Neoplasia Practice Questions

Q: Which of the following is NOT a tumor suppressor gene?

C-myc. ### Explanation The fundamental distinction in cancer genetics lies between **Proto-oncogenes** and **Tumor Suppressor Genes (TSGs)**. **Why C-myc is the correct answer:** **C-myc** is a **proto-oncogene**, not a tumor suppressor gene [1]. It encodes a transcription factor that promotes cell cycle progression (by activating cyclins) and cell growth [1]. When mutated or overexpressed (gain-of-function), it becomes an oncogene, leading to uncontrolled proliferation. It is classically associated with **Burkitt Lymphoma** via the **t(8;14)** translocation. **Why the other options are incorrect:** * **APC (Adenomatous Polyposis Coli):** A "Gatekeeper" TSG that downregulates the WNT signaling pathway by promoting the degradation of β-catenin. Mutations lead to Familial Adenomatous Polyposis (FAP). * **p53 (TP53):** Known as the "Guardian of the Genome," it is the most commonly mutated TSG in human cancers. It induces cell cycle arrest (via p21) or apoptosis (via BAX) in response to DNA damage. * **Rb (Retinoblastoma gene):** The "Governor of the Cell Cycle," it controls the G1/S checkpoint by sequestering the E2F transcription factor. It was the first TSG discovered, leading to Knudson’s "Two-Hit Hypothesis." **High-Yield Clinical Pearls for NEET-PG:** * **Two-Hit Hypothesis:** TSGs generally require **loss-of-function** in both alleles to promote cancer (recessive at the cellular level), whereas proto-oncogenes require only a **single "gain-of-function"** mutation (dominant). * **N-myc** is associated with Neuroblastoma; **L-myc** with Small Cell Carcinoma of the Lung. * **Li-Fraumeni Syndrome:** Germline mutation of **p53** leading to multiple diverse wheels (SBLA syndrome: Sarcoma, Breast, Leukemia, Adrenal). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 296-297.

Q: In carcinoma of unknown primary, if the tissue marker CDX-2 is positive, what does it indicate?

Gastrointestinal cancer. **Explanation:** **CDX-2 (Caudal-type homeobox 2)** is a transcription factor essential for the development and differentiation of intestinal epithelial cells. In the context of **Carcinoma of Unknown Primary (CUP)**, CDX-2 serves as a highly specific and sensitive immunohistochemical (IHC) marker for adenocarcinomas of **gastrointestinal origin**, particularly colorectal cancer (positive in >90% of cases). It is also frequently expressed in gastric and pancreaticoduodenal malignancies. **Analysis of Options:** * **Option B (Correct):** CDX-2 is the "master regulator" of the intestinal phenotype. Its expression in a metastatic lesion strongly points toward a primary site in the GI tract (Colorectal > Gastric/Small bowel). * **Option A (Bladder):** The primary marker for Urothelial carcinoma is **GATA-3**. While some urachal adenocarcinomas may express CDX-2, it is not the standard marker for bladder cancer. * **Option C (Lung):** The hallmark markers for primary lung adenocarcinoma are **TTF-1** (Thyroid Transcription Factor-1) and **Napsin A**. * **Option D (Thyroid):** Thyroid malignancies are characterized by **TTF-1** and **Thyroglobulin** (for papillary/follicular) or **Calcitonin** (for medullary carcinoma). **High-Yield Clinical Pearls for NEET-PG:** * **CK7-/CK20+/CDX-2+:** Classic IHC profile for **Colorectal Adenocarcinoma** [1]. * **CK7+/CK20-/TTF-1+:** Classic profile for **Lung Adenocarcinoma**. * **CK7+/CK20-:** Seen in Breast, Lung, and Thyroid cancers. * **PAX-8:** Highly specific for Renal, Ovarian, and Thyroid tumors. * **SATB2:** A newer, highly specific marker for colorectal origin, often used alongside CDX-2. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 819-821.

Q: Which of the following are expressed in breast cancer?

