Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following can cause pseudomyxoma peritonei?

A. Mucocele of appendix
B. Mucinous ovarian tumor
C. Ovarian dermoid
D. Adenocarcinoma of colon (Correct Answer)

Explanation: **Explanation:** **Pseudomyxoma peritonei (PMP)** is a clinical syndrome characterized by the accumulation of abundant gelatinous (mucinous) material within the peritoneal cavity, often referred to as "jelly belly" [1]. **Why Adenocarcinoma of the Colon is Correct:** While historically associated with various organs, modern immunohistochemistry and molecular studies have clarified that the vast majority of PMP cases arise from **mucinous tumors of the gastrointestinal tract**, most commonly the appendix. However, among the options provided, **Adenocarcinoma of the colon** (specifically the mucinous subtype) is a recognized primary source [1]. When these tumors rupture or spread to the peritoneum, they seed the cavity with mucus-producing cells that continue to secrete mucin, leading to the characteristic clinical picture [1]. **Analysis of Incorrect Options:** * **Mucocele of the appendix (Option A):** A mucocele is a generic clinical term for a dilated appendix filled with mucus. While a ruptured *mucinous neoplasm* of the appendix is the #1 cause of PMP, a simple non-neoplastic mucocele (e.g., from fecalith obstruction) does not typically cause the progressive, neoplastic seeding seen in true PMP. * **Mucinous ovarian tumor (Option B):** Historically, PMP was often attributed to the ovary. However, it is now established that most "ovarian" PMP cases are actually metastases from an appendiceal or GI primary [1], [2]. Primary ovarian mucinous tumors rarely cause PMP [2]. * **Ovarian dermoid (Option C):** These are mature cystic teratomas containing ectodermal tissues (hair, sebum). They do not produce the diffuse mucinous ascites characteristic of PMP. **High-Yield Pearls for NEET-PG:** * **Most Common Source:** Appendix (Low-grade Appendiceal Mucinous Neoplasm - LAMN). * **Clinical Sign:** "Jelly Belly" (distended abdomen with gelatinous ascites) [1]. * **Treatment:** Cytoreductive surgery (CRS) combined with Hyperthermic Intraperitoneal Chemotherapy (HIPEC). * **Pathology:** Characterized by "mucin pools" containing sparse neoplastic columnar cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 823-824. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1030-1032.

Question 172: Serum alpha-fetoprotein concentration is elevated in which of the following conditions?

A. Hepatoma, Hepatoblastoma, Endodermal sinus tumor, and Cirrhosis (Correct Answer)
B. Hepatoma and Cirrhosis
C. Hepatoblastoma and Endodermal sinus tumor
D. Hepatoblastoma, Endodermal sinus tumor, and Chromosomal trisomy

Explanation: **Explanation:** Alpha-fetoprotein (AFP) is a glycoprotein normally synthesized by the fetal liver, yolk sac, and gastrointestinal tract. In adults, elevated serum AFP serves as a crucial tumor marker for specific malignancies and a sensitive indicator of certain non-neoplastic liver conditions. **Why Option A is Correct:** * **Hepatoma (Hepatocellular Carcinoma):** AFP is the classic marker for HCC; levels >200 ng/mL are highly suggestive, and >400-500 ng/mL are diagnostic in the presence of a liver mass [1]. * **Hepatoblastoma:** This is the most common liver tumor in children [3]; AFP is elevated in over 90% of cases. * **Endodermal Sinus Tumor (Yolk Sac Tumor):** Since AFP is embryologically produced by the yolk sac, this tumor (ovarian or testicular) characteristically secretes very high levels of AFP [2]. * **Cirrhosis:** Non-neoplastic liver damage and subsequent regeneration (as seen in cirrhosis or acute hepatitis) cause a modest rise in AFP, typically <200 ng/mL [1]. **Analysis of Incorrect Options:** * **Options B & C:** These are incomplete. While they list conditions where AFP is elevated, they omit other clinically significant conditions included in Option A. * **Option D:** Chromosomal trisomies (specifically **Trisomy 21/Down Syndrome**) are associated with **decreased** maternal serum AFP (MSAFP) during pregnancy, not elevated levels. **NEET-PG High-Yield Pearls:** * **Elevated MSAFP:** Neural tube defects (spina bifida, anencephaly), abdominal wall defects (omphalocele, gastroschisis), and multiple gestations. * **Decreased MSAFP:** Down Syndrome (Trisomy 21), Edwards Syndrome (Trisomy 18), and gestational trophoblastic disease. * **Germ Cell Tumors:** AFP is elevated in Yolk Sac tumors but **never** in pure Seminomas/Dysgerminomas [4]. Mixed germ cell tumors may show elevation if a yolk sac component is present [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1035-1036. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 875-876. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982.

