General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 641: Ruston bodies are present in which of the following?

A. Apical periodontal cyst
B. Infected dentigerous cyst
C. Gingival cyst of neonate
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Rushton bodies** (also known as hyaline bodies) are unique, eosinophilic, linear, or curved microscopic structures found within the epithelial lining of various odontogenic cysts. 1. **Why "All of the above" is correct:** Rushton bodies are considered a product of the odontogenic epithelium [1]. They are most commonly associated with the **Radicular cyst (Apical periodontal cyst)**, occurring in approximately 10% of cases. However, they are not pathognomonic for a single entity and can be found in the lining of several other odontogenic cysts, including **Infected Dentigerous cysts**, **Gingival cysts**, and Odontogenic Keratocysts (OKC). Their presence is generally attributed to the degeneration of odontogenic epithelium or inflammatory exudates. 2. **Analysis of Options:** * **Apical Periodontal Cyst:** The most frequent site for Rushton bodies due to the chronic inflammatory nature of the lesion. * **Infected Dentigerous Cyst:** Inflammation often triggers the formation of these bodies within the reduced enamel epithelium. * **Gingival Cyst of Neonate:** Though less common, these bodies can be identified in the epithelial remnants (Rest of Serres) of the gingiva. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** They appear as "hairpin," "circular," or "polycyclic" structures and are often brittle, showing cracks. * **Staining:** They are **PAS-positive** and diastase-resistant, indicating a glycoprotein composition. * **Origin:** The most accepted theory is that they represent a secretory product of odontogenic epithelium (though some older theories suggested they were hematogenous in origin) [1]. * **Differential:** Do not confuse Rushton bodies with **Civatte bodies** (seen in Lichen Planus) or **Negri bodies** (seen in Rabies). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Question 642: Which of the following chemical mediators of inflammation is an example of a C-X-C or alpha chemokine?

A. Lipoxin LXA-4
B. Interleukin IL-8 (Correct Answer)
C. Interleukin IL-6
D. Monocyte chemoattractant protein MCP-1

Explanation: **Explanation:** Chemokines are a family of small (8–10 kDa) proteins that act primarily as chemoattractants for specific types of leukocytes [1]. They are classified into four groups based on the arrangement of conserved cysteine (C) residues [1]. **Why IL-8 is correct:** **Interleukin-8 (IL-8)**, also known as CXCL8, is the prototypical **C-X-C (alpha) chemokine** [1]. In this group, one amino acid separates the first two conserved cysteine residues. IL-8 is secreted by activated macrophages and endothelial cells and acts as a potent chemoattractant and activator specifically for **neutrophils**. **Analysis of Incorrect Options:** * **A. Lipoxin LXA-4:** These are anti-inflammatory lipid mediators derived from arachidonic acid. They inhibit neutrophil recruitment and promote the resolution of inflammation, rather than acting as chemokines [2]. * **C. Interleukin IL-6:** This is a multifunctional pro-inflammatory cytokine involved in the acute-phase response (stimulating CRP synthesis in the liver) and fever, but it does not belong to the chemokine family [1]. * **D. MCP-1 (CCL2):** Monocyte Chemoattractant Protein-1 belongs to the **C-C (beta) chemokine** group (where the first two cysteines are adjacent). It primarily recruits monocytes, eosinophils, and lymphocytes, but not neutrophils [1]. **High-Yield NEET-PG Pearls:** * **C-X-C (Alpha):** Act mainly on **neutrophils** (e.g., IL-8) [1]. * **C-C (Beta):** Act on monocytes, lymphocytes, and eosinophils (e.g., MCP-1, Eotaxin, RANTES, MIP-1α) [1]. * **C (Gamma):** Lacks the first and third cysteines; specific for lymphocytes (e.g., Lymphotactin) [1]. * **CX3C:** Contains three intervening amino acids; promotes strong adhesion of T-cells and monocytes (e.g., Fractalkine) [1]. * **Receptor Association:** Chemokines act through G-protein-coupled receptors (GPCRs). CXCR4 and CCR5 are notable as co-receptors for HIV entry [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Question 643: Which of the following proteins is NOT typically found in amyloid deposits in senile amyloidosis?

