Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 561: Which of the following is NOT a rare histological variant of carcinoma breast with a better prognosis?

A. Colloid carcinoma
B. Medullary carcinoma
C. Inflammatory carcinoma (Correct Answer)
D. Tubular carcinoma

Explanation: **Explanation:** In breast pathology, most invasive carcinomas are of the "No Special Type" (NST), which generally carry a standard prognosis [1]. However, certain histological variants are recognized for having a **favorable (better) prognosis** despite being invasive [1]. **1. Why Inflammatory Carcinoma is the correct answer:** Inflammatory carcinoma is **not** a histological variant but a **clinical diagnosis** characterized by "peau d'orange" (skin thickening and pitting) [3]. It is caused by extensive involvement of dermal lymphatic vessels by tumor emboli. It is the **most aggressive** form of breast cancer with a very poor prognosis (T4d in TNM staging), making it the opposite of a "better prognosis" variant. **2. Analysis of Incorrect Options (Favorable Variants):** * **Tubular Carcinoma (Option D):** Consists of well-formed tubules (>90%). It is the variant with the **best prognosis**; it is usually small, non-palpable, and rarely metastasizes. * **Colloid (Mucinous) Carcinoma (Option A):** Characterized by "clusters of cells floating in lakes of extracellular mucin." It typically occurs in older women and has a slow growth rate and excellent prognosis. * **Medullary Carcinoma (Option B):** Despite being high-grade (triple-negative) and having a fleshy appearance with lymphoid stroma, it paradoxically carries a better prognosis than standard NST carcinomas [2]. It is frequently associated with **BRCA1 mutations**. **NEET-PG High-Yield Pearls:** * **Best Prognosis:** Tubular Carcinoma. * **Worst Prognosis:** Inflammatory Carcinoma. * **Most Common Site:** Upper Outer Quadrant. * **Molecular Subtype with Best Prognosis:** Luminal A (ER/PR positive, HER2 negative, low Ki-67). * **Paget’s Disease of Nipple:** Indicates an underlying DCIS or invasive carcinoma; cells are PAS positive (mucin-producing) [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1068-1069. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1068. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 458-459.

Question 562: Which of the following parotid malignancies is known for perineural spread?

A. Pleomorphic adenoma
B. Adenoid cystic carcinoma (Correct Answer)
C. Warthin's tumor
D. Ductal papilloma

Explanation: **Explanation:** **Adenoid Cystic Carcinoma (ACC)** is the correct answer because it is classically characterized by its high propensity for **perineural invasion (PNI)**. In the context of the parotid gland, the tumor cells tend to track along the facial nerve (CN VII), often leading to facial nerve palsy—a clinical hallmark that distinguishes it from benign lesions. Histologically, it presents with a "Swiss-cheese" (cribriform) pattern, and its ability to spread along nerve sheaths often results in recurrence and late distant metastasis, even years after surgery. **Analysis of Incorrect Options:** * **Pleomorphic Adenoma (A):** This is the most common benign salivary gland tumor. While it can recur if the capsule is breached during surgery, it does not exhibit perineural spread. * **Warthin’s Tumor (C):** Also known as Papillary Cystadenoma Lymphomatosum, this is a benign tumor strongly associated with smoking. It is typically found in the tail of the parotid and does not invade nerves. * **Ductal Papilloma (D):** This is a rare, benign epithelial tumor of the salivary ducts. It lacks the invasive characteristics required for perineural spread. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site for ACC:** Submandibular gland (though it occurs in the parotid, it is the most common malignant tumor of the minor salivary glands) [1]. * **Histological Hallmark:** Cribriform pattern with "cylindromatous" appearance (basement membrane-like material in spaces). * **Clinical Sign:** Pain is a frequent early symptom in ACC due to its affinity for nerves. * **Prognosis:** Characterized by a "relentless" course; 5-year survival is good, but 10-20 year survival is poor due to late metastases (often to the lungs). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 753-755.

Question 563: Which of the following is NOT a feature of malignant transformation by cultured cells?

