Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 131: Which of the following conditions is associated with increased VMA?

A. Rhabdomyosarcoma
B. Pheochromocytoma (Correct Answer)
C. Nephroblastoma
D. Renal Cell Carcinoma (RCC)

Explanation: **Explanation:** **Pheochromocytoma** is a catecholamine-secreting tumor derived from chromaffin cells of the adrenal medulla. These tumors overproduce epinephrine and norepinephrine. In the body, catecholamines are metabolized by enzymes (MAO and COMT) into intermediate metabolites like metanephrines and finally into **Vanillylmandelic Acid (VMA)**. Because VMA is the stable end-product excreted in the urine, elevated 24-hour urinary VMA levels serve as a classic diagnostic marker for Pheochromocytoma [2]. **Analysis of Incorrect Options:** * **A. Rhabdomyosarcoma:** This is a malignant tumor of skeletal muscle origin [3]. It is associated with markers like Desmin and Myogenin, not catecholamine metabolites. * **C. Nephroblastoma (Wilms Tumor):** This is a common pediatric renal tumor derived from primitive blastema [3]. While it presents as an abdominal mass, it does not secrete catecholamines. * **D. Renal Cell Carcinoma (RCC):** This arises from renal tubular epithelium [1]. Common markers include CD10 and RCC antigen. It may cause paraneoplastic syndromes (like polycythemia due to EPO), but not increased VMA. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** Pheochromocytoma is 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), and 10% familial. * **Associated Syndromes:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL), and NF-1 [1]. * **Diagnosis:** While VMA is a classic exam answer, **plasma free metanephrines** are now considered the most sensitive screening test. * **Neuroblastoma:** It is important to remember that VMA is also elevated in Neuroblastoma (the most common extracranial solid tumor in children) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 419-420. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 483-484.

Question 132: All of the following constitute familial cancer syndromes except?

A. Xeroderma pigmentosum (Correct Answer)
B. Retinoblastoma
C. Neurofibromatosis
D. MEN-I

Explanation: To understand this question, it is essential to distinguish between the three categories of inherited predisposition to cancer: **Autosomal Dominant Cancer Syndromes**, **Autosomal Recessive Syndromes of Defective DNA Repair**, and **Familial Cancers** (uncertain inheritance) [3]. ### 1. Why Xeroderma Pigmentosum (XP) is the Correct Answer **Xeroderma pigmentosum** is classified as an **Autosomal Recessive Syndrome of Defective DNA Repair** [1]. While it is a hereditary condition that leads to cancer, it is technically distinct from the "Familial Cancer Syndromes" (which are typically Autosomal Dominant). In XP, there is a mutation in the nucleotide excision repair (NER) genes, making the skin hypersensitive to UV radiation, leading to early-onset squamous and basal cell carcinomas [1], [2]. ### 2. Analysis of Incorrect Options * **Retinoblastoma (RB):** This is the prototype of **Autosomal Dominant Cancer Syndromes**. It involves a germline mutation in the *RB1* tumor suppressor gene (Knudson’s Two-Hit Hypothesis) [3]. * **Neurofibromatosis (NF):** Both NF1 and NF2 are **Autosomal Dominant** syndromes [3]. NF1 involves mutations in the *neurofibromin* gene, leading to neurofibromas and optic gliomas. * **MEN-I (Multiple Endocrine Neoplasia Type I):** This is an **Autosomal Dominant** syndrome characterized by tumors of the "3 Ps": Parathyroid, Pancreas, and Pituitary [3]. ### 3. NEET-PG High-Yield Pearls * **Autosomal Dominant Syndromes:** Usually involve a single "hit" to a tumor suppressor gene (e.g., *RB, TP53, APC, BRCA1/2*) [3]. * **Autosomal Recessive Syndromes:** Usually involve defects in **DNA repair mechanisms**. Examples include Xeroderma pigmentosum, Ataxia-telangiectasia, Bloom syndrome, and Fanconi anemia [1]. * **Key Distinction:** In exams, if "Familial Cancer Syndrome" is used in a restrictive sense, it refers to the dominant inheritance patterns. XP is always the "odd one out" because of its recessive inheritance and specific DNA repair defect [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 332-333. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300.