A. Transthyretin
B. Beta-amyloid protein
C. Amyloid of prion
D. AL protein (Correct Answer)

Explanation: **Explanation:** The question asks to identify the protein **not** typically associated with senile amyloidosis. **Senile amyloidosis** refers to amyloid deposition occurring in elderly individuals, primarily affecting the heart (Senile Systemic Amyloidosis) or the brain (Alzheimer’s disease) [1]. **Why AL protein is the correct answer:** **AL (Amyloid Light Chain)** protein is derived from immunoglobulin light chains produced by plasma cells [1]. It is the hallmark of **Primary Amyloidosis**, which is associated with plasma cell dyscrasias like Multiple Myeloma [1]. While it can occur in elderly patients, it is a specific systemic disease process rather than a manifestation of "senile" or age-related degenerative amyloid deposition. **Analysis of incorrect options:** * **Transthyretin (ATTR):** This is the most common protein in **Senile Systemic Amyloidosis**. Normal (wild-type) transthyretin deposits in the hearts of elderly patients, leading to restrictive cardiomyopathy [1]. * **Beta-amyloid protein (Aβ):** This protein is derived from Amyloid Precursor Protein (APP) and forms the neuritic plaques found in the brains of patients with **Alzheimer’s disease**, the most common form of senile cerebral amyloidosis [1]. * **Amyloid of prion (PrP):** Prion proteins (PrPSc) can aggregate into amyloid plaques in the brain in age-related neurodegenerative conditions like Creutzfeldt-Jakob Disease (CJD) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** All amyloid types show **Apple-green birefringence** under polarized light after **Congo Red** staining [1]. * **Secondary Amyloidosis (AA):** Associated with chronic inflammation (e.g., TB, Rheumatoid Arthritis); derived from Serum Amyloid-Associated protein. * **Dialysis-associated Amyloidosis:** Caused by **β2-microglobulin** deposition [1]. * **Medullary Carcinoma of Thyroid:** Associated with **A-Cal (Calcitonin)** amyloid. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-270.

Question 644: Which of the following vascular lesions has the least clinical significance?

A. Monckeberg's medial calcification (Correct Answer)
B. Hyaline arteriolosclerosis
C. Hyperplastic arteriolosclerosis
D. Glomus tumor

Explanation: **Explanation:** The question asks to identify the vascular lesion with the **least clinical significance**. **1. Why Monckeberg’s Medial Calcification is the Correct Answer:** Monckeberg’s medial sclerosis is characterized by ring-like calcifications within the **tunica media** of medium-sized muscular arteries (e.g., radial and ulnar arteries). Crucially, these deposits **do not encroach upon the vessel lumen**. Because the blood flow remains unobstructed, it is typically an incidental finding on X-rays (appearing as "pipestem" arteries) and does not cause ischemia or clinical symptoms. It is most common in individuals over age 50. **2. Why the Other Options are Incorrect:** * **Hyaline Arteriolosclerosis:** Associated with benign hypertension and diabetes mellitus. It causes luminal narrowing and can lead to significant end-organ damage, particularly **nephrosclerosis** in the kidneys [1]. * **Hyperplastic Arteriolosclerosis:** Characteristic of **malignant hypertension**. It shows "onion-skin" thickening of the vessel wall, leading to severe luminal narrowing and fibrinoid necrosis, often resulting in acute renal failure [2]. * **Glomus Tumor:** A painful, benign vascular neoplasm arising from the glomus body (specialized arteriovenous anastomosis). While benign, it is **clinically significance** due to intense paroxysmal pain, typically occurring under the fingernails. **Clinical Pearls for NEET-PG:** * **Monckeberg’s:** "Medial" = Middle layer; "M" for Medial and "M" for Minimal clinical impact. * **Hyaline vs. Hyperplastic:** Hyaline is "pink/homogeneous" (benign HTN); Hyperplastic is "onion-skin" (malignant HTN) [2]. * **Arteriosclerosis vs. Atherosclerosis:** Arteriosclerosis is a general term for "hardening of arteries," while atherosclerosis is a specific type involving intimal plaques. Monckeberg’s is a form of arteriosclerosis but *not* atherosclerosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 645: Endotoxic shock is propagated by which of the following mechanisms?