A. Increased cell density
B. Increased requirement for growth factors (Correct Answer)
C. Alterations of cytoskeletal structures
D. Loss of anchorage

Explanation: ### Explanation The hallmark of malignant transformation in cultured cells (in vitro) is the acquisition of **autonomy** [1], [2]. Normal cells are dependent on external signals and physical constraints to grow, whereas malignant cells bypass these regulatory checkpoints. **Why Option B is the Correct Answer:** Malignant cells exhibit **decreased requirement for growth factors**, not an increased one [1]. This occurs because cancer cells often produce their own growth factors (autocrine stimulation), possess mutated receptors that are constitutively active, or have downstream signaling pathways (like RAS) that are permanently "turned on." Consequently, they can proliferate in culture media with significantly lower concentrations of serum or growth supplements compared to normal cells. **Analysis of Incorrect Options:** * **A. Increased cell density:** Normal cells exhibit **contact inhibition**; they stop dividing once they form a confluent monolayer [3]. Malignant cells lose this inhibition, piling up on top of one another to reach high cell densities (forming "foci"). * **C. Alterations of cytoskeletal structures:** Malignant transformation involves the reorganization of microfilaments (actin) and microtubules. This leads to changes in cell shape, increased motility, and the ability to invade [3]. * **D. Loss of anchorage:** Normal cells are "anchorage-dependent" and require attachment to a solid surface (extracellular matrix) to survive. Malignant cells can grow in suspension or semi-solid media (like agar), a phenomenon known as **anchorage independence**. **High-Yield NEET-PG Pearls:** * **Immortality:** Unlike normal cells (limited by the Hayflick limit), malignant cells express **telomerase**, allowing indefinite replication. * **Warburg Effect:** Malignant cells prefer aerobic glycolysis over oxidative phosphorylation, even in the presence of oxygen [1]. * **Gold Standard:** The most definitive proof of malignant transformation in vitro is the ability of the cultured cells to form a tumor when injected into a susceptible laboratory animal (e.g., nude mice). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 290-291. [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. 202-203. [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. 232-233.

Question 564: A 54-year-old woman diagnosed with early-stage breast cancer undergoes lumpectomy. The pathology report confirms the early stage and notes significant desmoplasia in the surrounding tissue. What does the term desmoplasia refer to?

A. An irregular accumulation of blood vessels.
B. Scanty connective tissue causing the neoplasm to be soft and fleshy.
C. Normal tissue misplaced within another organ.
D. Proliferation of non-neoplastic fibrous connective tissue. (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is Correct:** Desmoplasia refers to the **proliferation of non-neoplastic, reactive fibrous connective tissue** (stroma) induced by certain malignant tumors [1]. In many carcinomas, particularly breast and pancreatic cancers, the tumor cells secrete growth factors (like TGF-̢) that stimulate resident fibroblasts to produce abundant collagen [1]. This dense, collagenous stroma gives the tumor a characteristic **"stony hard" (scirrhous)** consistency upon palpation [3]. It is important to note that while the tumor cells are malignant, the desmoplastic stroma itself is a reactive, non-neoplastic host response. **2. Why the Other Options are Incorrect:** * **Option A:** An irregular accumulation of blood vessels describes **angiogenesis** or a **hemangioma**, not desmoplasia. * **Option B:** Scanty connective tissue results in a **"medullary"** or "fleshy" appearance (e.g., Medullary carcinoma of the breast) [2]. Desmoplasia is the exact opposite—it involves abundant connective tissue. * **Option C:** Normal tissue misplaced within another organ is the definition of a **Choristoma** (e.g., pancreatic tissue in the stomach wall). **3. NEET-PG High-Yield Pearls:** * **Scirrhous Morphology:** Tumors with prominent desmoplasia are called "scirrhous" tumors [3]. A classic example is **Infiltrating Ductal Carcinoma (IDC)** of the breast. * **Clinical Sign:** Desmoplasia in breast cancer often causes the pulling of Cooper’s ligaments, leading to **skin dimpling** or **nipple retraction** [1], [3]. * **Tumor Microenvironment:** Desmoplasia is not just structural; the dense stroma can create a physical barrier that limits the penetration of chemotherapy drugs. * **Linitis Plastica:** This is a "leather bottle" appearance of the stomach caused by diffuse desmoplasia in response to gastric adenocarcinoma. **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. 203-204. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 453-454.

