Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 971: Pro-apoptotic genes and anti-apoptotic genes belong to which gene family?

A. p53 (Tumor Suppressor Gene)
B. Bcl (B-cell lymphoma) (Correct Answer)
C. Rb (Retinoblastoma protein)
D. BRAF (B-Raf proto-oncogene)

Explanation: ***Bcl*** [1] - Pro-apoptotic and anti-apoptotic genes are part of the **Bcl-2 gene family**, which regulates apoptosis [1,2]. - This family includes key **regulators** that either promote or inhibit cell death, thus playing a crucial role in cellular health [1,2]. *BRAF* - BRAF is primarily known as a **proto-oncogene** that plays a role in cell signaling related to **cell growth** and **division** rather than apoptosis. - While it is important in cancer biology, it does not directly regulate apoptotic pathways like Bcl does. *Rb* - The Rb gene is a **tumor suppressor** involved in cell cycle regulation but does not classify as a direct modulator of apoptosis. - Its primary function is to prevent excessive cell growth by inhibiting progression through the cell cycle. *p53* - Although p53 is involved in regulating the **cell cycle** and can induce apoptosis under stress conditions, it is not part of the Bcl-2 gene family [1]. - It acts primarily as a **guardian of the genome**, responding to DNA damage rather than being classified as a pro- or anti-apoptotic gene per se [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 65-67; Neoplasia, pp. 303-304, 310-311.

Question 972: The following gene mutation protects tumor cells from apoptosis:

A. BRCA
B. RB
C. TGFβ
D. Bcl-2 (Correct Answer)

Explanation: ***bcl-2*** - The **bcl-2 gene** produces a protein that inhibits apoptosis, thereby allowing tumor cells to evade programmed cell death [1][2]. - Overexpression of **bcl-2** is associated with various cancers, making it pivotal in cancer biology [1]. *RB* - The **RB gene** is primarily a tumor suppressor, regulating the cell cycle, and does not directly prevent apoptosis. - Loss of RB function leads to unregulated cell division rather than inhibition of cell death. *TGFβ* - **TGFβ** acts as a tumor suppressor and can induce apoptosis in certain contexts, particularly in oncogenic processes. - Its primary role involves regulating cell growth and differentiation, not directly protecting against apoptosis. *BRCA* - **BRCA genes** (BRCA1 and BRCA2) are involved in DNA repair mechanisms; mutations increase cancer susceptibility but do not prevent apoptosis directly. - Dysfunction in BRCA proteins primarily impacts the repair of DNA damage, leading to genomic instability rather than apoptosis resistance. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310.

Question 973: Most common site of origin of pleomorphic adenoma is:

A. Parotid gland (Correct Answer)
B. Submandibular salivary gland
C. Minor salivary glands of soft and hard palate
D. Minor salivary glands of lip

Explanation: ***Parotid gland*** - The **parotid gland** is the most frequent site for the development of **pleomorphic adenomas**, accounting for approximately 80% of all cases [1]. - This benign mixed tumor predominantly affects the parotid gland due to its large size and complex ductal system [1]. *Submandibular salivary gland* - While pleomorphic adenomas can occur in the **submandibular gland**, they are far less common than in the parotid, representing only 10% of salivary gland pleomorphic adenomas [1]. - Tumors in this gland have a slightly higher risk of malignancy compared to parotid tumors [1]. *Minor salivary glands of soft and hard palate* - Pleomorphic adenomas can arise from **minor salivary glands**, with the palate being a relatively common site among these. - However, their overall incidence in minor salivary glands is significantly lower than in the major salivary glands, particularly the parotid. *Minor salivary glands of lip* - The **minor salivary glands of the lip** can be a site for pleomorphic adenoma, especially the upper lip. - Nevertheless, the frequency of these tumors in the lip is much lower compared to their occurrence in the parotid gland. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 751-753.

Question 974: Which tumor marker is associated with both colon carcinoma and pancreatic carcinoma?

