Neoplasia Practice Questions

Q: Regarding COX-2, which of the following is its function?

Cell proliferation. Cyclooxygenase-2 (COX-2) is an inducible enzyme primarily expressed during inflammation, injury, or stress [1, 3]. Unlike COX-1, which is "constitutive" and maintains physiological functions (like gastric protection), COX-2 is associated with pathological states, including carcinogenesis [3, 4]. **Why Cell Proliferation is correct:** COX-2 plays a critical role in **cell proliferation** and the inhibition of apoptosis [2]. It catalyzes the synthesis of Prostaglandin E2 (PGE2), which activates signaling pathways (like the Wnt/β-catenin and MAPK pathways) that drive the cell cycle forward. Overexpression of COX-2 is frequently observed in various cancers, most notably **Colorectal Carcinoma** [3]. By promoting proliferation and angiogenesis while suppressing programmed cell death, COX-2 facilitates tumor growth [2]. **Analysis of Incorrect Options:** * **A, C, & D (Cell adhesion, migration, and differentiation):** While COX-2 can indirectly influence the tumor microenvironment (e.g., promoting metastasis via matrix metalloproteinases), its primary, direct enzymatic hallmark in the context of molecular pharmacology and pathology is the stimulation of **proliferation** [2]. Adhesion and differentiation are more closely regulated by integrins and specific transcription factors rather than the prostaglandin pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Selective COX-2 Inhibitors (Celecoxib, Etoricoxib):** These drugs are preferred in patients with peptic ulcers because they spare the protective COX-1 in the stomach. * **Cardiovascular Risk:** COX-2 inhibitors increase the risk of MI and stroke because they inhibit PGI2 (vasodilator/anti-aggregatory) without affecting Thromboxane A2 (vasoconstrictor/pro-aggregatory) produced by COX-1. * **Cancer Prevention:** Regular use of Aspirin or NSAIDs is known to reduce the risk of colorectal polyps and cancer due to the inhibition of COX-2-mediated cell proliferation [3].

Q: A patient complains of epigastric pain that fails to respond to antacids. Endoscopy demonstrates an ulcerated mass on the greater curvature of the stomach. Genetic studies on the tumor demonstrate an altered DCC gene. Which of the following tumor suppressor genes is found on the same chromosome as DCC?

DPC. **Explanation:** The question tests your knowledge of tumor suppressor gene (TSG) chromosomal locations. The **DCC gene** (Deleted in Colorectal Carcinoma) is located on **Chromosome 18q**. **1. Why DPC is correct:** The **DPC4 gene** (Deleted in Pancreatic Carcinoma, also known as **SMAD4**) is also located on **Chromosome 18q**. Both genes are frequently mutated or deleted in gastrointestinal malignancies. While DCC is classically associated with colorectal cancer (and occasionally gastric cancer, as seen in this clinical vignette), DPC4/SMAD4 is a critical marker for pancreatic adenocarcinoma and juvenile polyposis syndrome. **2. Why other options are incorrect:** * **BRCA-1:** Located on **Chromosome 17q**. It is associated with hereditary breast and ovarian cancer. * **NF-1 (Neurofibromin):** Located on **Chromosome 17q**. Mutation leads to Neurofibromatosis Type 1 (von Recklinghausen disease). * **NF-2 (Merlin):** Located on **Chromosome 22q**. Mutation leads to Neurofibromatosis Type 2 (bilateral acoustic neuromas). **Clinical Pearls for NEET-PG:** * **Mnemonic for Chromosome 18:** Remember "**18** is **D**eleted in **D**PC and **D**CC" (The 3 Ds). * **SMAD4/DPC4** is a signaling transducer for the TGF-β pathway; its loss leads to unchecked cellular proliferation. * **Chromosome 17** is a high-yield "hotspot" containing **TP53** (17p), **NF-1** (17q), and **BRCA-1** (17q). * **Chromosome 13** contains **RB1** and **BRCA-2**. * **Chromosome 5** contains **APC** (Adenomatous Polyposis Coli). **Clinical Presentation Note:** Gastric adenocarcinomas may present as an ulcerated tumor [1], with common symptoms including dyspepsia and epigastric pain [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-781.

Q: Which of the following lesions is described as destructively invasive and locally malignant with rare metastasis?