Question 565: A patient presents with a mediastinal mass showing sheets of epithelial cells with an arborizing pattern and positivity for keratin, interspersed with lymphoid cells. What is the most likely diagnosis?

A. Thymoma (Correct Answer)
B. Thymic carcinoid
C. Primary mediastinal lymphoma
D. Non-Hodgkin lymphoma

Explanation: ### **Explanation** **Correct Answer: A. Thymoma** **Concept:** Thymomas are neoplasms derived from the **thymic epithelial cells** [4]. Histologically, they are characterized by a dual population of cells: neoplastic epithelial cells and non-neoplastic, reactive T-lymphocytes (thymocytes) [1]. The epithelial cells often form **sheets** or an **arborizing (branching) pattern** [1]. The definitive diagnostic feature in this question is the **positivity for keratin** (a marker for epithelial cells) within the cellular sheets, confirming their epithelial origin despite the heavy lymphoid infiltrate [2]. **Why other options are incorrect:** * **Thymic Carcinoid:** These are neuroendocrine tumors. While they appear in the mediastinum, they typically show an organoid, trabecular, or rosette-like growth pattern and are positive for neuroendocrine markers like **Chromogranin** and **Synaptophysin**, rather than just keratin [4]. * **Primary Mediastinal Lymphoma / Non-Hodgkin Lymphoma (NHL):** While these present as mediastinal masses, they consist of a monomorphic population of malignant lymphoid cells. They would be **negative for keratin** and positive for lymphoid markers like **CD20** (B-cell) or **CD3** (T-cell). They do not show an epithelial arborizing pattern. **Clinical Pearls for NEET-PG:** * **Most common association:** 30–50% of thymoma patients have **Myasthenia Gravis** [2]. Conversely, 15% of Myasthenia Gravis patients have a thymoma. * **Other associations:** Pure red cell aplasia, Hypogammaglobulinemia (Good Syndrome) [3]. * **Microscopy:** Look for **Hassall’s corpuscles** (though more common in the normal thymus, they can be seen in some variants) [2]. * **Classification:** The WHO classification (Type A, AB, B1, B2, B3) is based on the shape of epithelial cells (spindle vs. polygonal) and the ratio of lymphocytes to epithelial cells [3]. **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. 634-635. [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, p. 634. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 572-574. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 571-572.

Question 566: Keratin is a tumor marker for which of the following?

A. Carcinoma cervix (Correct Answer)
B. Neurofibroma
C. Rhabdomyosarcoma
D. Choriocarcinoma

Explanation: **Explanation:** **1. Why Carcinoma Cervix is Correct:** Keratin is an intermediate filament found in epithelial cells. It is the hallmark immunohistochemical (IHC) marker for **Carcinomas** (malignant tumors of epithelial origin) [1]. Since Carcinoma Cervix (most commonly Squamous Cell Carcinoma) arises from the epithelial lining of the cervix, it expresses Cytokeratin [2]. In pathology, "Keratin" or "Cytokeratin" (CK) is used to differentiate carcinomas from sarcomas, lymphomas, and melanomas [2]. **2. Why Other Options are Incorrect:** * **Neurofibroma (Option B):** This is a benign nerve sheath tumor. Its characteristic marker is **S-100**, reflecting its neural crest origin. * **Rhabdomyosarcoma (Option C):** This is a malignant tumor of skeletal muscle. Key markers include **Desmin**, **Myogenin**, and **MyoD1**. * **Choriocarcinoma (Option D):** This is a germ cell tumor/trophoblastic tumor. Its most specific diagnostic marker is **hCG** (human Chorionic Gonadotropin). **3. High-Yield Clinical Pearls for NEET-PG:** * **Cytokeratin (CK):** The most specific marker for epithelial differentiation (Carcinomas) [1]. * **Vimentin:** The marker for mesenchymal cells (Sarcomas). * **S-100:** Positive in Melanoma, Schwannoma, and Neurofibroma. * **LCA (CD45):** The primary marker for Lymphomas. * **Synaptophysin/Chromogranin:** Markers for Neuroendocrine tumors (e.g., Small cell carcinoma) [2]. * **PSA:** Marker for Prostatic Carcinoma. * **Thyroglobulin:** Marker for Thyroid Carcinoma (Papillary/Follicular). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, p. 1004. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 470-471.