Question 133: Which histological subtype of breast carcinoma has the best prognosis?

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

Explanation: **Explanation:** The prognosis of breast carcinoma is determined by its histological subtype, grade, and molecular profile [1]. **Tubular carcinoma** is associated with the most favorable prognosis among all invasive breast cancers, with a 10-year survival rate exceeding 95%. **1. Why Tubular Carcinoma is Correct:** Tubular carcinoma is a well-differentiated invasive ductal carcinoma characterized by the formation of small, regular, oval-to-pointed tubules lined by a single layer of epithelium [1]. It typically lacks a myoepithelial layer. These tumors are usually small (<1 cm), estrogen receptor (ER) and progesterone receptor (PR) positive, and HER2/neu negative. Their slow growth and low incidence of axillary lymph node metastasis contribute to their excellent prognosis [2]. **2. Analysis of Incorrect Options:** * **Colloid (Mucinous) Carcinoma:** Also carries a favorable prognosis, characterized by "islands of tumor cells floating in lakes of mucin" [1, 2]. However, its prognosis is slightly less favorable than the tubular subtype. * **Medullary Carcinoma:** Known for having a better prognosis than standard Invasive Carcinoma of No Special Type (NST) despite being high-grade (triple-negative) [2]. It is associated with BRCA1 mutations and dense lymphocytic infiltrates [1], but it does not surpass tubular carcinoma in survival outcomes. * **Lobular Carcinoma:** While often slow-growing, it is frequently multifocal and bilateral. Its long-term prognosis is generally comparable to or slightly worse than invasive ductal carcinoma (NST) [2]. **High-Yield NEET-PG Pearls:** * **Best Prognosis:** Tubular Carcinoma. * **Worst Prognosis:** Inflammatory Breast Carcinoma (due to dermal lymphatic invasion). * **Most Common Subtype:** Invasive Carcinoma of No Special Type (formerly Invasive Ductal Carcinoma). * **Tubular Carcinoma Rule:** To be classified as "tubular," >90% of the tumor must show tubular morphology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1064-1070. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 457-458.

Question 134: Which of the following is HMB45 negative?

A. Melanoma
B. Angiomyolipoma
C. Tendon clear cell sarcoma
D. Juxtaglomerular tumor (Correct Answer)

Explanation: **Explanation:** The question tests your knowledge of **HMB-45 (Human Melanoma Black-45)**, a monoclonal antibody that reacts against **gp100**, a glycoprotein found in premelanosomes. While primarily a marker for melanocytic tumors, it is also expressed in a specific family of tumors known as **PEComas** (Perivascular Epithelioid Cell tumors). **Why Juxtaglomerular Tumor is the Correct Answer:** A **Juxtaglomerular tumor (Reninoma)** is a rare benign tumor of the kidney arising from the juxtaglomerular cells. These cells are modified smooth muscle cells of the afferent arteriole. On immunohistochemistry (IHC), they are positive for **Renin, Vimentin, and CD117**, but they are **HMB-45 negative**. **Analysis of Incorrect Options:** * **Melanoma:** HMB-45 is highly specific for melanocytic differentiation. It is positive in the vast majority of malignant melanomas (except desmoplastic variants). * **Angiomyolipoma (AML):** This is the most common member of the **PEComa family**. Despite being a mesenchymal tumor (composed of blood vessels, smooth muscle, and fat), the "epithelioid" smooth muscle cells characteristically express melanocytic markers like **HMB-45 and Melan-A** [1]. * **Tendon Clear Cell Sarcoma:** Often referred to as "Melanoma of Soft Parts," this tumor harbor the **t(12;22)** translocation. It consistently expresses **HMB-45 and S100**, mimicking the IHC profile of melanoma. **High-Yield Clinical Pearls for NEET-PG:** * **PEComa Family:** Includes Angiomyolipoma (kidney), Lymphangiomyomatosis (lung), and Clear cell "sugar" tumor (lung). All are typically **HMB-45 positive** [1]. * **HMB-45 vs. S100:** HMB-45 is more specific for melanoma but less sensitive than S100. * **Juxtaglomerular Tumor Triad:** Hypertension, Hypokalemia, and High plasma renin activity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 957-958.

