Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 161: Kaposi sarcoma associated herpes virus causes all of the following, except?

A. Primary effusion lymphoma
B. Burkitt's lymphoma (Correct Answer)
C. Castleman disease
D. Kaposi sarcoma

Explanation: **Explanation:** The question tests your knowledge of **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi Sarcoma-associated Herpesvirus (KSHV), and its oncogenic associations [3]. **Why Burkitt’s Lymphoma is the correct answer:** Burkitt’s Lymphoma is strongly associated with **Epstein-Barr Virus (EBV)**, not HHV-8 [4]. In the endemic (African) form, EBV is found in nearly 100% of cases [3]. The hallmark genetic driver of Burkitt’s lymphoma is the **t(8;14)** translocation involving the *MYC* gene. **Analysis of incorrect options (HHV-8 associated conditions):** * **Kaposi Sarcoma:** HHV-8 is the primary causative agent for all four clinical subtypes (Classic, Endemic/African, Transplant-associated, and AIDS-associated) [1]. It infects endothelial cells, leading to characteristic spindle cell proliferation. * **Primary Effusion Lymphoma (PEL):** This is a rare B-cell lymphoma that presents as malignant effusions in body cavities (pleural, pericardial, peritoneal) without a discrete tumor mass [2]. It is **pathognomonic for HHV-8** infection, often occurring in HIV-positive patients [3]. * **Multicentric Castleman Disease (MCD):** HHV-8 infects B-cells in the mantle zones of lymph nodes, leading to this lymphoproliferative disorder. It is particularly common in the setting of HIV/AIDS. **High-Yield Clinical Pearls for NEET-PG:** * **HHV-8 Target:** It primarily infects vascular endothelial cells and B-lymphocytes. * **EBV vs. HHV-8:** While both are Gamma-herpesviruses, EBV is linked to Burkitt’s, Hodgkin’s, and Nasopharyngeal carcinoma; HHV-8 is strictly linked to Kaposi and specific B-cell lymphoproliferations [3]. * **LANA-1:** Latency-associated nuclear antigen (LANA) is a key immunohistochemical marker used to detect HHV-8 in tissue biopsies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [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. 604-605. [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. 219-220. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336.

Question 162: Which autosomal recessive condition presents as a cancer syndrome in children?

A. Neurofibromatosis
B. Ataxia-telangiectasia (Correct Answer)
C. Sturge-Weber syndrome
D. Tuberous sclerosis complex

Explanation: **Explanation:** The correct answer is **Ataxia-telangiectasia (AT)**. This condition is a classic example of a **DNA repair defect syndrome** inherited in an **autosomal recessive (AR)** pattern [1], [2]. **Why Ataxia-telangiectasia is correct:** AT is caused by a mutation in the **ATM gene** (located on chromosome 11q23), which encodes a protein kinase responsible for sensing double-stranded DNA breaks. When this "sensor" is defective, cells cannot repair DNA damage or initiate p53-mediated apoptosis, leading to genomic instability. Clinically, it presents in childhood with cerebellar ataxia, oculocutaneous telangiectasias, and immunodeficiency [1]. Most importantly, these children have a significantly increased risk of developing malignancies, particularly **leukemias and lymphomas**. **Why the other options are incorrect:** * **Neurofibromatosis (Type 1 & 2):** These are **Autosomal Dominant (AD)** conditions. NF1 is caused by mutations in the *NF1* gene (neurofibromin) on chromosome 17. * **Tuberous Sclerosis Complex (TSC):** This is an **Autosomal Dominant (AD)** neurocutaneous syndrome caused by mutations in *TSC1* (hamartin) or *TSC2* (tuberin). * **Sturge-Weber Syndrome:** This is a **sporadic** condition (not inherited) caused by a somatic mutation in the *GNAQ* gene. It is characterized by port-wine stains and leptomeningeal angiomas but is not primarily a cancer predisposition syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **DNA Repair Defects (AR):** Remember the triad of AR cancer syndromes: **Ataxia-telangiectasia, Xeroderma Pigmentosum, and Fanconi Anemia.** [2] * **Laboratory Marker:** Patients with AT often show **elevated Alpha-Fetoprotein (AFP)** levels, a key diagnostic clue. * **Radiosensitivity:** Because they cannot repair double-stranded breaks, AT patients are hypersensitive to ionizing radiation (X-rays/CT scans) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1300-1301. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323.

