Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 381: Which of the following statements about p53 is false?

A. It encodes a 53 kDa protein.
B. It is located on chromosome 17.
C. It arrests the cell cycle at the G1 phase.
D. Wild type p53 is associated with childhood tumors. (Correct Answer)

Explanation: **Explanation:** The p53 protein, often called the "Guardian of the Genome," is a tumor suppressor gene that plays a critical role in maintaining genomic stability [1]. **Why Option D is the Correct (False) Statement:** Wild-type p53 is the **normal, functional form** of the protein. It acts as a tumor suppressor by inducing cell cycle arrest, DNA repair, or apoptosis [2]. Therefore, it prevents tumor formation. It is the **mutated** p53 (loss of function) that is associated with various cancers, including Li-Fraumeni syndrome. While p53 mutations are common in adult epithelial cancers, they are less frequently the primary driver in common childhood tumors (like Wilms tumor or Retinoblastoma), which often involve other specific genes (WT1, RB1) [1]. **Analysis of Incorrect Options:** * **Option A:** p53 is named after its molecular weight; it encodes a protein that weighs **53 kiloDaltons (kDa)**. * **Option B:** The TP53 gene is located on the short arm of **chromosome 17 (17p13.1)** [1]. Deletions of this region are common in many malignancies. * **Option C:** Upon sensing DNA damage, p53 upregulates **p21** (a CDK inhibitor), which inhibits Cyclin E-CDK2 complexes, effectively **arresting the cell cycle at the G1 phase** to allow for DNA repair [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in TP53 leading to a 25-fold increased risk of developing multiple tumors (SBLA: Sarcoma, Breast, Leukemia, Adrenal gland) by age 50. * **Mechanism:** p53 induces **BAX** (pro-apoptotic) and inhibits **BCL-2** (anti-apoptotic) if DNA repair fails. * **Degradation:** In normal cells, p53 levels are kept low by **MDM2**, which facilitates its degradation via the ubiquitin-proteasome pathway. * **Most Common Mutation:** TP53 is the most frequently mutated gene in human cancer (>50% of all cases) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 226-228. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303.

Question 382: Carcinoembryonic antigen (CEA) is elevated in all of the following conditions except:

A. Lung cancer
B. Breast cancer
C. Colon cancer
D. Osteogenic sarcoma (Correct Answer)

Explanation: **Explanation:** Carcinoembryonic antigen (CEA) is a high-molecular-weight oncofetal glycoprotein. It is normally produced during fetal development in the gastrointestinal tract, but its expression is suppressed after birth. In adults, elevated levels are primarily associated with **adenocarcinomas** arising from endodermal tissues. **Why Osteogenic Sarcoma is the correct answer:** CEA is a marker for epithelial tumors (carcinomas). **Osteogenic sarcoma** is a primary malignant tumor of the bone derived from mesenchymal cells [1], [2]. Mesenchymal tumors do not express CEA; instead, they often express markers like Alkaline Phosphatase (ALP). Therefore, CEA levels remain normal in bone sarcomas. **Analysis of incorrect options:** * **Colon Cancer:** CEA is the classic tumor marker for colorectal carcinoma. While not used for primary screening due to low specificity, it is the "gold standard" for monitoring recurrence and response to therapy. * **Lung Cancer:** CEA is frequently elevated in non-small cell lung cancer (NSCLC), particularly **adenocarcinoma** of the lung. * **Breast Cancer:** CEA, along with CA 15-3, is often elevated in advanced or metastatic breast cancer and is used to monitor treatment efficacy. **NEET-PG High-Yield Pearls:** * **Oncofetal Antigens:** These include CEA and Alpha-fetoprotein (AFP). * **CEA Non-specificity:** Elevated CEA is not pathognomonic for cancer; it can be raised in benign conditions like **heavy smoking**, alcoholic cirrhosis, pancreatitis, and ulcerative colitis. * **Clinical Use:** The primary role of CEA is **post-operative surveillance** to detect early recurrence of colorectal cancer. * **Other markers:** Remember **CA-125** (Ovarian cancer), **CA 19-9** (Pancreatic cancer), and **PSA** (Prostate cancer). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-674. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1198-1205.

