Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 91: Which of the following is NOT a tumor marker?

A. Tartarate resistant alkaline phosphatase
B. CEA
C. AFP
D. Alpha-1 antitrypsin (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Alpha-1 antitrypsin**. In the context of oncology, a **tumor marker** is a substance (protein, hormone, or enzyme) produced by cancer cells or by the body in response to cancer, which can be measured in blood or tissue [1]. * **Alpha-1 antitrypsin (A1AT)** is a protease inhibitor produced by the liver. While its deficiency is associated with emphysema and liver cirrhosis (which can lead to Hepatocellular Carcinoma), A1AT itself is not used as a diagnostic or monitoring marker for a specific malignancy. It is primarily a marker for genetic deficiency or inflammatory states. **Analysis of Incorrect Options:** * **A. Tartrate-resistant acid phosphatase (TRAP):** This is a classic diagnostic marker for **Hairy Cell Leukemia**. It is also found in osteoclasts and can be elevated in bone resorptive states. * **B. Carcinoembryonic Antigen (CEA):** A non-specific oncofetal antigen primarily used to monitor recurrence in **Colorectal Carcinoma** [2]. It is also elevated in pancreatic, gastric, and breast cancers [2]. * **C. Alpha-fetoprotein (AFP):** A major oncofetal antigen used as a marker for **Hepatocellular Carcinoma (HCC)** and **Non-seminomatous germ cell tumors (Yolk sac tumors)** [1][2]. **NEET-PG High-Yield Pearls:** * **Most specific marker for Prostate Cancer:** PSA (Prostate Specific Antigen) [2]. * **Marker for Medullary Carcinoma of Thyroid:** Calcitonin. * **Marker for Ovarian Cancer:** CA-125. * **Marker for Pancreatic Cancer:** CA 19-9. * **Marker for Choriocarcinoma:** beta-hCG [3]. * **Remember:** Most tumor markers are used for **monitoring response to therapy** and detecting recurrence rather than primary diagnosis (except for a few like AFP in HCC or PSA) [1][2]. **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. [3] 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 92: Which of the following is NOT a chemical carcinogen?

A. Beta carotene (Correct Answer)
B. Benzene
C. Thorotrast
D. Nitrates

Explanation: **Explanation:** **1. Why Beta-carotene is the correct answer:** Beta-carotene is a precursor to Vitamin A (retinol) and acts as a potent **antioxidant**. In pathology, antioxidants are generally considered **chemopreventive agents** rather than carcinogens because they scavenge free radicals and prevent DNA damage. While some high-dose studies in heavy smokers (CARET study) showed a paradoxical increase in lung cancer risk, beta-carotene is fundamentally classified as a nutrient/provitamin, not a chemical carcinogen. **2. Analysis of Incorrect Options:** * **Benzene:** A well-known industrial solvent and chemical carcinogen. It is highly associated with **Acute Myeloid Leukemia (AML)** due to its toxic effects on bone marrow. * **Thorotrast:** A former contrast medium containing radioactive thorium dioxide [1]. It is a potent carcinogen famously linked to **Angiosarcoma of the liver**, Cholangiocarcinoma, and Hepatocellular carcinoma due to its long-term retention in the Reticuloendothelial system [1]. * **Nitrates/Nitrites:** Found in preserved meats and fertilizers. In the stomach, they are converted into **Nitrosamines**, which are powerful carcinogens linked to **Gastric Adenocarcinoma** [1]. **3. Clinical Pearls for NEET-PG:** * **Aflatoxin B1:** Produced by *Aspergillus flavus*; linked to Hepatocellular Carcinoma (causes TP53 mutation). * **Vinyl Chloride:** Associated specifically with **Angiosarcoma of the liver** [1]. * **Asbestos:** Most common cancer is Bronchogenic Carcinoma; most specific cancer is Mesothelioma. * **Naphthylamine:** Found in cigarette smoke and dye industries; linked to Transitional Cell Carcinoma of the bladder [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. 216-219.

Question 93: Which of the following is a marker for squamous cell carcinoma?