Question 135: Which tumor arises from the organ of Zuckerkandl?

A. Paraganglioma (Correct Answer)
B. Schwannoma
C. Astrocytoma
D. Medulloblastoma

Explanation: **Explanation:** **Correct Answer: A. Paraganglioma** The **Organ of Zuckerkandl** is a collection of extra-adrenal chromaffin tissue derived from the neural crest [1]. It is typically located at the origin of the inferior mesenteric artery or near the aortic bifurcation [1]. A tumor arising from these extra-adrenal chromaffin cells is termed a **Paraganglioma** [1]. While histologically identical to a Pheochromocytoma (which arises from the adrenal medulla), the term Paraganglioma is specifically used for extra-adrenal sites [1]. The Organ of Zuckerkandl is the most common site for extra-adrenal paragangliomas [1]. **Why other options are incorrect:** * **B. Schwannoma:** These are benign nerve sheath tumors arising from Schwann cells, not chromaffin tissue. * **C. Astrocytoma:** These are primary central nervous system (CNS) tumors arising from astrocytes (glial cells). * **D. Medulloblastoma:** This is a highly malignant primitive neuroectodermal tumor (PNET) located in the cerebellum (posterior fossa) of children [2]. **NEET-PG High-Yield Pearls:** * **Rule of 10s for Pheochromocytoma:** 10% are extra-adrenal (Paragangliomas), 10% are bilateral, 10% are malignant, and 10% occur in children. * **Zuckerkandl Clinical Presentation:** Like pheochromocytomas, these can secrete catecholamines, leading to the classic triad of episodic headache, sweating, and palpitations (hypertension) [1]. * **Staining:** Paragangliomas are positive for **Chromogranin** and **Synaptophysin**. The characteristic histological pattern is the **"Zellballen" appearance** (nests of cells surrounded by vascular stroma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 748-749. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 483-484.

Question 136: All of the following are tumor suppressor genes except?

A. NF1
B. pRb
C. SMAD1 (Correct Answer)
D. p53

Explanation: ### Explanation The correct answer is **SMAD1**. **1. Why SMAD1 is the correct answer:** Tumor Suppressor Genes (TSGs) act as "brakes" on cell proliferation [1]. While several members of the SMAD family (specifically **SMAD2** and **SMAD4**) function as tumor suppressors within the TGF-β signaling pathway, **SMAD1** is primarily involved in the Bone Morphogenetic Protein (BMP) signaling pathway. SMAD1 typically promotes cell growth, differentiation, and development rather than acting as a traditional tumor suppressor. In many cancers, SMAD1 is actually associated with promoting epithelial-mesenchymal transition (EMT) and metastasis. **2. Analysis of Incorrect Options:** * **NF1 (Neurofibromin 1):** A classic TSG located on chromosome 17q. It acts as a GTPase-activating protein (GAP) that negatively regulates the **RAS** signaling pathway. Mutations lead to Neurofibromatosis Type 1. * **pRb (Retinoblastoma Protein):** Known as the "Governor of the Cell Cycle," pRb (encoded by the *RB1* gene on chromosome 13q) prevents cells from entering the S-phase by sequestering the E2F transcription factor [2]. It was the first TSG discovered [3]. * **p53:** Known as the "Guardian of the Genome," p53 (encoded by *TP53* on chromosome 17p) triggers cell cycle arrest, DNA repair, or apoptosis in response to DNA damage [2], [4]. It is the most commonly mutated gene in human cancers [2]. **3. NEET-PG High-Yield Pearls:** * **SMAD4** is also known as **DPC4** (Deleted in Pancreatic Cancer) and is a high-yield marker for pancreatic adenocarcinoma. * **Two-Hit Hypothesis:** Most TSGs require both alleles to be inactivated to promote oncogenesis (Knudson’s hypothesis), whereas oncogenes require only a single "gain-of-function" mutation [1], [4]. * **Li-Fraumeni Syndrome:** Germline mutation of *TP53* leading to multiple early-onset cancers (SBLA: Sarcoma, Breast, Leukemia, Adrenal). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 301-302. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300. [4] 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.