A. Endothelial injury
B. Peripheral vasodilation
C. Increased vascular permeability
D. Cytokine action (Correct Answer)

Explanation: **Explanation:** **Why Cytokine Action is Correct:** Endotoxic shock (a form of septic shock) is primarily triggered by **Lipopolysaccharide (LPS)**, an endotoxin found in the outer membrane of Gram-negative bacteria [1]. The core mechanism involves LPS binding to **CD14** on the surface of monocytes and macrophages via Toll-like receptor 4 (**TLR-4**) [2]. This interaction triggers a massive systemic release of **pro-inflammatory cytokines**, most notably **TNF-α, IL-1, and IL-6**. These cytokines act as the primary mediators (the "cytokine storm") that subsequently drive the systemic inflammatory response syndrome (SIRS), leading to the clinical manifestations of shock [2]. **Why Other Options are Incorrect:** * **A, B, and C (Endothelial injury, Peripheral vasodilation, Increased vascular permeability):** While these three processes are critical components of the pathophysiology of shock, they are **downstream effects** or consequences of cytokine action [3]. Cytokines (like TNF-α) induce the production of Nitric Oxide (causing vasodilation) and damage the endothelium (causing leakage and injury). The question asks for the mechanism that *propagates* or drives the shock state, which is the cytokine cascade itself [2]. **NEET-PG High-Yield Pearls:** * **Primary Mediator:** TNF-α is considered the "master regulator" and the first cytokine to rise in endotoxic shock. * **Receptor:** TLR-4 is the specific pattern recognition receptor for LPS. * **Coagulation:** Cytokines also induce Tissue Factor expression, leading to **DIC** (Disseminated Intravascular Coagulation), a common complication [1]. * **Metabolic Shift:** Cytokines promote insulin resistance and hyperglycemia initially, followed by liver failure and hypoglycemia. **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. 63-64. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 142. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 142-143.

Question 646: Which one of the following manifestations is more likely to be found in the diffuse form of systemic sclerosis than in the limited variant?

A. Esophageal dysmotility
B. Pulmonary involvement (Correct Answer)
C. Distal skin thickening
D. Renal disease

Explanation: **Explanation:** Systemic Sclerosis (Scleroderma) is a multi-system autoimmune disorder characterized by excessive fibrosis. It is broadly classified into two types: **Limited** and **Diffuse**. [1] **Why Pulmonary Involvement is the Correct Answer:** While both variants can involve the lungs, **interstitial lung disease (ILD)** and significant pulmonary fibrosis occur much earlier and more frequently in the **Diffuse Cutaneous Systemic Sclerosis (dcSSc)** variant. [1] In contrast, the limited variant is more typically associated with isolated pulmonary arterial hypertension (PAH) later in the disease course. [1] The diffuse form is characterized by rapid progression and early involvement of internal organs (lungs, heart, and kidneys). [3] **Analysis of Incorrect Options:** * **A. Esophageal dysmotility:** This is a common feature of **both** variants. [3] It is a classic component of the **CREST syndrome** (the limited variant). [2] * **C. Distal skin thickening:** This is the hallmark of **Limited Scleroderma**. In the limited form, skin thickening is restricted to the hands, forearms, and face (distal to elbows/knees). [1] In the diffuse form, thickening is **proximal** (trunk, thighs, and upper arms). [2] * **D. Renal disease:** While **Scleroderma Renal Crisis** is a classic complication of the diffuse form, recent NEET-PG trends and standard textbooks (like Robbins) emphasize that **Pulmonary involvement** (specifically ILD) is now the leading cause of mortality and a more frequent systemic manifestation in the diffuse variant compared to the limited form. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Antibody Association:** * **Limited (CREST):** Anti-Centromere antibodies (Highly specific). [1] * **Diffuse:** Anti-Scl-70 (Anti-topoisomerase I) and Anti-RNA polymerase III. [1] * **CREST Syndrome:** Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia. [2] * **Mortality:** Lung disease (ILD) is currently the #1 cause of death in Systemic Sclerosis. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 238-239. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 689-690. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 237-238.