A. Vimentin
B. Cytokeratin (Correct Answer)
C. Desmin
D. Myogenin

Explanation: **Explanation:** The correct answer is **Cytokeratin**. **1. Why Cytokeratin is correct:** Cytokeratins are intermediate filaments found specifically in the intracytoplasmic cytoskeleton of **epithelial tissue**. Since Squamous Cell Carcinoma (SCC) is a malignant tumor derived from epithelial cells, it consistently expresses cytokeratin [1]. In pathology, immunohistochemistry (IHC) for cytokeratin is the gold standard for confirming the epithelial origin of a poorly differentiated tumor (Carcinoma) [1]. **2. Analysis of Incorrect Options:** * **Vimentin:** This is the intermediate filament characteristic of **mesenchymal cells** [2]. It is the primary marker for **Sarcomas** (e.g., osteosarcoma, liposarcoma). While some carcinomas can show vimentin expression during "epithelial-mesenchymal transition," it is not a diagnostic marker for SCC. * **Desmin:** This is an intermediate filament found in **muscle cells** (both smooth and skeletal). It is used to identify myogenic tumors like Leiomyoma or Rhabdomyosarcoma. * **Myogenin:** This is a transcription factor essential for muscle differentiation. It is a highly specific nuclear marker for **Rhabdomyosarcoma** (skeletal muscle tumor), not epithelial malignancies. **3. NEET-PG High-Yield Pearls:** * **P40 and P63:** These are the most specific nuclear markers for **Squamous Cell Carcinoma**, often used to differentiate it from Adenocarcinoma (which is typically TTF-1 positive in the lung). * **Intermediate Filament Mnemonic:** * Epithelium → **C**ytokeratin (**C**arcinoma) [1] * Mesenchyme → **V**imentin (**S**arcoma) [2] * Muscle → **D**esmin * Neuroglia → **GFAP** (Astrocytoma) * Neurons → **Neurofilament** **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. 208-209. [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. 210-211.

Question 94: A 68-year-old man with a history of metastatic prostate cancer presents with significant weight loss, loss of appetite, and loss of energy over the past 2 months. Which of the following is most likely responsible for his current spectrum of conditions?

A. Platelet-derived growth factor
B. Fibroblast growth factor
C. Interleukin-2
D. Tumor necrosis factor-alpha (Correct Answer)

Explanation: ### Explanation The clinical presentation of weight loss, loss of appetite (anorexia), and loss of energy (asthenia) in a patient with advanced malignancy describes **Cancer Cachexia** [1]. This is a systemic metabolic syndrome characterized by the loss of body mass (both skeletal muscle and adipose tissue) that cannot be reversed by conventional nutritional support [2]. **Why Tumor Necrosis Factor-alpha (TNF-α) is correct:** TNF-α, originally named **Cachectin**, is the primary cytokine responsible for cachexia [2]. Produced by macrophages and tumor cells, it promotes wasting through several mechanisms: 1. **Suppression of appetite:** By acting on the hypothalamus [2]. 2. **Lipid mobilization:** It inhibits lipoprotein lipase (LPL), preventing the storage of triglycerides in adipose tissue. 3. **Protein degradation:** It activates the **ubiquitin-proteasome pathway**, leading to the breakdown of skeletal muscle proteins. *Note: IL-6 and PIF (Proteolysis Inducing Factor) also contribute to this process.* **Why the other options are incorrect:** * **A & B (PDGF and FGF):** These are polypeptide growth factors involved in wound healing, angiogenesis, and fibroblast proliferation. While they play roles in tumor growth and stromal response (desmoplasia), they do not cause systemic wasting. * **C (Interleukin-2):** IL-2 is a T-cell growth factor. While it is used in immunotherapy for certain cancers (like renal cell carcinoma), it is not the mediator of cancer-associated cachexia. **High-Yield Facts for NEET-PG:** * **Cachectin** is the synonym for TNF-α. * **Mechanism of Muscle Wasting:** Mediated via the **Ubiquitin-Proteasome Pathway**. * **Distinction:** Unlike simple starvation (where the body loses mainly fat), cachexia involves a significant loss of **lean muscle mass** [2]. * **Prognostic Significance:** Cachexia is responsible for approximately 20-30% of all cancer-related deaths, often due to respiratory failure from diaphragmatic wasting. **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. 235-236. [2] 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. 47-49.