Question 383: Which of the following is NOT a recognized tumor marker?

A. Beta HCG
B. Beta 2 microglobulin
C. Alpha fetoprotein
D. None of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **None of the above** because all three listed substances (Beta-HCG, Beta-2 microglobulin, and Alpha-fetoprotein) are well-established tumor markers used in clinical oncology for diagnosis, monitoring, and prognosis. [3] **Analysis of Options:** * **Beta-HCG (Human Chorionic Gonadotropin):** This is a glycoprotein hormone normally produced by syncytiotrophoblasts. [2] It is a highly sensitive marker for **Gestational Trophoblastic Disease (Hydatidiform mole/Choriocarcinoma)** and certain **Germ Cell Tumors**, specifically non-seminomatous germ cell tumors of the testis and dysgerminomas. [1] [4] * **Beta-2 Microglobulin:** This is a component of the MHC Class I molecule found on the surface of nucleated cells. It serves as a crucial prognostic marker for hematological malignancies, most notably **Multiple Myeloma** and certain **B-cell Lymphomas**. Elevated levels correlate with a higher tumor burden and renal dysfunction. * **Alpha-fetoprotein (AFP):** This is a plasma protein produced by the fetal yolk sac and liver. In adults, pathologically elevated levels are classic markers for **Hepatocellular Carcinoma (HCC)** and **Yolk Sac Tumors** (Endodermal sinus tumors) of the ovary or testes. [3] **High-Yield Clinical Pearls for NEET-PG:** * **AFP + Beta-HCG:** Used together to classify and monitor testicular germ cell tumors. * **Calcitonin:** Highly specific marker for Medullary Carcinoma of the Thyroid. * **CA-125:** Primary marker for monitoring epithelial ovarian cancer. * **PSA (Prostate Specific Antigen):** Used for screening and monitoring adenocarcinoma of the prostate, though it is organ-specific, not cancer-specific. * **CEA (Carcinoembryonic Antigen):** Primarily used for monitoring recurrence in Colorectal Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1035-1036. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 512-513. [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. 254-255. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982.

Question 384: Human papillomavirus (HPV) is etiologically associated with which of the following carcinomas?

A. Carcinoma of the cervix (Correct Answer)
B. Gastric carcinoma
C. Maxillary carcinoma
D. Colon carcinoma

Explanation: **Explanation:** **1. Why Option A is Correct:** Human Papillomavirus (HPV), particularly high-risk strains **16 and 18**, is the primary causative agent for **Cervical Carcinoma** [1]. The oncogenic potential of HPV lies in its viral proteins: * **E6:** Binds to and facilitates the degradation of the **p53** tumor suppressor protein [2]. * **E7:** Binds to the **RB (Retinoblastoma)** protein, displacing E2F transcription factors and promoting uncontrolled cell cycle progression from G1 to S phase [2], [3]. This molecular synergy leads to genomic instability and malignant transformation of the cervical transformation zone [3]. **2. Why Other Options are Incorrect:** * **B. Gastric Carcinoma:** Primarily associated with *Helicobacter pylori* infection and dietary factors (nitrosamines). * **C. Maxillary Carcinoma:** Usually linked to occupational exposures (wood dust, nickel) or chronic sinusitis; it is not typically associated with HPV. * **D. Colon Carcinoma:** Arises via the APC/β-catenin pathway or Microsatellite Instability (MSI) pathway; it has no established link to HPV. **3. High-Yield Clinical Pearls for NEET-PG:** * **HPV 6 & 11:** Low-risk types; cause Genital Warts (Condyloma acuminatum) and Laryngeal Papillomas [1], [4]. * **Other HPV-associated cancers:** Anal, Vulvar, Vaginal, Penile, and Oropharyngeal (especially tonsillar) carcinomas [3]. * **Koilocytes:** The hallmark cytological finding of HPV infection (shrunken "raisin-like" nucleus with a large perinuclear halo) [4]. * **Vaccination:** The quadrivalent vaccine (Gardasil) targets types 6, 11, 16, and 18 [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 219-220. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 334-335. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1006-1007. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 466-467.