Question 647: Cloudy swelling is:

A. Irreversible
B. Reversible (Correct Answer)
C. Physiological and never pathological
D. Late manifestation of cell injury

Explanation: **Explanation:** **Cloudy swelling** (also known as hydropic change or vacuolar degeneration) is the **earliest and most common form of reversible cell injury** [1]. **1. Why the correct answer (B) is right:** The underlying mechanism is the failure of energy-dependent ion pumps (Na⁺-K⁺ ATPase) in the plasma membrane [1]. When a cell is injured (e.g., by hypoxia or toxins), ATP levels drop, causing the pump to fail. This leads to an accumulation of intracellular sodium and an obligatory entry of water into the cell to maintain osmotic equilibrium [1]. This results in cellular swelling and the formation of small clear vacuoles within the cytoplasm (representing distended endoplasmic reticulum) [1]. Since the cell can return to its normal homeostatic state if the injurious stimulus is removed, it is classified as **reversible** [1]. **2. Why the incorrect options are wrong:** * **Option A:** Irreversible injury is characterized by severe mitochondrial dysfunction and membrane damage (e.g., necrosis or apoptosis) [1]. Cloudy swelling precedes these stages. * **Option C:** Cloudy swelling is always a **pathological** response to stress or injury; it is never a normal physiological process. * **Option D:** It is an **early** (initial) manifestation of cell injury, not a late one [1]. Late manifestations typically involve nuclear changes (pyknosis, karyorrhexis) or membrane rupture. **NEET-PG High-Yield Pearls:** * **Gross Appearance:** The affected organ (liver, kidney, or heart) appears enlarged, pale, and heavy with rounded margins. * **Microscopic Hallmark:** Small, clear vacuoles in the cytoplasm; this is why it is also called **Hydropic Degeneration** [1]. * **Sequence of Reversible Injury:** Decreased ATP → Failure of Na⁺-K⁺ pump → Influx of Na⁺ and H₂O → Efflux of K⁺ → Cellular Swelling [1]. * **Distinction:** Unlike fatty change (another reversible injury), the vacuoles in cloudy swelling do not stain with Sudan Black or Oil Red O [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. 49-53.

Question 648: In which phase of the cell cycle is the cellular content of DNA doubled?

A. S phase (Correct Answer)
B. M phase
C. G1 phase
D. G2 phase

Explanation: ### Explanation The cell cycle is a highly regulated sequence of events that leads to cell division [1]. The correct answer is **S phase (Synthesis phase)**. **1. Why S phase is correct:** The S phase is the period during which **DNA replication** occurs. The cell synthesizes a complete copy of the DNA in its nucleus. By the end of this phase, the DNA content of the cell doubles (from 2n to 4n in diploid cells), ensuring that when the cell eventually divides, each daughter cell receives an identical and complete set of genetic material. **2. Why the other options are incorrect:** * **G1 phase (Gap 1):** This is the pre-synthetic phase. The cell grows in size and synthesizes RNA and proteins required for DNA replication, but the DNA content remains constant (2n) [1]. * **G2 phase (Gap 2):** This is the post-synthetic phase. While the DNA has already doubled, this phase is dedicated to further cell growth and the synthesis of proteins (like tubulin) needed for the mitotic spindle [1]. * **M phase (Mitosis):** This is the phase of actual nuclear and cytoplasmic division. While the DNA is organized into chromosomes and separated, the "doubling" process has already been completed during the S phase [1]. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Interphase:** Consists of G1, S, and G2. It is the longest part of the cell cycle. * **Quiescent Phase (G0):** Cells that have exited the cycle (e.g., neurons, cardiac myocytes) are in G0 [1]. * **Checkpoints:** The **G1-S checkpoint** (regulated by p53 and Rb protein) is the most critical "restriction point." If DNA damage is detected here, the cell cycle arrests to prevent the replication of mutated DNA [2]. * **Cyclins and CDKs:** The cell cycle is driven by Cyclin-Dependent Kinases. For example, **Cyclin D-CDK4** is essential for the G1 to S transition [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303.

Question 649: Which cells are most sensitive to hypoxic injury?