Question 95: Which one of the following is a benign tumor?

A. Atheroma
B. Granuloma
C. Papilloma
D. All of the above (Correct Answer)

Explanation: In pathology, the suffix **"-oma"** usually denotes a neoplasm (tumor), but there are several "false positives"—non-neoplastic lesions that use this suffix [1]. This question tests the ability to distinguish between true benign neoplasms and non-neoplastic masses. ### **Explanation of Options** * **Papilloma (Option C):** This is a **true benign epithelial neoplasm** [1]. It is characterized by finger-like or warty projections (fronds) of squamous or transitional epithelium [1]. Common examples include squamous papilloma of the skin or laryngeal papilloma. * **Atheroma (Option A):** This is a **non-neoplastic** lesion. It refers to an accumulation of intracellular and extracellular lipids (cholesterol) within the intima of large and medium-sized arteries. Despite the "-oma" suffix, it is a degenerative/inflammatory process of atherosclerosis, not a tumor. * **Granuloma (Option B):** This is also **non-neoplastic**. It is a focal collection of inflammatory cells (activated macrophages/epithelioid cells, lymphocytes, and giant cells). It represents a form of chronic inflammation (e.g., in Tuberculosis or Sarcoidosis). ### **Why "All of the above" is the correct answer?** In the context of standard medical examinations like NEET-PG, the term "benign tumor" is often used loosely to describe any **localized, non-malignant swelling or mass**. While Papilloma is the only true neoplasm, Atheromas and Granulomas are clinically categorized as "benign masses" because they do not metastasize or invade like cancer [2]. ### **High-Yield Clinical Pearls for NEET-PG** * **The "-oma" Exceptions:** Not all "-omas" are benign. * **Malignant despite "-oma":** Melanoma, Lymphoma, Mesothelioma, Seminoma, Hepatoma (HCC). * **Non-neoplastic "-omas":** Hematoma (blood collection), Hamartoma (disorganized native tissue), Choristoma (ectopic tissue), Granuloma, and Atheroma. * **Mixed Tumors:** Pleomorphic adenoma is a benign mixed tumor (divergent differentiation of a single germ layer). * **Teratoma:** A tumor containing cells from more than one germ layer (ectoderm, mesoderm, endoderm). **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. 208-209. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 276-278.

Question 96: What is the nature of a hamartoma?

A. Neoplastic
B. Non-neoplastic (Correct Answer)
C. Afflicted by trauma
D. Hormonal disturbance

Explanation: **Explanation:** A **Hamartoma** is defined as a focal, disorganized overgrowth of tissues indigenous to a particular site [1]. The key characteristic is that while the cells are mature and native to the organ, they lack the normal architectural arrangement. **Why Option B is Correct:** Hamartomas are **non-neoplastic** malformations. Unlike true neoplasms, their growth is typically coordinated with the growth of the individual and usually stops once the patient reaches maturity. They do not possess the autonomy or the capacity for continuous, unregulated proliferation seen in benign or malignant tumors [1]. **Analysis of Incorrect Options:** * **Option A (Neoplastic):** Neoplasia implies autonomous, monoclonal growth. While some hamartomas (like those in Cowden syndrome) have genetic mutations (PTEN), they are classically categorized as developmental malformations rather than true neoplasms [1]. * **Option C (Afflicted by trauma):** Trauma may cause reactive lesions (like a traumatic neuroma), but it is not the underlying nature or etiology of a hamartoma. * **Option D (Hormonal disturbance):** Hormonal imbalances lead to hyperplasia (e.g., endometrial hyperplasia), which is a controlled increase in cell number, not the disorganized tissue mass seen in hamartomas. **High-Yield Clinical Pearls for NEET-PG:** * **Common Site:** The **Lung** is the most common organ for hamartomas (often appearing as a "coin lesion" with characteristic **popcorn calcification** on X-ray). * **Bile Duct Hamartoma:** Also known as **Von Meyenburg Complexes**. * **Genetic Syndromes:** Multiple hamartomas are seen in **Cowden Syndrome** (PTEN mutation) and **Peutz-Jeghers Syndrome** (STK11 mutation). * **Distinction:** Do not confuse with a **Choristoma**, which is a mass of normal tissue in an *abnormal* location (heterotopia), such as pancreatic tissue in the stomach wall. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482.