Question 163: Beta-naphthyl amine dyes predispose to which of the following cancers?

A. Urinary bladder carcinoma (Correct Answer)
B. Renal carcinoma
C. Hepatic carcinoma
D. Lung carcinoma

Explanation: **Explanation:** **Correct Answer: A. Urinary bladder carcinoma** The association between aromatic amines and bladder cancer is a classic example of chemical carcinogenesis [1]. **Beta-naphthylamine** (found in rubber, dye, and cigarette smoke) is a pro-carcinogen [2]. Once absorbed, it is detoxified in the liver via conjugation with glucuronic acid. However, when this conjugate reaches the urinary bladder, the enzyme **beta-glucuronidase** (produced by bladder mucosal cells or bacteria) hydrolyzes the bond, releasing the active, carcinogenic free naphthylamine. This metabolite causes DNA damage specifically in the urothelium, leading to **Transitional Cell Carcinoma (TCC)** of the bladder [1]. **Analysis of Incorrect Options:** * **B. Renal carcinoma:** While some chemicals like cadmium are linked to renal cell carcinoma, aromatic amines specifically target the lower urinary tract where the active metabolite is liberated. * **C. Hepatic carcinoma:** Although the liver metabolizes beta-naphthylamine, it does so by converting it into a non-toxic conjugated form. Therefore, the liver is protected from its carcinogenic effects, unlike the bladder. * **D. Lung carcinoma:** Lung cancer is primarily associated with polycyclic aromatic hydrocarbons (from tobacco), asbestos, and radon, rather than aniline dyes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Occupational Risk:** Classic history involves workers in the **rubber, dye, and leather industries** [1]. * **Latency:** There is a long latent period (often 15–40 years) between exposure and tumor development [2]. * **Other Bladder Carcinogens:** Schistosoma haematobium (Squamous cell carcinoma), Cyclophosphamide (Acrolein metabolite), and Phenacetin [2]. * **Screening:** Workers in high-risk industries are often screened using urine cytology to detect early malignant cells. **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. 217-218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 968-970.

Question 164: All of the following cancers commonly metastasize to the liver EXCEPT?

A. Breast
B. Prostate (Correct Answer)
C. Colon
D. Pancreas

Explanation: **Explanation:** The liver is the most common site for blood-borne metastasis due to its dual blood supply (portal vein and hepatic artery) and fenestrated endothelium. However, the pattern of spread depends heavily on the primary site's venous drainage. **Why Prostate is the correct answer:** Prostate cancer characteristically metastasizes to the **bone** (specifically the axial skeleton) via the **Batson venous plexus**, a valveless vertebral venous system [2]. When it spreads viscerally, it more commonly involves the lungs or pelvic lymph nodes [3]. While liver metastasis can occur in advanced, terminal stages, it is statistically rare compared to the other options provided [1]. **Analysis of Incorrect Options:** * **Colon:** The liver is the most common site of metastasis for colorectal cancer. This is because the venous drainage of the intestinal tract occurs via the **portal vein**, which leads directly to the liver. * **Pancreas:** Similar to the colon, the pancreas drains into the portal system. Liver metastasis is frequently present at the time of diagnosis in pancreatic adenocarcinoma. * **Breast:** Breast cancer spreads via the systemic circulation (hematogenous). The liver is one of the most frequent sites of distant metastasis for breast cancer, alongside the lungs, bones, and brain. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site of metastasis overall:** Lymph nodes. * **Most common organ for metastasis:** Liver (second only to lymph nodes). * **Most common primary causing liver metastasis:** Colon > Pancreas > Breast > Lung. * **Prostate Cancer Hallmark:** Characterized by **osteoblastic** (bone-forming) metastases, unlike most other cancers which are osteolytic [1], [2]. * **Batson Plexus:** Explains why prostate and thyroid cancers spread to the vertebrae without involving the lungs first. **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. 501-502. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 993-994. [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. 989-990.