A. CA-125
B. CA-19-9 (Correct Answer)
C. CA-15-3
D. None of the options

Explanation: ***CA-19-9*** - This **glycoprotein** tumor marker is commonly elevated in both **pancreatic adenocarcinoma** and, to a lesser extent, in **colorectal carcinoma**. - Its primary utility is in monitoring treatment response and recurrence, rather than as a screening tool, given its **low sensitivity and specificity**. *CA-125* - **CA-125** is primarily associated with **ovarian cancer** and is often used for screening high-risk individuals, monitoring treatment, and detecting recurrence. - While it can be elevated in other conditions like **endometriosis** or certain benign pelvic masses, it is not a primary marker for colon or pancreatic carcinoma. *CA-15-3* - **CA-15-3** is predominantly used as a tumor marker for **breast cancer**, particularly for monitoring disease progression and recurrence in metastatic cases. - It has limited utility in the diagnosis or management of colon or pancreatic malignancies. *None of the options* - This option is incorrect because **CA-19-9** is indeed a tumor marker associated with both colon and pancreatic carcinoma, making it the correct answer.

Question 975: What is the most common malignant tumor of the parotid gland?

A. Oncocytoma
B. Adenoid cystic carcinoma
C. Mucoepidermoid carcinoma (Correct Answer)
D. Warthin's tumor

Explanation: ***Mucoepidermoid carcinoma*** - This is the **most common malignant tumor** of the **major and minor salivary glands**, including the parotid gland [1]. - It arises from **ductal and myoepithelial cells** and presents with a wide range of histological grades (low, intermediate, high). *Oncocytoma* - This is a **rare, benign tumor** composed of oncocytes, which are large epithelial cells with abundant granular eosinophilic cytoplasm. - It is **not malignant** and does not represent the most common parotid malignancy. *Warthin's tumor* - Also known as papillary cystadenoma lymphomatosum, this is the **second most common benign parotid tumor** [1] after pleomorphic adenoma. - It is **benign** and primarily affects older men, often smokers. *Adenoid cystic carcinoma* - While a **malignant tumor**, it is **less common** than mucoepidermoid carcinoma in the parotid gland [1]. - It is known for its characteristic **perineural invasion** and a high propensity for distant metastases, even years after resection [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 753-755.

Question 976: Which of the following cancers is associated with osteolytic metastases?

A. Lung
B. Kidney
C. Thyroid
D. All of the options (Correct Answer)

Explanation: ***All of the options*** - **Lung**, **kidney**, and **thyroid** cancers are all known to frequently produce **osteolytic bone metastases** [1]. - These cancers release factors that stimulate **osteoclast activity**, leading to bone destruction rather than new bone formation. *Lung* - **Non-small cell lung cancer** often metastasizes to bone and commonly causes **osteolytic lesions** [2]. - Bone metastases are a frequent complication, particularly in advanced stages, and are associated with **pain** and **pathological fractures**. *Kidney* - **Renal cell carcinoma** is notorious for causing highly vascularized and often **osteolytic metastases** in bone [1]. - These lesions can be aggressive, leading to significant **bone destruction** and **hypercalcemia**. *Thyroid* - **Follicular thyroid carcinoma** and, less commonly, **papillary thyroid carcinoma** are known to cause **osteolytic bone metastases** [1]. - Thyroid cancer metastases in bone can be slow-growing but are typically **destructive** and may cause **pain** or **fractures**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725.

Question 977: Serum lactate dehydrogenase (LDH) increased with normal alpha-fetoprotein (AFP) is seen with:

A. Yolk sac tumor
B. Brenner's tumor
C. Mucinous cystadenocarcinoma
D. Dysgerminoma (Correct Answer)

Explanation: ***Dysgerminoma*** - Dysgerminoma is associated with **increased serum lactate dehydrogenase (LDH)** levels due to high cellular turnover [1]. - It typically presents with a **normal alpha-fetoprotein (AFP)** level, which helps distinguish it from other germ cell tumors [1]. *Mucinous cystodenocarcinoma* - This tumor typically elevates **CA-125** rather than LDH, and serum AFP is not relevant. - It primarily arises from **epithelial ovarian tissue**, which does not correlate with LDH elevation. *Yolk sac tumor* - Yolk sac tumors typically show **elevated AFP** levels, not just LDH, which is a contrasting feature. - They are germ cell tumors that are associated with **high AFP** and low LDH. *Brenner's* - Brenner tumor usually does not have significant changes in **LDH** and is associated with **normal tumor markers** like AFP. - It is classified as a **benign or low malignant potential ovarian tumor**, not typically linked with elevated LDH. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1034-1035.