A. Neurons (Correct Answer)
B. Myocardial cells
C. Skeletal muscles
D. All of the above

Explanation: The sensitivity of a cell to hypoxia depends on its metabolic rate and its ability to utilize anaerobic glycolysis. **Neurons** are the most sensitive cells in the body to hypoxic-ischemic injury because they have a high metabolic demand for oxygen and very limited glycogen stores [1], [2], [3]. Irreversible damage to neurons occurs within **3 to 5 minutes** of total oxygen deprivation [1]. **Analysis of Options:** * **A. Neurons (Correct):** Specifically, the **Pyramidal cells of the Hippocampus (Sommer sector)** and **Purkinje cells of the Cerebellum** are the most vulnerable "watershed" areas in the brain [3]. * **B. Myocardial cells:** These are also highly sensitive but more resilient than neurons. Irreversible injury (infarction) in cardiac myocytes typically occurs after **20 to 30 minutes** of ischemia [1]. * **C. Skeletal muscles:** These cells are relatively resistant to hypoxia. They possess significant glycogen stores and can rely on anaerobic metabolism for several hours (up to **2–3 hours**) before irreversible damage occurs [1]. * **D. All of the above:** While all these cells are affected by hypoxia, the question asks for the *most* sensitive, which is uniquely the neuron. **NEET-PG High-Yield Pearls:** 1. **Hierarchy of Sensitivity:** Neurons (3–5 mins) > Myocytes/Hepatocytes/Renal tubular cells (30–120 mins) > Skeletal muscle/Fibroblasts (hours) [1]. 2. **Most sensitive area in the brain:** Hippocampus (CA1 area/Sommer sector) [3]. 3. **Morphological Sign:** The earliest light microscopic sign of neuronal hypoxic injury is the **"Red Neuron"** (shrunken cell body, pyknotic nucleus, and intense eosinophilia), seen 12–24 hours after injury. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 140-142. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1265-1266. [3] 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. 150-151.

Question 650: The Cyclin D-IGH fusion gene is associated with which of the following conditions?

A. Mantle cell lymphoma
B. Follicular lymphoma
C. Melanoma
D. Burkitt lymphoma (Correct Answer)

Explanation: The question identifies **Burkitt lymphoma** as the correct answer; however, it is critical to note a common point of confusion in medical genetics. While the provided answer key selects Burkitt lymphoma, the **Cyclin D1-IGH** fusion is classically the hallmark of **Mantle Cell Lymphoma** [1]. In the context of Burkitt lymphoma, the characteristic fusion involves **c-MYC and IGH** [4]. ### **Explanation of Options** * **Burkitt Lymphoma (Correct per key):** Characterized by the **t(8;14)** translocation, which fuses the **c-MYC** proto-oncogene on chromosome 8 with the **Immunoglobulin Heavy chain (IGH)** locus on chromosome 14 [4]. This leads to constitutive expression of c-MYC, driving rapid cell proliferation ("Starry sky" appearance) [4]. * **Mantle Cell Lymphoma (MCL):** This is the classic association for **Cyclin D1-IGH**. It involves **t(11;14)**, where the *CCND1* gene (Cyclin D1) is translocated to the IGH locus [1]. Overexpression of Cyclin D1 promotes the G1 to S phase transition in the cell cycle. * **Follicular Lymphoma:** Associated with **t(14;18)**, involving the fusion of **BCL-2** with the IGH locus [2]. This leads to the overexpression of BCL-2, an anti-apoptotic protein, preventing programmed cell death [3]. * **Melanoma:** Typically associated with mutations in **BRAF (V600E)** or **p16/INK4a** deletions, rather than IGH translocations. ### **High-Yield Clinical Pearls for NEET-PG** * **t(8;14):** c-MYC; Burkitt Lymphoma (Starry sky pattern, EBV association) [4]. * **t(11;14):** Cyclin D1; Mantle Cell Lymphoma (CD5+ B-cells) [1]. * **t(14;18):** BCL-2; Follicular Lymphoma (Centrocytes and centroblasts) [2]. * **t(9;22):** BCR-ABL; CML (Philadelphia chromosome). * **t(15;17):** PML-RARα; APML (M3 subtype of AML; responds to ATRA). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 610-612. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

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