Question 165: What is the most common carcinoma of the breast?

A. Ductal carcinoma (Correct Answer)
B. Colloid carcinoma
C. Lobular carcinoma
D. Sarcoma phylloides

Explanation: Explanation: Invasive Ductal Carcinoma (IDC), also known as "Invasive Carcinoma of No Special Type (NST)," is the most common histological subtype of breast cancer, accounting for approximately 70–80% of all cases [1]. It originates from the ductal epithelium and is characterized by its ability to incite a prominent fibrotic response (desmoplasia), which gives the tumor its classic "hard" or "scirrhous" consistency on palpation. Analysis of Options: * B. Colloid (Mucinous) Carcinoma: This is a rare subtype (approx. 2–3%) typically seen in elderly women. It is characterized by clusters of tumor cells floating in "pools of mucus" and generally carries a better prognosis than IDC. * C. Lobular Carcinoma: This is the second most common type (approx. 10–15%) [2]. It is unique for its "Indian file" pattern of cell arrangement and is frequently bilateral and multicentric due to the loss of E-cadherin expression [2]. * D. Sarcoma Phylloides: This is a fibroepithelial tumor, not a carcinoma. While it can be malignant, it arises from the intralobular stroma and is much rarer than epithelial ductal cancers. NEET-PG High-Yield Pearls: * Most common site: Upper Outer Quadrant (UOQ) of the breast. * Molecular Marker: Loss of E-cadherin is the hallmark of Lobular Carcinoma; it is present in Ductal Carcinoma. * Mammography: IDC often presents as a radiodense mass with "spiculated" margins. * Prognostic Factor: The most important prognostic factor for breast cancer is the axillary lymph node status, while the most important factor for long-term survival is the tumor stage at diagnosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1064. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 454-455.

Question 166: Which virus is implicated in Burkitt's lymphoma?

A. EBV (Correct Answer)
B. HTLV
C. HPV
D. HHV8

Explanation: **Explanation:** **Epstein-Barr Virus (EBV)** is the correct answer [1]. EBV is a gamma-herpesvirus that infects B cells via the **CD21 receptor** [3]. In Burkitt’s lymphoma, EBV acts as a potent mitogen. While the virus drives B-cell proliferation, the definitive oncogenic event is the **t(8;14) translocation**, which moves the **c-MYC** proto-oncogene next to the Ig heavy chain promoter, leading to constitutive expression of MYC and uncontrolled cell growth. EBV is found in nearly 100% of African (Endemic) Burkitt’s cases and about 15-20% of sporadic cases [2]. **Analysis of Incorrect Options:** * **HTLV-1 (Human T-cell Lymphotropic Virus):** Associated with **Adult T-cell Leukemia/Lymphoma (ATLL)**, characterized by flower cells and lytic bone lesions [1]. * **HPV (Human Papillomavirus):** High-risk types (16, 18) are linked to squamous cell carcinomas of the cervix, anus, and oropharynx via E6 and E7 oncoproteins [4]. * **HHV8 (Human Herpesvirus 8):** Also known as KSHV, it is the causative agent of **Kaposi Sarcoma** and Primary Effusion Lymphoma [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages against a background of neoplastic B cells). * **Genetics:** t(8;14) is most common; t(2;8) and t(22;8) are variants. * **Cytology:** Deeply basophilic cytoplasm with **lipid vacuoles**. * **EBV Association:** Also linked to Nasopharyngeal Carcinoma, Hodgkin Lymphoma (Mixed Cellularity), and Oral Hairy Leukoplakia [5]. **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. 219-220. [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. [5] 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. 220-221.

Question 167: The BRCA2 gene is associated with which type of carcinoma?