Question 173: Which of the following is an example of a mixed tumor?

A. Adenoacanthoma (Correct Answer)
B. Hamartoma
C. Glomus Tumor
D. Osteoma

Explanation: ### Explanation **Correct Answer: A. Adenoacanthoma** **Concept of Mixed Tumors:** In pathology, a **mixed tumor** refers to a neoplasm where the tumor cells undergo divergent differentiation. This can occur in two ways: 1. **Monoclonal origin:** A single germ layer (progenitor cell) differentiates into more than one cell type (e.g., Pleomorphic adenoma) [1]. 2. **Divergent differentiation of a single cell type:** A tumor showing two different morphological patterns of the same lineage. Adenoacanthoma is a classic example of divergent differentiation. It is an **adenocarcinoma** (glandular differentiation) that contains areas of **benign squamous metaplasia**. Since it displays both glandular and squamous components originating from the same epithelial lineage, it is classified as a mixed tumor. --- **Analysis of Incorrect Options:** * **B. Hamartoma:** This is not a true neoplasm. It is a **disorganized mass** of indigenous tissue (tissue native to the site) that grows at the same rate as the surrounding area (e.g., Pulmonary hamartoma). * **C. Glomus Tumor:** This is a benign vascular tumor arising from the specialized arteriovenous anastomosis (glomus body), typically found under the fingernails. It is a **pure mesenchymal tumor**, not mixed. * **D. Osteoma:** This is a benign, slow-growing **monomorphic tumor** composed of mature compact or cancellous bone [2]. --- **NEET-PG High-Yield Pearls:** * **Pleomorphic Adenoma (Salivary Gland):** The most common mixed tumor (epithelial elements + myxoid/chondroid stroma) [1]. * **Teratoma:** Unlike mixed tumors, teratomas originate from **totipotent germ cells** and contain derivatives of **all three germ layers** (ectoderm, mesoderm, endoderm) [3]. * **Collision Tumor:** Two independent primary tumors arising in the same organ (e.g., Squamous cell carcinoma and Small cell carcinoma in the lung). Unlike mixed tumors, these have different clonal origins. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 274-276. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 276-278. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1033-1034.

Question 174: Alpha-fetoprotein (AFP) is raised in which of the following conditions?

A. Renal carcinoma
B. Pancreatic carcinoma
C. Prostatic carcinoma
D. Hepatic carcinoma (Correct Answer)

Explanation: **Explanation:** **Alpha-fetoprotein (AFP)** is a glycoprotein normally synthesized by the fetal liver and yolk sac. In adults, it serves as a highly specific **tumor marker** when its levels are significantly elevated. **Why Hepatic Carcinoma is Correct:** AFP is the gold-standard serum marker for **Hepatocellular Carcinoma (HCC)** [1]. It is produced by malignant hepatocytes that have reverted to a fetal phenotype. A level >400 ng/mL in a patient with a liver mass is highly suggestive of HCC. Additionally, AFP is elevated in **Non-seminomatous Germ Cell Tumors (NSGCT)**, specifically Yolk Sac Tumors (Endodermal Sinus Tumors). **Why Other Options are Incorrect:** * **Renal Carcinoma:** Associated with markers like HIF-1α or CA-IX (in clear cell type), but not AFP. * **Pancreatic Carcinoma:** The primary marker is **CA 19-9**. * **Prostatic Carcinoma:** The specific marker is **PSA (Prostate-Specific Antigen)**; Acid Phosphatase may also be elevated in metastatic cases. **High-Yield Clinical Pearls for NEET-PG:** * **Triple Marker Test:** AFP is used in prenatal screening. Low levels are associated with **Down Syndrome**, while high levels in amniotic fluid/maternal serum indicate **Neural Tube Defects** (e.g., Anencephaly, Spina Bifida). * **Differential Diagnosis:** Moderate elevations of AFP can occur in non-neoplastic conditions like **Cirrhosis** and **Chronic Hepatitis**, so it must be correlated with imaging. * **Yolk Sac Tumor:** AFP is the most sensitive marker for diagnosis and monitoring recurrence in these pediatric germ cell tumors. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400.