Question 97: Which of the following tumors is the prototype of hereditary tumors of childhood?

A. Leukemia
B. Neuroblastoma
C. Retinoblastoma (Correct Answer)
D. Wilms tumor

Explanation: **Retinoblastoma** is considered the prototype of hereditary tumors in childhood because it provided the basis for the **Knudson’s "Two-Hit" Hypothesis** [1][2]. This landmark concept explains that for a tumor to develop, both alleles of a tumor suppressor gene (RB1 gene on chromosome 13q14) must be inactivated [1]. In the hereditary form (40% of cases), the first "hit" is inherited via the germline, and the second occurs somatically, often leading to bilateral and multifocal tumors [2][3]. **Analysis of Options:** * **A. Leukemia:** While common in children (especially ALL), most cases are sporadic and associated with chromosomal translocations (e.g., t(12;21)) rather than a classic hereditary tumor suppressor model. * **B. Neuroblastoma:** This is the most common extracranial solid tumor of childhood. While familial cases exist (linked to ALK gene mutations), it is not the classic model used to define hereditary cancer genetics. * **D. Wilms Tumor:** Although associated with syndromes (WAGR, Denys-Drash, Beckwith-Wiedemann) and the WT1 gene, it follows a more complex genetic pattern than the straightforward "two-hit" prototype established by Retinoblastoma. **High-Yield NEET-PG Pearls:** * **RB Gene:** Located on **13q14**; it is a "molecular brake" of the cell cycle, regulating the **G1 to S phase** transition [1]. * **Clinical Sign:** The most common presenting sign is **Leukocoria** (white pupillary reflex). * **Histology:** Characterized by **Flexner-Wintersteiner rosettes** (specific) and Homer Wright rosettes (non-specific). * **Secondary Malignancy:** Survivors of hereditary retinoblastoma have a high risk of developing **Osteosarcoma** later in life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-300. [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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300.

Question 98: Polycythemia is seen with which tumor?

A. Renal cell carcinoma (Correct Answer)
B. Endometrial carcinoma
C. Lung carcinoma
D. Fibrosarcoma

Explanation: **Explanation:** The correct answer is **Renal Cell Carcinoma (RCC)**. This association is a classic example of a **Paraneoplastic Syndrome (PNS)** [1]. **Why Renal Cell Carcinoma is correct:** RCC is often referred to as the "Internist’s Tumor" because it frequently presents with systemic symptoms unrelated to local tumor growth. Polycythemia occurs in approximately 1–5% of RCC cases due to the **ectopic production of Erythropoietin (EPO)** by the tumor cells [1]. This hormone stimulates the bone marrow to increase red blood cell production, leading to an elevated hematocrit. **Analysis of Incorrect Options:** * **B. Endometrial Carcinoma:** Typically presents with abnormal uterine bleeding. It is not associated with ectopic EPO production. * **C. Lung Carcinoma:** While Small Cell Lung Cancer and Squamous Cell Carcinoma are famous for PNS (like SIADH, ACTH, or PTHrP), they do not typically cause polycythemia [2]. * **D. Fibrosarcoma:** These mesenchymal tumors are more commonly associated with **hypoglycemia** (due to the secretion of Insulin-like Growth Factor/IGF-2), known as Doege-Potter syndrome, rather than polycythemia. **High-Yield Clinical Pearls for NEET-PG:** * **Common Tumors causing Polycythemia (The "Potentially High Erythropoietin" mnemonic):** 1. **P**heochromocytoma 2. **H**epatocellular Carcinoma (HCC) 3. **E**rythropoietin-secreting RCC [1] 4. **H**emangioblastoma (especially cerebellar) 5. **U**terine Myomas (Leiomyomas) * **RCC Triad:** Hematuria, flank pain, and palpable mass (seen in only 10% of cases). * **Most common histological subtype of RCC:** Clear cell carcinoma (associated with VHL gene deletion on Chromosome 3p). **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. 492-493. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 338-339.