A. Breast (Correct Answer)
B. Lung
C. Liver
D. Gastric

Explanation: **Explanation:** **BRCA2 (Breast Cancer 2)** is a tumor suppressor gene located on **chromosome 13q12.3**. Its primary function is to encode a protein involved in the repair of double-stranded DNA breaks via **homologous recombination**. When this gene undergoes a germline mutation, the DNA repair mechanism is compromised, leading to genomic instability and a significantly increased risk of malignancies, most notably **Breast Carcinoma** [1]. * **Why Option A is Correct:** BRCA2 mutations are associated with a high lifetime risk of female breast cancer (approx. 45%) and are the most common cause of **hereditary male breast cancer**. * **Why Options B, C, and D are Incorrect:** While BRCA2 mutations increase the risk of several systemic cancers, they are not classically associated with primary Lung, Liver, or Gastric carcinomas. Lung cancer is primarily linked to smoking and EGFR/ALK mutations; Liver cancer to HBV/HCV and cirrhosis; and Gastric cancer to *H. pylori* and CDH1 mutations. **High-Yield Clinical Pearls for NEET-PG:** 1. **Chromosome Locations:** BRCA1 is on **17q21**, while BRCA2 is on **13q12**. (Mnemonic: BRCA**1** is on **17**, BRCA**2** is on **13**). 2. **Associated Malignancies:** Beyond breast cancer, BRCA2 is strongly linked to **Ovarian cancer** (though less than BRCA1), **Prostate cancer** (aggressive forms), and **Pancreatic cancer** [1]. 3. **Fanconi Anemia:** Biallelic mutations in BRCA2 (FANCD1) result in a subtype of Fanconi Anemia. 4. **Treatment:** Tumors with BRCA mutations are particularly sensitive to **PARP inhibitors** (e.g., Olaparib) due to the concept of synthetic lethality. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1059.

Question 168: What is the term for a benign tumor of voluntary muscle?

A. Leiomyoma
B. Rhabdomyoma (Correct Answer)
C. Rhabdomyosarcoma
D. Leiomyosarcoma

Explanation: ### Explanation **Correct Answer: B. Rhabdomyoma** **1. Why Rhabdomyoma is correct:** In pathology nomenclature, the prefix **"Rhabdo-"** refers to striated muscle (skeletal or voluntary muscle), and the suffix **"-oma"** denotes a benign tumor [3]. Therefore, a **Rhabdomyoma** is a benign neoplasm arising from voluntary (skeletal) muscle fibers. While rare in adults, cardiac rhabdomyomas are the most common primary cardiac tumors in children and are strongly associated with Tuberous Sclerosis [1]. **2. Why the other options are incorrect:** * **A. Leiomyoma:** The prefix **"Leio-"** refers to smooth (involuntary) muscle [3]. Leiomyomas are benign tumors most commonly found in the uterus (fibroids), gastrointestinal tract, and skin (pilar leiomyoma). * **C. Rhabdomyosarcoma:** The suffix **"-sarcoma"** indicates a malignant tumor of mesenchymal origin [3]. Rhabdomyosarcoma is the malignant counterpart of rhabdomyoma and is the most common soft tissue sarcoma in children (specifically the embryonal subtype) [2]. * **D. Leiomyosarcoma:** This is the malignant tumor of smooth muscle. It is commonly found in the retroperitoneum, uterus, and large blood vessels. **3. NEET-PG High-Yield Pearls:** * **Cardiac Rhabdomyoma:** Often presents as "spider cells" (cells with central nuclei and radiating cytoplasmic processes) on histology. * **Rhabdomyosarcoma Marker:** **Desmin** and **Myogenin (MyoD1)** are the most specific immunohistochemical (IHC) markers used for diagnosis [2]. * **Sarcoma Botryoides:** A variant of embryonal rhabdomyosarcoma that presents as a "grape-like" mass protruding from the vagina in young girls (under age 5) [2]. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225. [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. 208-209.

Question 169: Which of the following is NOT a feature of dyskeratosis?