Question 175: All of the following conditions are premalignant except?

A. Ulcerative colitis
B. Crohn's disease
C. Bronchiectasis (Correct Answer)
D. Paget disease of bone

Explanation: **Explanation:** The correct answer is **Bronchiectasis**. In pathology, a premalignant (precancerous) condition is a clinical state associated with a significantly increased risk of developing cancer [1]. **Why Bronchiectasis is the correct answer:** Bronchiectasis is a chronic inflammatory condition characterized by the permanent dilation of bronchi and bronchioles due to the destruction of muscle and elastic tissue. While it involves chronic inflammation and squamous metaplasia, it is **not** considered a classic premalignant condition [3]. It does not carry a statistically significant risk of progressing to bronchogenic carcinoma, unlike other chronic lung conditions like idiopathic pulmonary fibrosis. **Analysis of Premalignant Options:** * **Ulcerative Colitis (UC):** Long-standing UC is a well-known precursor to **Colorectal Carcinoma**. The risk increases with the duration of the disease (usually after 8–10 years) and the extent of colon involvement (pancolitis) [1]. * **Crohn’s Disease:** Although the risk is slightly lower than in UC, Crohn’s disease is also a premalignant condition that increases the risk of intestinal adenocarcinoma [1]. * **Paget Disease of Bone:** This condition involves disordered bone remodeling. In approximately 1% of cases (higher in polyostotic forms), it can transform into **Osteosarcoma**, typically in elderly patients. **NEET-PG High-Yield Pearls:** * **Other Premalignant Conditions:** Actinic keratosis (Squamous cell carcinoma), Leukoplakia (Oral cancer), Barrett’s esophagus (Adenocarcinoma), and Xeroderma pigmentosum (Skin cancers) [2]. * **Hyperplasia vs. Neoplasia:** While most hyperplasias are controlled, **Atypical Endometrial Hyperplasia** is a major premalignant condition. * **Regenerative Nodules:** Cirrhosis of the liver is the most common premalignant condition for Hepatocellular Carcinoma (HCC). Notably, while bronchiectasis itself is not a precursor, lung carcinoma can lead to secondary bronchiectasis due to airway obstruction [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 286-287. [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. 222-223. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 723. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725.

Question 176: Which of the following agents is associated with Burkitt's lymphoma?

A. HTLV-1
B. HTLV-3
C. HPV
D. EBV (Correct Answer)

Explanation: **Explanation:** **Epstein-Barr Virus (EBV)** is the correct answer. EBV is a double-stranded DNA virus belonging to the Herpesviridae family [1]. It shows a strong tropism for B cells via the **CD21 receptor** (CR2) [3]. In the pathogenesis of Burkitt’s lymphoma, EBV acts as a potent mitogen, leading to B-cell proliferation. This increased turnover predisposes the cells to a characteristic **t(8;14) translocation**, which results in the overexpression of the **c-MYC oncogene**, driving uncontrolled cell growth. **Analysis of Incorrect Options:** * **HTLV-1 (Human T-cell Lymphotropic Virus-1):** This retrovirus is specifically associated with **Adult T-cell Leukemia/Lymphoma (ATLL)**, primarily seen in Japan and the Caribbean [1]. It utilizes the Tax protein for oncogenesis. * **HTLV-3:** This is an older nomenclature for **HIV-1**. While HIV increases the risk of various lymphomas (including Burkitt’s) due to immunosuppression, it is not the direct transforming agent [4]. * **HPV (Human Papillomavirus):** High-risk strains (16, 18) are associated with squamous cell carcinomas of the cervix, oropharynx, and anogenital region via E6 and E7 oncoproteins, not lymphomas [1], [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Burkitt’s Lymphoma Variants:** The **Endemic (African)** form is nearly 100% associated with EBV and typically presents as a jaw mass [2]. The **Sporadic** form is associated with EBV in only 15-20% of cases and usually presents as an ileocecal mass [2]. * **Morphology:** Characterized by a **"Starry-sky appearance"** (tingible body macrophages against a background of neoplastic B-cells). * **Other EBV Associations:** Nasopharyngeal carcinoma, Hodgkin Lymphoma (Mixed cellularity type), and Oral Hairy Leukoplakia [1]. **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. 219-221. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-369. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262.

