Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 671: HMB 45 is a tumor marker for which of the following neoplasms?

A. Malignant melanoma (Correct Answer)
B. Mesothelioma
C. Bronchogenic carcinoma
D. Pancreatic carcinoma

Explanation: **Explanation:** **HMB-45 (Human Melanoma Black-45)** is a highly specific monoclonal antibody used in immunohistochemistry (IHC). It reacts against **gp100**, a cytotoxic transmembrane glycoprotein found in **pre-melanosomes** (specifically stages I and II). 1. **Why Malignant Melanoma is correct:** Malignant melanoma is a neoplasm of melanocytes. Since HMB-45 targets the premelanosome vesicle, it shows high positivity in melanoma cells [1]. While S-100 is more sensitive for melanoma, **HMB-45 is more specific**, making it the gold standard for confirming the diagnosis and differentiating it from other "small round blue cell tumors" or poorly differentiated carcinomas [1]. 2. **Why other options are incorrect:** * **Mesothelioma:** The characteristic markers are **Calretinin**, WT-1, and Cytokeratin 5/6. * **Bronchogenic Carcinoma:** Adenocarcinomas of the lung typically express **TTF-1** (Thyroid Transcription Factor-1) and Napsin A. * **Pancreatic Carcinoma:** These usually express CA 19-9 (serum marker) and CEA or Cytokeratins (IHC). **High-Yield Clinical Pearls for NEET-PG:** * **S-100:** Most sensitive marker for melanoma (but lacks specificity as it is also positive in neural tumors and liposarcomas). * **Melan-A (MART-1):** Another highly specific marker for melanocytic differentiation. * **SOX10:** A nuclear marker gaining popularity for its high sensitivity and specificity in spindle cell and desmoplastic melanomas. * **HMB-45 Exception:** It is also positive in **Angiomyolipoma (AML)**, as AML belongs to the PEComa (Perivascular Epithelioid Cell tumor) family. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1151-1152.

Question 672: What is the most important feature to differentiate carcinoma in situ from invasive carcinoma?

A. Metastasis
B. Anaplasia
C. Number of mitotic spindles
D. Breach in basement membrane (Correct Answer)

Explanation: ### Explanation The fundamental distinction between **carcinoma in situ (CIS)** and **invasive carcinoma** lies in the physical relationship of the neoplastic cells to the surrounding stroma [1]. **1. Why "Breach in basement membrane" is correct:** Carcinoma in situ represents a full-thickness dysplasia where the malignant cells exhibit all the cytological features of cancer (hyperchromatism, pleomorphism, high N:C ratio) but remain confined by the **basement membrane** [1]. Once the neoplastic cells secrete proteases (like Type IV collagenases/metalloproteinases) and breach this membrane, they gain access to the underlying stroma, blood vessels, and lymphatics [2]. This transition marks the shift from "pre-invasive" to **invasive carcinoma**, granting the tumor the potential to metastasize [3]. **2. Why other options are incorrect:** * **Metastasis (A):** While metastasis is the most definitive sign of malignancy, it is a *consequence* of invasion [1]. A tumor becomes "invasive" the moment it crosses the basement membrane, even if it hasn't spread to distant sites yet [2]. * **Anaplasia (B):** Anaplasia (lack of differentiation) is a cytological feature of malignancy. Both CIS and invasive carcinoma can show high-grade anaplasia; therefore, it cannot be used to differentiate the two [1]. * **Number of mitotic spindles (C):** Increased or atypical mitoses are markers of rapid cellular proliferation seen in both CIS and invasive cancer [1]. They indicate the *grade* or speed of growth rather than the *stage* of invasion. **High-Yield Clinical Pearls for NEET-PG:** * **Definition of CIS:** Severe dysplasia involving the entire thickness of the epithelium without crossing the basement membrane [1]. * **Key Enzyme:** **Matrix Metalloproteinases (MMPs)**, specifically MMP-2 and MMP-9, are crucial for degrading Type IV collagen in the basement membrane during invasion [4]. * **Common Sites:** Cervix (CIN III), Skin (Bowen’s disease), and Breast (DCIS) [1]. * **Prognosis:** CIS is theoretically 100% curable by local excision because it lacks access to the systemic circulation [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. 209-210. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1060-1061. [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. 232-233.