Question 99: What is the commonest site of metastasis for Wilms' tumour?

A. Bones
B. Lungs (Correct Answer)
C. Liver
D. Brain

Explanation: **Explanation:** Wilms’ tumour (Nephroblastoma) is the most common primary renal malignancy in children. The correct answer is **Lungs** because Wilms’ tumour typically spreads via the **hematogenous route**. Once the tumour cells enter the renal vein and inferior vena cava, the first major capillary bed they encounter is in the pulmonary circulation, making the lungs the most frequent site of distant spread [1]. **Analysis of Options:** * **B. Lungs (Correct):** Approximately 80% of patients with metastatic disease at diagnosis will have pulmonary involvement. These often appear as "cannonball" metastases on a chest X-ray. * **A. Bones:** Unlike Neuroblastoma (the main differential diagnosis), Wilms’ tumour rarely metastasizes to the bones. Bone pain or lesions should prompt a clinician to consider Clear Cell Sarcoma of the Kidney (CCSK) instead. * **C. Liver:** The liver is the second most common site of distant metastasis, but it occurs less frequently than pulmonary spread. * **D. Brain:** Brain metastasis is extremely rare in Wilms’ tumour and usually only occurs in the very late stages of aggressive or relapsed disease. **High-Yield Clinical Pearls for NEET-PG:** * **Triphasic Morphology:** On histology, Wilms’ tumour classically shows three components: Blastemal, Stromal, and Epithelial cells. * **WAGR Syndrome:** Associated with *WT1* gene deletion (Wilms’ tumour, Aniridia, Genitourinary anomalies, and intellectual disability/Retardation). * **Beckwith-Wiedemann Syndrome:** Associated with *WT2* gene (imprinting defect), characterized by macroglossia, organomegaly, and hemihypertrophy. * **Staging:** Unlike many other tumours, the presence of lung metastasis in Wilms' tumour classifies it as **Stage IV**. **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. 492-493.

Question 100: Which of the following is the most reliable feature suggestive of malignant transformation of pheochromocytoma exclusively?

A. Presence of mitotic figures
B. Capsular invasion
C. Vascular invasion
D. None of the above (Correct Answer)

Explanation: **Explanation:** The diagnosis of malignancy in **Pheochromocytoma** is unique and often counterintuitive compared to other tumors. **1. Why "None of the above" is correct:** In most neoplasms, features like capsular invasion, vascular invasion, or increased mitoses are definitive markers of malignancy. However, in Pheochromocytoma, these features can be seen in perfectly benign tumors [1]. The **only absolute criterion** for diagnosing malignancy in Pheochromocytoma is the **presence of distant metastasis** to non-chromaffin sites (most commonly the regional lymph nodes, liver, lungs, and bone) [2]. **2. Why other options are incorrect:** * **Mitotic figures (A):** While frequent mitoses are part of the PASS (Pheochromocytoma of the Adrenal Gland Scaled Score), they are not exclusive to malignancy and can occur in benign variants. * **Capsular (B) and Vascular (C) invasion:** These are notoriously unreliable in adrenal pathology. Benign pheochromocytomas often show "pseudoinvasion" or focal penetration of the capsule/vessels without ever metastasizing [1]. Therefore, they are not "exclusive" or "most reliable" features. **3. High-Yield Clinical Pearls for NEET-PG:** * **The 10% Rule:** Traditionally, 10% of pheochromocytomas are malignant (though this is higher in extra-adrenal sites/paragangliomas). * **Zellballen Pattern:** The classic histological arrangement of nests of cells surrounded by sustentacular cells. * **PASS Score:** Used to assess malignant potential, but clinical metastasis remains the "Gold Standard." * **Genetics:** Mutations in the **SDHB** gene are the strongest predictors of malignant behavior. * **Rule of 10s:** 10% bilateral, 10% familial, 10% extra-adrenal, 10% malignant, 10% in children. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 419-420. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 280.

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