Question 177: Which of the following is the site of malignant transformation of melanocytes in melanoma?

A. Junctional melanocytes (Correct Answer)
B. Epidermal cells
C. Basal cells
D. Follicular cells

Explanation: **Explanation:** **Why Junctional Melanocytes are Correct:** Melanoma arises from the malignant transformation of melanocytes [3]. In the skin, melanocytes are primarily located at the **dermo-epidermal junction** [2] (the interface between the epidermis and dermis). The initial phase of most melanomas involves the proliferation of these **junctional melanocytes** [1]. Whether the melanoma arises *de novo* or from a pre-existing nevus (like a junctional or compound nevus), the transformation begins at this specific histological site [3]. This is reflected in the "radial growth phase," where malignant cells spread laterally within the junctional layer before invading deeper into the dermis (vertical growth phase) [1]. **Why Incorrect Options are Wrong:** * **B. Epidermal cells:** This is a broad term. While melanocytes reside in the epidermis, the term "epidermal cells" usually refers to keratinocytes. Malignancy of keratinocytes leads to Squamous Cell Carcinoma, not melanoma. * **C. Basal cells:** These are the keratinocytes of the *stratum basale* [2]. Malignant transformation of these cells leads to **Basal Cell Carcinoma (BCC)**, the most common skin cancer, which is distinct from melanoma. * **D. Follicular cells:** These cells make up the hair follicle. While rare variants of melanoma can involve the follicular epithelium (e.g., lentigo maligna), it is not the primary or standard site of origin for cutaneous melanoma. **High-Yield Clinical Pearls for NEET-PG:** * **ABCDE Criteria:** Used for clinical diagnosis (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving). * **Prognostic Marker:** The **Breslow Thickness** (measured in mm from the granular layer to the deepest tumor cell) is the most important prognostic factor [3]. * **Common Mutation:** **BRAF V600E** mutation is found in approximately 50% of cutaneous melanomas. * **S-100 & HMB-45:** These are the most specific immunohistochemical (IHC) markers for melanoma [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1151-1152. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 633-634. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 649-650.

Question 178: All of the following are examples of tumour markers, except:

A. Alpha-HCG (Correct Answer)
B. AFP
C. NSE
D. CEA

Explanation: **Explanation:** The correct answer is **Alpha-HCG**. Human Chorionic Gonadotropin (HCG) is a glycoprotein hormone consisting of two subunits: alpha (α) and beta (β). The **alpha subunit** is identical to those found in LH, FSH, and TSH, making it non-specific. In clinical oncology, the **Beta-HCG (β-HCG)** subunit is the specific tumor marker used for diagnosis and monitoring, as it is unique to HCG [1]. Therefore, Alpha-HCG is not used as a tumor marker. **Analysis of other options:** * **AFP (Alpha-Fetoprotein):** A major marker for **Hepatocellular Carcinoma (HCC)** and non-seminomatous germ cell tumors (specifically **Yolk Sac Tumors**) [2], [4]. * **NSE (Neuron-Specific Enolase):** An enzyme found in neurons and neuroendocrine cells. It is a marker for **Small Cell Lung Cancer (SCLC)**, Neuroblastoma, and Carcinoid tumors. * **CEA (Carcinoembryonic Antigen):** A classic oncofetal antigen used primarily for monitoring recurrence in **Colorectal Carcinoma**, but also elevated in pancreatic, gastric, and breast cancers [4]. **Clinical Pearls for NEET-PG:** * **β-HCG** is the marker of choice for Choriocarcinoma and Hydatidiform mole [3]. * **Calcitonin** is the specific marker for Medullary Carcinoma of the Thyroid. * **CA-125** is associated with Ovarian Cancer, while **CA 19-9** is associated with Pancreatic Cancer. * **PSA (Prostate Specific Antigen)** is the only marker used for organ-specific screening (Prostate Cancer) [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 512-513. [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. 254-255. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1035-1036. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 346.

Question 179: DNA probes are valuable in the identification of genes in which of the following neoplasms?