Question 385: Which of the following is an example of a tumor suppressor gene?

A. myc
B. fos
C. ras
D. RB (Correct Answer)

Explanation: **Explanation:** The correct answer is **RB (Retinoblastoma gene)**. **1. Why RB is the correct answer:** The **RB gene**, located on chromosome **13q14** [2], is the "governor" of the cell cycle and the first tumor suppressor gene (TSG) discovered. It acts as a negative regulator of the cell cycle by controlling the **G1 to S phase transition** [1]. In its hypophosphorylated (active) state, RB binds to the **E2F transcription factor**, preventing the cell from entering the S-phase [1]. Loss of both alleles (Knudson’s "Two-Hit" Hypothesis) leads to uncontrolled cell proliferation, resulting in tumors like Retinoblastoma and Osteosarcoma [2]. **2. Why other options are incorrect:** * **A (myc):** This is a **proto-oncogene** that encodes a nuclear transcription factor. *c-myc* is associated with Burkitt Lymphoma, while *n-myc* is linked to Neuroblastoma. * **B (fos):** This is a **proto-oncogene** (specifically an early response gene) that forms the AP-1 transcription factor complex, promoting cell growth. * **C (ras):** This is the most common **proto-oncogene** mutated in human cancers. It encodes a GTP-binding protein involved in signal transduction. Mutations in *K-ras* are frequently seen in pancreatic and colon cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Guardian of the Genome:** p53 (most commonly mutated gene in cancer) [1]. * **Governor of the Cell Cycle:** RB gene [1]. * **Two-Hit Hypothesis:** Proposed by Knudson specifically for the RB gene [2]. * **Quiescence vs. Senescence:** RB-mediated G1 arrest can lead to temporary (quiescence) or permanent (senescence) exit from the cell cycle [1]. * **HPV Connection:** The E7 protein of High-risk Human Papillomavirus (HPV 16, 18) binds and inactivates the RB protein, leading to cervical cancer [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 301-302. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300.

Question 386: The tumor suppressor gene P53 induces cell arrest at which phase?

A. G2-M phase
B. S-G2 phase
C. G1-S phase (Correct Answer)
D. G0 phase

Explanation: **Explanation:** The **TP53 gene**, located on chromosome 17p13.1, is known as the "Guardian of the Genome" [1]. Its primary function is to monitor DNA integrity. When DNA damage is detected, the p53 protein levels rise and trigger the transcription of **p21** (a Cyclin-Dependent Kinase Inhibitor) [1]. p21 inhibits the Cyclin E/CDK2 complex, preventing the phosphorylation of the Retinoblastoma (Rb) protein. This keeps the cell sequestered in the **G1 phase**, preventing it from entering the **S (Synthesis) phase** [1], [2]. This **G1-S checkpoint** allows time for DNA repair; if repair fails, p53 induces apoptosis via the BAX/BAK pathway [1], [2]. **Analysis of Options:** * **G1-S phase (Correct):** This is the primary site of p53 action. By arresting the cell here, p53 ensures that damaged DNA is not replicated during the S phase [2]. * **G2-M phase (Incorrect):** While p53 can play a minor role at the G2-M checkpoint by regulating 14-3-3σ and Cdc25C, its classic, most significant, and exam-relevant action is at the G1-S transition. * **S-G2 phase (Incorrect):** The transition from DNA synthesis to the pre-mitotic phase is not the primary regulatory target of p53. * **G0 phase (Incorrect):** G0 is a quiescent state. p53 acts on actively cycling cells that have encountered genomic stress, rather than pulling them out of the resting state. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in TP53 leading to a high risk of multiple diverse tumors (SBLA: Sarcoma, Breast, Leukemia, Adrenal gland). * **Most Common Mutation:** TP53 is the most commonly mutated gene in human cancers [1]. * **Mechanism of Degradation:** In normal cells, p53 is kept at low levels by **MDM2**, which facilitates its degradation via the ubiquitin-proteasome pathway. * **HPV Connection:** The E6 protein of High-risk Human Papillomavirus (HPV 16, 18) degrades p53, leading to cervical cancer. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 301-303. [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 387: Ectopic rest of normal tissue is known as?