Question 567: Germline mutations in which of the following genes are not associated with hereditary breast cancer?

A. CHEK2
B. GATA2 (Correct Answer)
C. BRCA2
D. TP53

Explanation: **Explanation:** The development of hereditary breast cancer is primarily linked to germline mutations in genes involved in DNA repair pathways and cell cycle regulation [1]. **Why GATA2 is the correct answer:** **GATA2** is a transcription factor essential for the proliferation and survival of hematopoietic stem cells. Germline mutations in *GATA2* lead to **GATA2 deficiency syndrome**, which is characterized by immunodeficiency (MonoMAC syndrome), lymphedema (Emberger syndrome), and a high predisposition to **Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML)**. It has no established association with hereditary breast cancer. **Analysis of incorrect options:** * **BRCA2 (Option C):** The most well-known high-penetrance gene associated with breast cancer [2]. It is involved in homologous recombination repair of double-strand DNA breaks. Mutations significantly increase the risk of breast, ovarian, prostate, and pancreatic cancers. * **TP53 (Option D):** Mutations in this "guardian of the genome" cause **Li-Fraumeni Syndrome** [3]. This syndrome is characterized by a high incidence of early-onset breast cancer, along with sarcomas, brain tumors, and adrenocortical carcinomas [3]. * **CHEK2 (Option A):** This gene encodes a cell cycle checkpoint kinase. Mutations in *CHEK2* (specifically the 1100delC variant) are associated with a moderate risk of breast cancer in both females and males. **High-Yield Clinical Pearls for NEET-PG:** * **Most common gene in hereditary breast cancer:** *BRCA1* (followed by *BRCA2*) [2]. * **Cowden Syndrome:** *PTEN* mutation (Breast cancer + Thyroid cancer + Endometrial cancer). * **Peutz-Jeghers Syndrome:** *STK11* mutation (Breast cancer + GI polyps + Perioral pigmentation). * **Hereditary Diffuse Gastric Cancer (HDGC):** *CDH1* mutation (Lobular breast cancer + Diffuse gastric cancer). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1058. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1059. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060.

Question 568: All the following can cause GIT cancers except?

A. Hepatitis B virus (Correct Answer)
B. EBV
C. HIV
D. H. pylori

Explanation: **Explanation:** The correct answer is **A. Hepatitis B virus**. While Hepatitis B Virus (HBV) is a potent oncogenic virus, its primary target is the liver, where it causes **Hepatocellular Carcinoma (HCC)** [4]. It is not associated with cancers of the Gastrointestinal Tract (GIT) such as the esophagus, stomach, or intestines. **Analysis of Options:** * **EBV (Epstein-Barr Virus):** EBV is strongly associated with **Gastric Adenocarcinoma** and nasopharyngeal cancer [1]. Although primarily known for Burkitt lymphoma [2], its oncogenic potential extends to these epithelial sites. * **HIV:** HIV increases the risk of GIT malignancies indirectly through immunosuppression [3]. It is a major risk factor for **Kaposi Sarcoma** (which can involve the entire GIT) and **Non-Hodgkin Lymphoma** (specifically primary GI lymphomas). It is also associated with Anal Squamous Cell Carcinoma via co-infection with HPV [3]. * **H. pylori:** This bacterium is the most common cause of GIT-related malignancy. It is classified as a Class I carcinogen and is linked to **Gastric Adenocarcinoma** and **MALToma** (Mucosa-Associated Lymphoid Tissue lymphoma). **High-Yield Clinical Pearls for NEET-PG:** * **H. pylori** is the only bacterium recognized as a direct carcinogen. * **EBV** is associated with the "nasopharyngeal-gastric" axis of epithelial cancers [1], in addition to Burkitt Lymphoma. * **HBV/HCV** are strictly hepatotropic regarding oncogenesis; they do not cause luminal GI tract cancers [4]. * **Anal Cancer** in HIV patients is primarily driven by **HPV (Types 16, 18)** due to decreased immune surveillance [3]. **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. Diseases of the Immune System, pp. 261-262. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 336-337.