Question 137: Which of the following is associated with primary hepatic malignancy?

A. Cadmium
B. Vinyl chloride (Correct Answer)
C. Chromium compounds
D. Asbestos

Explanation: **Explanation:** The correct answer is **Vinyl chloride**. This association is a classic high-yield topic in oncology and occupational pathology. **1. Why Vinyl Chloride is Correct:** Vinyl chloride monomer (used in the plastics industry to produce PVC) is a potent chemical carcinogen [1]. Chronic exposure is specifically linked to **Hepatic Angiosarcoma**, a rare and aggressive primary malignancy of the liver's vascular endothelium [2]. It can also lead to hepatocellular carcinoma (HCC). The mechanism involves the formation of reactive metabolites (chloroethylene oxide) that bind to DNA, causing mutations. **2. Analysis of Incorrect Options:** * **A. Cadmium:** Primarily associated with **Prostate cancer** and **Lung cancer**. It is also a significant cause of obstructive lung disease and renal tubular damage (Itai-itai disease). * **C. Chromium compounds:** Hexavalent chromium (found in electroplating and pigments) is a well-known risk factor for **Bronchogenic carcinoma** and perforation of the nasal septum. * **D. Asbestos:** Strongly associated with **Mesothelioma** (pleural and peritoneal) and **Bronchogenic carcinoma** [1]. It does not have a primary association with hepatic malignancy. **3. NEET-PG Clinical Pearls:** * **Angiosarcoma of the Liver:** Associated with **Vinyl chloride**, **Thorotrast** (radioactive contrast) [2], and **Arsenic** [1]. * **Aflatoxin B1:** Produced by *Aspergillus flavus*; it is the most common dietary risk factor for **Hepatocellular Carcinoma (HCC)** [3], often causing a mutation in the **p53 gene (codon 249)** [4]. * **Arsenic:** Unique for causing a "triad" of cancers: **Skin** (Squamous cell carcinoma), **Lung**, and **Liver** (Angiosarcoma) [1]. * **Benzene:** Associated with **Acute Myeloid Leukemia (AML)** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 286. [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. 216-217. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 876-877. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 331-332.

Question 138: Which chromosome is associated with retinoblastoma?

A. 13 (Correct Answer)
B. 11
C. 17
D. 15

Explanation: **Explanation:** **Retinoblastoma** is the most common intraocular tumor of childhood. It is caused by a mutation or deletion in the **RB1 gene**, which is located on **Chromosome 13q14** [1], [2]. 1. **Why Option A is correct:** The RB1 gene is a classic **tumor suppressor gene**. According to **Knudson’s "Two-Hit" Hypothesis**, both alleles of the RB1 gene must be inactivated for the tumor to develop [1]. In familial cases, the first "hit" is inherited (germline), and the second occurs somatically [2]. In sporadic cases, both "hits" occur somatically in the same retinal cell. The RB protein (pRB) regulates the **G1 to S phase transition** of the cell cycle by binding to the E2F transcription factor [1]. 2. **Why other options are incorrect:** * **Option B (11):** Associated with the **WT1 gene** (Wilms tumor) and the **PAX6 gene** (Aniridia). * **Option C (17):** Associated with the **TP53 gene** (Li-Fraumeni syndrome) and **NF1** (Neurofibromatosis type 1) [2]. * **Option D (15):** Associated with **Prader-Willi** and **Angelman syndromes** (15q11-q13). **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** The most common sign is **Leukocoria** (white pupillary reflex). * **Histopathology:** Characterized by **Flexner-Wintersteiner rosettes** (highly specific) and Homer Wright rosettes. * **Trilateral Retinoblastoma:** Bilateral retinoblastoma associated with a pineal tumor (Pineoblastoma). * **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, p. 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.

Question 139: Familial tendency is not seen in which of the following malignancies?