All of the above. Breast cancer is a heterogeneous disease driven by a variety of genetic alterations, including the activation of oncogenes and the inactivation of tumor suppressor genes [1]. **Explanation of the Correct Answer:** The correct answer is **D (All of the above)** because breast tumorigenesis involves a complex interplay of these three specific biomarkers: 1. **HER2/neu (ERBB2):** This is a proto-oncogene located on chromosome 17q. It is overexpressed (via gene amplification) in approximately 15–20% of breast cancers [1]. It serves as both a prognostic marker (associated with aggressive disease) and a predictive marker (indicating response to Trastuzumab). 2. **P53 (TP53):** This is the "guardian of the genome" (tumor suppressor gene). Mutations in *TP53* are the most common genetic alterations in human cancer. In breast cancer, *p53* mutations are frequently seen, particularly in the aggressive "Triple Negative" and "HER2-enriched" subtypes [1]. 3. **BRCA1:** This is a tumor suppressor gene involved in DNA repair (homologous recombination) [1]. Germline mutations in *BRCA1* significantly increase the lifetime risk of breast and ovarian cancer. Even in sporadic cases, the *BRCA1* pathway may be functionally impaired. **High-Yield Clinical Pearls for NEET-PG:** * **Molecular Subtypes:** Luminal A (ER+/PR+, HER2-), Luminal B (ER+, HER2+/-), HER2-enriched, and Basal-like (Triple Negative) [1]. * **Li-Fraumeni Syndrome:** Characterized by germline *p53* mutations; breast cancer is a core component [1]. * **BRCA1 vs. BRCA2:** *BRCA1* is more commonly associated with Triple Negative Breast Cancer (TNBC), while *BRCA2* is more often ER-positive. * **Nottingham Grading System:** Uses tubule formation, nuclear pleomorphism, and mitotic count to grade breast carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1060.

Question 1

A 3-year-old child presents with an abdominal mass originating from the right adrenal gland. Biopsy reveals sheets of small cells with hyperchromatic nuclei, forming occasional pseudorosettes with central young nerve fibers. Which oncogene is associated with this tumor?

Accepted Answer

N-myc

Answer

erb-B2

Answer

c-myc

Answer

L-myc

Question 2

Which of the following are oncogenic viruses in humans?

Accepted Answer

All of the above

Answer

Human Papillomavirus (HPV)

Answer

Epstein-Barr Virus (EBV)

Answer

Hepatitis B Virus

Question 3

Which of the following is NOT a tumor suppressor gene?

Accepted Answer

C-myc

Answer

APC

Answer

p53

Answer

Rb

Question 4

The paraneoplastic hypercalcemia in lymphoma is due to ectopic production of which of the following?

Accepted Answer

1,25 dihydroxyvitamin D

Answer

Parathyroid hormone-related protein

Answer

Parathyroid hormone

Answer

Prostaglandin E2

Question 5

Lynch syndrome is associated with which of the following conditions?

Accepted Answer

Hereditary nonpolyposis colorectal cancer

Answer

Gastric adenocarcinoma

Answer

Hepatoma

Answer

Familial adenomatous polyposis of the colon

Question 6

What is the normal level of Prostate-Specific Antigen (PSA) in males?

Accepted Answer

Less than 4 ng/ml

Answer

4-10 ng/ml

Answer

Greater than 10 ng/ml

Answer

PSA is not produced by normal males

Question 7

In carcinoma of unknown primary, if the tissue marker CDX-2 is positive, what does it indicate?

Accepted Answer

Gastrointestinal cancer

Answer

Bladder cancer

Answer

Lung cancer

Answer

Thyroid cancer

Question 8

Which of the following statements regarding Carcinoembryonic Antigen (CEA) is false?

Accepted Answer

Elevated only when there is hepatic metastasis

Answer

A prognostic indicator

Answer

A glycoprotein

Answer

Elevated in colorectal carcinoma

Question 9

Which of the following is NOT a premalignant ulcer?

Accepted Answer

Bazin's ulcer

Answer

Paget's disease of nipple

Answer

Marjolin's ulcer

Answer

Lupus vulgaris

Question 10

Which of the following are expressed in breast cancer?

Accepted Answer

All of the above

Answer

HER2/neu

Answer

P53

Answer

BRCA1

Neoplasia — MCQs

Neoplasia — MCQs

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