Question 569: Which among the following is a marker of carcinoma?

A. Cytokeratin (Correct Answer)
B. Vimentin
C. Calretinin
D. CD 45

Explanation: **Explanation:** The identification of tumors using Immunohistochemistry (IHC) is based on the presence of specific **Intermediate Filaments**, which serve as tissue-specific markers. **Why Cytokeratin is correct:** **Cytokeratin** is the characteristic intermediate filament found in **epithelial cells**. Since **Carcinomas** are malignant tumors of epithelial origin [1], Cytokeratin is the primary diagnostic marker used to identify them. It helps differentiate carcinomas from sarcomas or lymphomas [1], [2]. **Analysis of Incorrect Options:** * **Vimentin:** This is the intermediate filament marker for **mesenchymal cells**. It is the primary marker for **Sarcomas** (e.g., Osteosarcoma, Liposarcoma) [1]. It is also expressed in melanomas and some carcinomas (like Renal Cell Carcinoma). * **Calretinin:** This is a calcium-binding protein used as a highly specific marker for **Mesothelioma**. It is also seen in sex cord-stromal tumors of the ovary. * **CD 45 (LCA - Leukocyte Common Antigen):** This is the definitive marker for **Lymphomas** and leukemias. It is expressed on all hematopoietic cells except mature erythrocytes and platelets. **High-Yield Clinical Pearls for NEET-PG:** * **Desmin:** Marker for Muscle tumors (Rhabdomyosarcoma, Leiomyosarcoma). * **GFAP (Glial Fibrillary Acidic Protein):** Marker for Glial tumors (Astrocytoma, Ependymoma). * **S-100:** Marker for Melanoma, Schwannoma, and Langerhans Cell Histiocytosis (LCH). * **Synaptophysin/Chromogranin:** Markers for Neuroendocrine tumors (e.g., Carcinoid, Small cell carcinoma). * **PSA:** Specific for Prostate cancer. **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. 208-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 341-342.

Question 570: In Burkitt's lymphoma, which chromosomal translocation is typically seen?

A. t(12;14)
B. t(8;14) (Correct Answer)
C. t(4;8)
D. t(12;18)

Explanation: ### Explanation **1. Why t(8;14) is Correct:** Burkitt’s Lymphoma is a highly aggressive B-cell neoplasm characterized by the translocation of the **c-MYC proto-oncogene** from chromosome 8 to the **Immunoglobulin Heavy chain (IgH)** locus on chromosome 14 [1]. * **Mechanism:** The IgH promoter is constitutively active in B-cells. When c-MYC (a transcription factor promoting cell cycle progression) is moved adjacent to this promoter, it leads to the massive over-expression of the MYC protein, resulting in rapid cellular proliferation [1]. * *Note:* Variants include t(2;8) involving the kappa light chain and t(8;22) involving the lambda light chain [1]. **2. Analysis of Incorrect Options:** * **t(12;14):** This is not a classic translocation associated with major lymphomas. However, t(11;14) is the hallmark of **Mantle Cell Lymphoma** (Cyclin D1/BCL-1). * **t(4;8) and t(12;18):** These are not standard diagnostic translocations in common hematological malignancies. For NEET-PG, remember t(14;18) for **Follicular Lymphoma** (BCL-2) [3] and t(9;22) for **CML** (BCR-ABL). **3. NEET-PG High-Yield Clinical Pearls:** * **Morphology:** Characterized by a **"Starry Sky" appearance** (tingible body macrophages acting as "stars" against a background of dark neoplastic B-cells) [2]. * **Associations:** Strongly linked to **Epstein-Barr Virus (EBV)**, especially the endemic (African) variety involving the jaw. * **Immunophenotype:** CD19+, CD20+, CD10+, and BCL-6+. Crucially, it is **BCL-2 negative**. * **Proliferation Index:** Ki-67 index is typically near **100%**, reflecting the extremely rapid doubling time [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [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, p. 606. [3] 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.

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