A. Sarcomas
B. Stomach carcinoma
C. Colon carcinoma
D. Laryngeal carcinoma (Correct Answer)

Explanation: **Explanation:** The correct answer is **Laryngeal carcinoma (Option D)**. This malignancy is primarily associated with environmental and lifestyle factors rather than a genetic or familial predisposition [1]. The strongest risk factors are chronic tobacco smoking and excessive alcohol consumption, which act synergistically [1]. While some head and neck cancers are linked to HPV, laryngeal cancer lacks a defined hereditary syndrome or familial clustering pattern. **Why other options are incorrect:** * **Sarcomas (Option A):** Many sarcomas exhibit a strong familial tendency. For example, **Li-Fraumeni Syndrome** (germline mutation of the *TP53* gene) predisposes individuals to soft tissue and osteosarcomas [3]. Additionally, Retinoblastoma survivors have a high risk of developing osteosarcoma later in life. * **Stomach Carcinoma (Option B):** Approximately 1–3% of gastric cancers are familial [3]. **Hereditary Diffuse Gastric Cancer (HDGC)**, caused by mutations in the *CDH1* gene (encoding E-cadherin), is a well-known autosomal dominant condition [2]. * **Colon Carcinoma (Option C):** This is one of the most common cancers with a familial link [3]. Examples include **FAP (Familial Adenomatous Polyposis)** due to *APC* gene mutations and **Lynch Syndrome (HNPCC)** due to mutations in DNA mismatch repair genes (*MLH1, MSH2*). **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** Remember the "SBLA" mnemonic (Sarcoma, Breast, Leukemia, Adrenal gland) for cancers associated with *TP53* mutations. * **E-cadherin (CDH1):** Loss of this protein leads to the "signet ring cell" morphology in hereditary diffuse gastric cancer. * **Laryngeal Cancer:** The most common site is the glottis (vocal cords), and the most common histological type is Squamous Cell Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 746-747. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 778-779. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 287-288.

Question 140: What is the most common sarcoma in a person receiving immunosuppressive treatment?

A. Kaposi's sarcoma (Correct Answer)
B. Lymphoma sarcoma
C. Osteosarcoma
D. Angiosarcoma

Explanation: **Explanation:** **1. Why Kaposi’s Sarcoma (KS) is correct:** Kaposi’s sarcoma is a vascular neoplasm caused by **Human Herpesvirus-8 (HHV-8)**. It is the most common malignancy associated with immunosuppression, particularly in patients with HIV/AIDS (AIDS-defining illness) and those receiving **post-transplant immunosuppressive therapy** [1]. In transplant recipients, the risk of KS is increased up to 500-fold compared to the general population. The mechanism involves the reactivation of latent HHV-8 due to the loss of T-cell mediated surveillance, leading to the proliferation of spindle cells and neoangiogenesis [1]. **2. Why the other options are incorrect:** * **Lymphoma sarcoma:** While Non-Hodgkin Lymphomas (especially DLBCL and Burkitt lymphoma) are highly prevalent in immunosuppressed patients, they are classified as **hematological malignancies**, not sarcomas [1]. * **Osteosarcoma:** This is the most common primary malignant bone tumor in children and adolescents, but its incidence is not specifically linked to immunosuppressive treatment. * **Angiosarcoma:** Although KS is a type of vascular sarcoma, "Angiosarcoma" typically refers to high-grade malignant tumors of endothelial cells (often associated with chronic lymphedema or radiation) [3]. It is much rarer than KS in the context of immunosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Characterized by "slit-like" vascular spaces containing extravasated RBCs and spindle-shaped cells [2]. * **Transplant-associated KS:** Often regresses if immunosuppressive doses are reduced or switched to **Sirolimus (mTOR inhibitors)**, which has anti-neoplastic properties. * **Most common site:** Skin (purple/red plaques or nodules), but can involve the GI tract and lungs [2]. * **Other HHV-8 associations:** Primary Effusion Lymphoma and Multicentric Castleman Disease. **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 Infancy and Childhood, pp. 526-527. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 527-528.

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