CEA**, making its absence a useful marker in differentiating mesothelioma from adenocarcinoma [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 731.

Question 806: Which is not a characteristic of Li-Fraumeni syndrome?

A. p53 mutation
B. Multiple primary tumors
C. Autosomal recessive (Correct Answer)
D. Early onset cancers

Explanation: ***Autosomal recessive*** - Li-Fraumeni syndrome is inherited in an **autosomal dominant** pattern, not autosomal recessive [1]. - This means only one copy of the altered gene in each cell is sufficient to cause the disorder. *p53 mutation* - Li-Fraumeni syndrome is directly caused by a **germline mutation** in the **TP53 tumor suppressor gene**, which codes for the p53 protein [2]. - The p53 protein normally plays a critical role in **cell cycle arrest**, DNA repair, and apoptosis, preventing tumor formation [2]. *Multiple primary tumors* - Individuals with Li-Fraumeni syndrome have a significantly increased risk of developing **multiple independent primary cancers** throughout their lifetime [1]. - These can include soft tissue sarcomas, osteosarcomas, brain tumors, adrenocortical carcinomas, and breast cancer. *Early onset cancers* - A hallmark of Li-Fraumeni syndrome is the development of **cancers at unusually young ages**, often in childhood or early adulthood. - This early onset is a key diagnostic criterion, differentiating it from sporadic cancers that typically appear later in life [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [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. 227-228.

Question 807: Best marker for distinguishing reactive from neoplastic mesothelial proliferation?

A. Calretinin
B. WT1
C. D2-40
D. BAP1 loss (Correct Answer)

Explanation: ***BAP1 loss*** - Biallelic **BAP1 inactivation**, detected as a loss of nuclear BAP1 immunoreactivity, is a highly specific marker for distinguishing **malignant mesothelioma** from benign reactive mesothelial proliferations. - While other markers confirm mesothelial lineage, only **BAP1 loss** directly points towards malignancy in this context. *Calretinin* - **Calretinin** is a sensitive marker for **mesothelial differentiation**, meaning it is expressed in both reactive and neoplastic mesothelial cells. - Therefore, it cannot differentiate between **benign reactive mesothelium** and **malignant mesothelioma**. *WT1* - **WT1 (Wilms Tumor 1)** is another valuable marker for **mesothelial lineage**, showing nuclear staining in both reactive and neoplastic mesothelial cells. - Like calretinin, its presence indicates mesothelial origin but does not distinguish between **benign and malignant processes**. *D2-40* - **D2-40 (podoplanin)** is a cell surface glycoprotein that is reliably expressed by normal and neoplastic mesothelial cells. - It is used to confirm the **mesothelial nature** of a proliferation but is not specific for malignancy.

Question 808: Most specific marker for distinguishing seminoma from embryonal carcinoma?

A. CD30 (Correct Answer)
B. OCT3/4
C. SALL4
D. PLAP

Explanation: ***CD30*** - **CD30** is highly specific for **embryonal carcinoma** among germ cell tumors, showing strong and diffuse positivity. - Its presence helps differentiate embryonal carcinoma from seminoma, which is consistently **CD30-negative**. *SALL4* - **SALL4** is a pan-germ cell marker, meaning it is expressed in both **seminoma** and **embryonal carcinoma**, so it cannot distinguish between them. - It is useful for identifying germ cell tumors in general but lacks specificity for subtyping. *OCT3/4* - **OCT3/4** is also a pan-germ cell marker expressed in both **seminoma** and **embryonal carcinoma** [1]. - Its utility lies in confirming germ cell origin but not in differentiating between specific subtypes [1]. *PLAP* - **PLAP (Placental alkaline phosphatase)** is typically positive in both **seminoma** and **embryonal carcinoma**, thus not useful for distinguishing these two entities [1]. - While helpful in diagnosing germ cell tumors, it lacks the specificity needed for subtyping in this context [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-982.

Question 809: A patient with gastric cancer shows positive CEA. What is its significance?

A. Prognostic (Correct Answer)
B. Diagnostic
C. Therapeutic
D. Screening

Explanation: ***Prognostic*** - A positive **carcinoembryonic antigen (CEA)** in gastric cancer indicates **larger tumor burden** and more advanced disease [1] - Elevated preoperative CEA levels are associated with **poorer prognosis**, higher risk of recurrence, and decreased survival [1] - CEA levels can be used to **monitor treatment response** and detect early recurrence after curative resection [1] - Higher CEA values correlate with advanced stage, lymph node involvement, and distant metastases *Diagnostic* - CEA is **not specific enough** for diagnosing gastric cancer as it can be elevated in other malignancies (colorectal, pancreatic, lung) and benign conditions (smoking, cirrhosis, inflammatory bowel disease) [2] - Diagnosis of gastric cancer requires **endoscopic biopsy** with histopathological examination - CEA may be normal even in confirmed gastric cancer cases (limited sensitivity) [2] *Therapeutic* - CEA is a **tumor marker**, not a therapeutic agent or treatment modality - While CEA levels help guide treatment decisions and monitor response, the marker itself has no therapeutic role - Treatment decisions are based on staging, histology, and patient factors, not solely on CEA values *Screening* - CEA lacks sufficient **sensitivity and specificity** for population-based screening of gastric cancer [2] - Screening for gastric cancer uses **endoscopy** in high-risk populations, not serum tumor markers - CEA is primarily used for post-treatment surveillance in patients with known cancer, not for detecting occult disease in asymptomatic individuals **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. 254-255. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 346.

Question 810: Which of the following is not a tumor suppressor gene?

A. p53
B. HER2 (Correct Answer)
C. RB
D. BRCA1

Explanation: ***HER2*** - **HER2** (**Human Epidermal growth factor Receptor 2**) is an **oncogene**, meaning it promotes cell growth and division when overexpressed [1]. - It is a **receptor tyrosine kinase** that, when activated, signals cells to grow and divide, and its amplification is associated with aggressive forms of breast cancer [1]. *p53* - **p53** is a well-known **tumor suppressor gene** that plays a critical role in cell cycle control and apoptosis. - It detects DNA damage and can halt cell division or initiate programmed cell death to prevent the proliferation of damaged cells. *BRCA1* - **BRCA1** (**BReast CAncer gene 1**) is a **tumor suppressor gene** involved in DNA repair. - Mutations in BRCA1 are strongly associated with increased risk of hereditary breast and ovarian cancers due to compromised DNA damage repair mechanisms. *RB* - The **retinoblastoma protein (RB)** is a classic example of a **tumor suppressor gene**. - It acts as a gatekeeper for cell cycle progression from G1 to S phase, preventing uncontrolled cell division by binding to and inactivating E2F transcription factors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 291-294.

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Neoplasia — MCQs

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