A. Premalignant leukoplakia
B. Atrophy and telangiectasia
C. Hypopigmented macules
D. Most common congenital syndrome involving nails (Correct Answer)

Explanation: This question tests the distinction between the **histopathological process** of dyskeratosis and the **clinical syndrome** known as Dyskeratosis Congenita. ### **Understanding the Concept** **Dyskeratosis** is a histopathological term referring to premature or abnormal keratinization of individual cells below the stratum granulosum. However, the question refers to **Dyskeratosis Congenita (DKC)**, a rare progressive multisystem telomere biology disorder. ### **Why Option D is the Correct Answer?** While Dyskeratosis Congenita is characterized by a classic clinical triad, it is **not** the most common congenital syndrome involving nails. That distinction typically belongs to **Pachyonychia Congenita** or simple **hereditary nail dysplasia**. In DKC, nail dystrophy is a major feature, but the syndrome itself is extremely rare (estimated 1 in 1 million). ### **Analysis of Other Options (Features of DKC)** * **Option A (Premalignant leukoplakia):** This is part of the classic clinical triad of DKC. Oral leukoplakia in these patients has a high rate of malignant transformation into Squamous Cell Carcinoma. * **Option B & C (Atrophy, telangiectasia, and hypopigmented macules):** These describe the **"poikilodermatous" skin pigmentation** (another part of the triad). Patients develop a reticular pattern of hyper/hypopigmentation, skin atrophy, and telangiectasia, usually on the neck and chest. ### **Clinical Pearls for NEET-PG** * **Classic Triad of Dyskeratosis Congenita:** 1. Abnormal skin pigmentation, 2. Nail dystrophy, 3. Oral leukoplakia. * **Pathophysiology:** Mutations in genes maintaining telomeres (e.g., *DKC1* encoding dyskerin, *TERC*, *TERT*). * **Major Complication:** Bone marrow failure (the leading cause of mortality) and increased risk of malignancy (SCC and AML). * **Histology Tip:** In general pathology, "Dyskeratotic cells" are seen in conditions like Squamous Cell Carcinoma, Bowen’s disease, and Darier’s disease (corps ronds and grains).

Question 170: Sarcoma of the soft tissues spreads by which of the following routes?

A. Blood vessels (Correct Answer)
B. Lymphatics
C. Direct invasion
D. Local infiltration

Explanation: **Explanation:** **1. Why Blood Vessels (Hematogenous Spread) is Correct:** The primary mode of metastasis for **sarcomas** (malignant tumors of mesenchymal origin) is the hematogenous route [1]. This occurs because sarcomas are typically highly vascularized and lack a well-developed lymphatic drainage system within the tumor stroma. Consequently, malignant cells invade thin-walled veins and capillaries, commonly leading to secondary deposits in the **lungs** (the most frequent site of distant metastasis for most sarcomas) [1]. **2. Analysis of Incorrect Options:** * **Lymphatics:** This is the characteristic route for **carcinomas** (malignant tumors of epithelial origin) [1]. While most sarcomas avoid lymphatics, there are notable exceptions (see Clinical Pearls). * **Direct Invasion & Local Infiltration:** While sarcomas are locally aggressive and infiltrate surrounding tissues (muscles, fascia), these terms describe **local growth patterns** rather than the primary route of distant metastasis. In the context of "spread" in oncology exams, the question usually refers to the mode of systemic dissemination. **3. Clinical Pearls for NEET-PG:** * **The "Rule of Exceptions":** While sarcomas spread via blood, remember the mnemonic **SCARE** for sarcomas that frequently spread via **lymphatics**: * **S**ynovial sarcoma * **C**lear cell sarcoma * **A**ngiosarcoma * **R**habdomyosarcoma * **E**pithelioid sarcoma * **Carcinoma Exception:** Conversely, Renal Cell Carcinoma (RCC), Hepatocellular Carcinoma (HCC), Follicular Carcinoma of Thyroid, and Choriocarcinoma prefer **hematogenous spread** over lymphatics [1]. * **First Site:** For most sarcomas, the first evidence of hematogenous spread is seen on a Chest X-ray or CT as "cannon-ball" pulmonary nodules [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 282.

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Neoplasia — MCQs

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