A. Choristoma (Correct Answer)
B. Hamartoma
C. Pseudotumor
D. Lymphoma

Explanation: **Explanation:** The correct answer is **Choristoma**. This question tests the fundamental definitions of developmental growth disturbances often confused with true neoplasia. **1. Why Choristoma is correct:** A **Choristoma** is defined as a mass formed by **microscopically normal cells or tissues** present in an **abnormal (ectopic) location**. It is a developmental anomaly rather than a true neoplasm. A classic example is a nodule of well-organized pancreatic tissue found in the submucosa of the stomach or small intestine. **2. Why the other options are incorrect:** * **Hamartoma:** This is a focal overgrowth of cells and tissues **native** to the organ in which it occurs (e.g., a pulmonary hamartoma containing cartilage, bronchial epithelium, and fat). Unlike choristoma, the tissue is in the *correct* location but grows in a disorganized mass. * **Pseudotumor:** This is a non-specific clinical term for a non-neoplastic lesion that mimics a tumor (e.g., Inflammatory Myofibroblastic Tumor). * **Lymphoma:** This is a **malignant neoplasm** of lymphoid tissue [1]. It is not a developmental rest but a clonal proliferation of malignant cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Choristoma vs. Hamartoma:** Remember the mnemonic: **C**horistoma = **C**hange in location; **H**amartoma = **H**ome (native location). * **Common Choristomas:** Pancreatic tissue in the gallbladder/stomach or gastric mucosa in Meckel’s diverticulum. * **Common Hamartomas:** Lungs (most common site), Bile duct hamartomas (Von Meyenburg complexes), and Cowden Syndrome (multiple hamartomas). * Both Choristomas and Hamartomas end in the suffix **"-oma,"** but they are **benign developmental malformations**, not true cancers [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 208-209.

Question 388: For which one of the following tumors, Gastrin is a biochemical marker?

A. Medullary carcinoma of thyroid
B. Pancreatic neuroendocrine tumor (Correct Answer)
C. Pheochromocytoma
D. Gastrointestinal stromal tumor

Explanation: **Explanation:** The correct answer is **Pancreatic neuroendocrine tumor (PanNET)**. Gastrin is a peptide hormone primarily secreted by G-cells in the gastric antrum and duodenum. However, it serves as a specific biochemical marker for **Gastrinomas** [1], which are a subtype of functional pancreatic neuroendocrine tumors. These tumors often present as **Zollinger-Ellison Syndrome (ZES)**, characterized by hypergastrinemia, fulminant peptic ulcer disease, and diarrhea [2]. **Analysis of Options:** * **Medullary Carcinoma of Thyroid (MTC):** The hallmark biochemical marker is **Calcitonin**, secreted by parafollicular C-cells. Carcinoembryonic antigen (CEA) is also used for monitoring. * **Pheochromocytoma:** This tumor of the adrenal medulla secretes catecholamines. The diagnostic markers are urinary and plasma **Metanephrines** and Vanillylmandelic acid (VMA). * **Gastrointestinal Stromal Tumor (GIST):** These are mesenchymal tumors, not endocrine ones. Their primary diagnostic marker is the immunohistochemical expression of **CD117 (c-KIT)** or DOG1, rather than a secreted hormone. **High-Yield Clinical Pearls for NEET-PG:** * **Gastrinoma Triangle:** Most gastrinomas are found in this anatomical region (bounded by the confluence of cystic/common bile duct, junction of 2nd/3rd parts of the duodenum, and neck/body of the pancreas) [1]. * **MEN1 Association:** Approximately 25% of gastrinomas occur as part of Multiple Endocrine Neoplasia Type 1 (MEN1), alongside parathyroid and pituitary tumors [2]. * **General NET Marker:** **Chromogranin A** is the most sensitive universal serum marker for most neuroendocrine tumors, regardless of their specific hormone production. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1124-1125. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1125.