Ameloblastoma. **Explanation:** The question describes a classic pathological behavior known as **"locally malignant"** or **"borderline"** neoplasia. **Why Ameloblastoma is correct:** Ameloblastoma is a primary odontogenic tumor, most commonly occurring in the mandible [2]. It is characterized by a "locally aggressive" nature. While it is histologically benign in most cases, it is **destructively invasive**, often causing significant bone resorption and expansion. Despite its ability to infiltrate surrounding tissues extensively, it has a **very low potential for metastasis** (rarely spreading to the lungs). This combination of local destruction without systemic spread defines its classification as a locally malignant tumor. **Why other options are incorrect:** * **A. Fibroma:** This is a purely **benign** mesenchymal tumor. It is encapsulated, slow-growing, and does not invade surrounding tissues or metastasize. * **C. Papilloma:** This is a **benign** epithelial tumor. While it can grow outward (exophytic), it does not show destructive invasion into the underlying stroma. **High-Yield NEET-PG Pearls:** * **Radiological Appearance:** Ameloblastoma typically presents as a **"soap-bubble"** or **"honeycomb"** multilocular radiolucency. * **Histopathology:** Look for "Vickers-Gorlin" criteria—palisading columnar cells with **reverse polarity** (nuclei away from the basement membrane) and central stellate reticulum-like cells. * **Other Locally Malignant Tumors:** Basal Cell Carcinoma (Rodent ulcer), Giant Cell Tumor of bone (Osteoclastoma), and Craniopharyngioma. These are frequent "except" type questions in NEET-PG [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 644-645. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Q: Which of the following is NOT a component of Carney's triad?

Osteomas. **Explanation:** **Carney’s Triad** is a rare, non-hereditary syndrome primarily affecting young females. It is characterized by the synchronous or metachronous occurrence of three specific tumors. 1. **Why Option C is correct:** **Osteomas** are not a component of Carney’s triad. Osteomas (particularly of the mandible and skull) are classic features of **Gardner Syndrome**, which is a variant of Familial Adenomatous Polyposis (FAP) associated with intestinal polyps and soft tissue tumors. 2. **Why the other options are incorrect:** * **Option A (GIST):** These are typically multifocal and epithelioid in Carney’s triad. Unlike sporadic GISTs, these are usually **SDH-deficient** (succinate dehydrogenase) and do not harbor KIT or PDGFRA mutations. * **Option B (Pulmonary chondromas):** These are benign cartilaginous tumors of the lung. They are often asymptomatic and discovered incidentally on imaging. * **Option D (Extra-adrenal paraganglioma):** These are catecholamine-secreting tumors arising from the sympathetic chain [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Triad" vs. Reality:** Although called a triad, only about 25% of patients present with all three tumors simultaneously. The presence of any **two** is sufficient for diagnosis. * **Carney-Stratakis Syndrome:** Do not confuse Carney’s Triad with Carney-Stratakis Syndrome. The latter is a **hereditary** dyad (GIST and Paraganglioma) caused by germline mutations in SDH subunits (A, B, C, or D) [1]. * **Carney Complex:** This is a distinct autosomal dominant condition (PRKAR1A mutation) characterized by "NAME" or "LAMB" syndrome (Myxomas, spotty skin pigmentation, and endocrine overactivity). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 748-749.

Question 1

Which gene is associated with superficial papillary urothelial neoplasm?

Accepted Answer

p16

Answer

p53

Answer

p7

Answer

KRAS

Question 2

Regarding COX-2, which of the following is its function?

Accepted Answer

Cell proliferation

Answer

Cell adhesion

Answer

Cell migration

Answer

Cell differentiation

Question 3

Which type of cancer is most commonly associated with radiation exposure?

Accepted Answer

Leukemia

Answer

Bronchogenic carcinoma

Answer

Thyroid carcinoma

Answer

Breast cancer

Question 4

Which of the following statements about the p53 gene is FALSE?

Accepted Answer

The wild-type, non-mutated form is associated with an increased risk of childhood tumors.

Answer

It arrests the cell cycle at the G1 phase.

Answer

Its product is a 53 kD protein.

Answer

It is located on chromosome 17.

Question 5

What is the most common extragonadal site for germ cell tumors?

Accepted Answer

Mediastinum

Answer

Retroperitoneum

Answer

Sacrococcygeal region

Answer

Pineal gland

Question 6

A patient complains of epigastric pain that fails to respond to antacids. Endoscopy demonstrates an ulcerated mass on the greater curvature of the stomach. Genetic studies on the tumor demonstrate an altered DCC gene. Which of the following tumor suppressor genes is found on the same chromosome as DCC?

Accepted Answer

DPC

Answer

BRCA-1

Answer

NF-1

Answer

NF-2

Question 7

Which of the following lesions is described as destructively invasive and locally malignant with rare metastasis?

Accepted Answer

Ameloblastoma

Answer

Fibroma

Answer

Papilloma

Answer

None of the above

Question 8

HER-2/neu gene amplification causes breast carcinoma due to:

Accepted Answer

Overexpression

Answer

Suppression

Answer

Mutation

Answer

Translocation

Question 9

What is the most suggestive sign or symptom of metastatic disease?

Accepted Answer

Paresthesia

Answer

Sudden swelling

Answer

Root resorption

Answer

Diffuse radiolucency

Question 10

Which of the following is NOT a component of Carney's triad?

Accepted Answer

Osteomas

Answer

Gastrointestinal stromal tumors (GIST)

Answer

Pulmonary chondromas

Answer

Extra-adrenal paraganglioma

Neoplasia — MCQs

Neoplasia — MCQs

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