A. Neuroblastoma
B. Breast cancer
C. Lymphomas
D. Gliomas (Correct Answer)

Explanation: **Explanation** The correct answer is **Gliomas**. **1. Why Gliomas is correct:** In the context of molecular pathology, DNA probes are essential for identifying specific genetic alterations that have both diagnostic and prognostic value in gliomas. Specifically, **Fluorescence In Situ Hybridization (FISH)** using DNA probes is the gold standard for detecting the **1p/19q co-deletion**, which is the hallmark of oligodendrogliomas [1]. Additionally, DNA probes are used to identify **EGFR amplification** (common in glioblastomas) and **IDH1/2 mutations** [1]. These molecular markers are now mandatory for the integrated diagnosis of CNS tumors according to the WHO classification. **2. Why other options are incorrect:** * **Neuroblastoma:** While N-myc amplification is a key prognostic factor, it is traditionally associated with PCR or Southern Blotting in older literature, though FISH is used now. However, in the context of classic pathology questions, gliomas are more frequently linked to the specific diagnostic utility of DNA probes for chromosomal deletions. * **Breast Cancer:** While HER2/neu status is checked via FISH, the primary screening and identification are typically done via Immunohistochemistry (IHC) [3]. * **Lymphomas:** Diagnosis primarily relies on morphology, flow cytometry, and IHC. While cytogenetics (translocations) are important, DNA probes are considered supplementary to immunophenotyping [2]. **High-Yield Clinical Pearls for NEET-PG:** * **1p/19q co-deletion:** Diagnostic for Oligodendroglioma; predicts a better response to chemotherapy. * **Psammoma bodies** in the brain are most commonly seen in **Meningiomas**. * **Rosenthal fibers** are characteristic of **Pilocytic Astrocytoma**. * The most common primary malignant brain tumor in adults is **Glioblastoma Multiforme (GBM)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1312. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 342-343. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060.

Question 180: Which is a specific marker for prostatic cancer?

A. Prostate specific antigen (Correct Answer)
B. Lactate dehydrogenase (LDH)
C. Chromogranin
D. Carbohydrate antigen 19-9 (CA 19-9)

Explanation: **Explanation:** **Prostate Specific Antigen (PSA)** is the correct answer as it is a glycoprotein enzyme produced by the epithelial cells of the prostate gland. In clinical practice, PSA is the most widely used tumor marker for the screening, diagnosis, and monitoring of prostate cancer [1]. While PSA is "organ-specific" (produced only by prostatic tissue), it is not strictly "cancer-specific," as levels can also rise in benign prostatic hyperplasia (BPH) and prostatitis [1]. However, significantly elevated levels or a rapid "PSA velocity" are highly suggestive of malignancy [1]. **Analysis of Incorrect Options:** * **Lactate Dehydrogenase (LDH):** A non-specific marker of cell turnover. It is elevated in various conditions, including lymphomas, germ cell tumors (especially dysgerminoma), and hemolytic anemias. * **Chromogranin:** A marker for neuroendocrine tumors (e.g., carcinoid tumors, small cell carcinoma of the lung, or pheochromocytoma). * **CA 19-9:** A tumor marker primarily associated with pancreatic adenocarcinoma and cholangiocarcinoma. **NEET-PG High-Yield Pearls:** * **Free vs. Bound PSA:** A *lower* percentage of free PSA is more indicative of prostate cancer, whereas a higher percentage is seen in BPH [1]. * **PSA Density:** Calculated by dividing the PSA level by the prostate volume (measured via ultrasound); higher density increases the suspicion of cancer [1]. * **Prostatic Acid Phosphatase (PAP):** An older marker for prostate cancer, now largely replaced by PSA, but still relevant for identifying metastatic spread to the bone. * **Gleason Scoring:** The definitive histological grading system for prostate cancer prognosis based on glandular architecture. **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. 992-994.

Practice by Chapter

Nomenclature and Classification of Tumors

Practice Questions

Characteristics of Benign and Malignant Neoplasms

Practice Questions

Molecular Basis of Cancer

Practice Questions

Carcinogenesis and Carcinogens

Practice Questions

Tumor Progression and Metastasis

Practice Questions

Tumor Markers

Practice Questions

Paraneoplastic Syndromes

Practice Questions

Genetic Basis of Cancer

Practice Questions

Tumor Immunity

Practice Questions

Cancer Epidemiology and Prevention

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Neoplasia — MCQs

Neoplasia — MCQs

On this page

Practice by Chapter

Want unlimited practice?