Question 389: Kaposi sarcoma is commonly seen in which condition?

A. Leukemia
B. Lymphoma
C. AIDS (Correct Answer)
D. Cytomegalovirus infections

Explanation: **Explanation:** **Kaposi Sarcoma (KS)** is a vascular neoplasm caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi Sarcoma-associated Herpesvirus (KSHV) [1]. While it can occur in various clinical settings, it is most strongly associated with **AIDS** (Acquired Immunodeficiency Syndrome), where it serves as an **AIDS-defining illness** [1], [2]. 1. **Why AIDS is Correct:** In HIV-infected patients, profound immunosuppression allows HHV-8 to infect endothelial cells and drive spindle cell proliferation [1]. The **AIDS-associated (Epidemic) form** is the most aggressive variant, often presenting with widespread cutaneous lesions, mucosal involvement (especially the palate), and visceral spread [1]. 2. **Why Other Options are Incorrect:** * **Leukemia & Lymphoma:** While these are malignancies of the lymphoid/hematopoietic system and can involve immunosuppression, they are not the primary drivers or classic associations for Kaposi Sarcoma [1]. * **Cytomegalovirus (CMV):** Although CMV is a common opportunistic infection in AIDS patients, it causes conditions like retinitis or esophagitis. It is HHV-8, not CMV, that is the oncogenic driver for KS. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for "slit-like vascular spaces" containing RBCs and "spindle-shaped" stromal cells. * **Variants:** 1. **Classic (European):** Older Mediterranean men; indolent; distal limbs. 2. **Endemic (African):** Pre-AIDS era; can be very aggressive in children (lymphadenopathic). 3. **Iatrogenic:** Post-transplant patients on immunosuppressants. 4. **AIDS-associated:** Most common HIV-related malignancy [1]. * **Markers:** CD31 (vascular marker) and HHV-8 LNA-1 (latent nuclear antigen) are positive on IHC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-263. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 260-261.

Question 390: Gleason's staging is done in which of the following cancers?

A. Carcinoma of the prostate (Correct Answer)
B. Carcinoma of the pancreas
C. Carcinoma of the kidney
D. Carcinoma of the cervix

Explanation: **Explanation:** **Gleason’s Scoring System** is the gold standard for determining the histological grade and prognosis of **Prostate Adenocarcinoma** (Option A) [1]. Unlike many other systems, it is based entirely on **architectural patterns** of the tumor glands rather than individual cellular features (like nuclear atypia). The system assigns a primary grade (most common pattern) and a secondary grade (second most common pattern), each on a scale of 1 to 5. The sum of these two provides the **Gleason Score** (ranging from 2 to 10). A higher score indicates a more poorly differentiated tumor and a worse prognosis [1]. Modern practice utilizes the ‘Grade Group (1-5)’ system to further refine these scores for clinical decision-making. **Why other options are incorrect:** * **Carcinoma of the Pancreas (B):** Graded based on the degree of glandular differentiation and mitotic activity, but does not use the Gleason system. * **Carcinoma of the Kidney (C):** Renal Cell Carcinoma (RCC) is primarily graded using the **Fuhrman Grading System** (or the updated WHO/ISUP system), which focuses on nuclear size, contour, and nucleolar prominence. * **Carcinoma of the Cervix (D):** Staged using the **FIGO system**, which is based on clinical and radiological extent rather than a specific architectural grading system like Gleason. **High-Yield Clinical Pearls for NEET-PG:** * **Gleason Grade 1:** Small, uniform, closely packed glands (well-differentiated). * **Gleason Grade 5:** No glandular differentiation; solid sheets, cords, or single cells (poorly differentiated). * **Prostate Cancer Marker:** PSA (Prostate Specific Antigen) is used for screening, while Gleason score is the best predictor of biological behavior [1]. * **Common Site:** Most prostate cancers arise in the **peripheral zone** [1]. **References:** [1] 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.

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