Question 978: Inflammatory carcinoma of the breast is classified under which category?

A. T4b
B. T4c
C. T4d (Correct Answer)
D. T3

Explanation: ***T4d*** - **Inflammatory carcinoma of the breast** is specifically classified as **T4d** in the TNM staging system, regardless of tumor size. - This classification reflects its unique clinical presentation with **diffuse erythema, edema, and peau d'orange** (orange peel skin) due to lymphatic invasion [1]. *T4b* - **T4b** refers to breast cancer with clinically evident **edema, ulceration of the skin of the breast**, or satellite skin nodules in the same breast [2]. - While inflammatory carcinoma might have edema, the hallmark features of widespread erythema and lymphatic involvement distinguish T4d. *T4c* - **T4c** is used when a tumor exhibits **both T4a and T4b features**. - **T4a** involves chest wall fixation, and T4b involves skin edema/ulceration; neither specifically defines inflammatory breast cancer [2]. *T3* - **T3** classifies breast tumors larger than **5 cm in greatest dimension** but without features of T4. - Inflammatory breast cancer is defined by its characteristic skin changes and lymphatic involvement, not solely by tumor size. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 453-454. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1068.

Question 979: Krukenberg tumors originate from:

A. Liver
B. Stomach (Correct Answer)
C. Ovary
D. Gallbladder

Explanation: ***Stomach*** - **Krukenberg tumors** are **metastatic signet-ring cell adenocarcinomas** of the ovary. - The **stomach** is the **most common primary site** (70-80% of cases), particularly **gastric adenocarcinoma** [1]. - These tumors typically involve **both ovaries bilaterally** and are characterized by **mucin-producing signet-ring cells** [1]. - Metastasis occurs via **lymphatic or hematogenous spread** [2] or by **direct transperitoneal seeding**. *Liver* - The liver is a common site of metastasis for many GI malignancies, but it is **not the primary origin** of Krukenberg tumors. - **Hepatocellular carcinoma** has a different metastatic pattern and histology (not signet-ring cells). *Ovary* - The ovary is the **site of metastasis**, not the primary origin. - **Primary ovarian malignancies** have different histological features (serous, mucinous, endometrioid) and lack the characteristic signet-ring cell morphology from GI primaries. *Gallbladder* - Gallbladder adenocarcinoma can rarely metastasize to the ovaries, but is an **uncommon source** compared to gastric primaries. - **Gallbladder cancer** typically spreads to liver and regional lymph nodes rather than ovaries. **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. 355-356.

Question 980: What is the primary cause of Mesothelioma?

A. Silicosis
B. Baggasosis
C. Anthracosis
D. Asbestos exposure (Correct Answer)

Explanation: ***Asbestosis*** - Mesothelioma is primarily caused by **exposure to asbestos**, which leads to malignant changes in the mesothelial cells [1][2][3]. - Asbestosis results in **lung scarring** and is a well-established risk factor for the development of mesothelioma. *Silicosis* - Caused by inhalation of **silica dust**, primarily affecting individuals in construction or mining [1][4]. - While it can cause lung diseases, it does not lead to mesothelioma specifically. *Anthracosis* - Results from **coal dust exposure**, leading to the accumulation of carbon in the lungs [1]. - It is associated with chronic bronchitis and other respiratory issues but not with mesothelioma. *Baggasosis* - Caused by exposure to **bagasse** (sugarcane residue), mainly leading to lung inflammation [1]. - It does not have a recognized link to mesothelioma and largely affects the respiratory system differently. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 695. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 339-340. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 697-698. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 697.

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Neoplasia — MCQs

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