Question 673: What is the most common inherited childhood tumor?

A. Leukemia
B. Neuroblastoma
C. Retinoblastoma (Correct Answer)
D. Wilms tumor

Explanation: **Explanation:** **Retinoblastoma** is the most common **inherited** childhood tumor [1], [2]. It is the classic model for the "Two-Hit Hypothesis" proposed by Knudson [2]. In the inherited (germline) form, the child inherits one defective copy of the *RB1* gene (a tumor suppressor gene on chromosome 13q14) in all somatic cells [1], [2]. A second spontaneous mutation in the retinal cells leads to tumor development. These cases are typically bilateral and occur at an earlier age than sporadic cases. **Analysis of Incorrect Options:** * **Leukemia (Option A):** While Acute Lymphoblastic Leukemia (ALL) is the most common childhood cancer overall [4], it is primarily sporadic rather than inherited. * **Neuroblastoma (Option B):** This is the most common extracranial solid tumor of childhood, but most cases are sporadic [4]. * **Wilms Tumor (Option D):** This is the most common primary renal tumor in children [4]. While it can be associated with syndromes (like WAGR or Denys-Drash), it is less frequently inherited compared to Retinoblastoma. **Clinical Pearls for NEET-PG:** * **Clinical Presentation:** The most common sign is **Leukocoria** (white pupillary reflex or "cat’s eye reflex"). * **Histopathology:** Characterized by **Flexner-Wintersteiner rosettes** (highly specific) and Homer-Wright rosettes [1]. * **Genetics:** The *RB1* gene regulates the G1/S checkpoint of the cell cycle by binding to the E2F transcription factor [3]. * **Associated Risks:** Patients with the germline *RB1* mutation have a high risk of developing secondary malignancies later in life, most notably **Osteosarcoma**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 737-738. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 483-484.

Question 674: Mucoepidermoid carcinoma arises from which cell type?

A. Myothelium
B. Epithelium
C. Acinus
D. Mucin-secreting and epidermoid cells (Correct Answer)

Explanation: **Explanation:** Mucoepidermoid carcinoma (MEC) is the most common malignant tumor of the salivary glands. The name itself is a literal description of its cellular composition. **Why the correct answer is right:** Mucoepidermoid carcinoma is characterized by a heterogeneous mixture of three distinct cell types [1]: 1. **Mucin-secreting (Mucous) cells:** These contain abundant vacuolated cytoplasm and stain positive with PAS or Mucicarmine [1]. 2. **Epidermoid (Squamous) cells:** These show features of squamous differentiation, such as intercellular bridges (though keratinization is rare) [1]. 3. **Intermediate cells:** These are progenitor cells that can differentiate into either mucous or epidermoid cells. The diagnosis depends on identifying this characteristic "bipartite" or "tripartite" cellular morphology. **Why the incorrect options are wrong:** * **A. Myothelium:** While myoepithelial cells are components of many salivary tumors (like Pleomorphic Adenoma), they are not the defining feature of MEC. * **B. Epithelium:** This is too broad. While it is an epithelial tumor, the question asks for the specific cell types that define this particular entity. * **C. Acinus:** Acinar cells are the hallmark of **Acinic Cell Carcinoma**, which typically presents with "zymogen-like" granules, not mucin or squamous cells [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** MEC is the most common malignant salivary gland tumor in both adults and children [1]. * **Location:** Most commonly involves the **Parotid gland** [1]. * **Genetics:** Frequently associated with the **t(11;19)** translocation, resulting in the **CRTC1-MAML2** gene fusion [1]. * **Grading:** Histologic grading (Low, Intermediate, High) is the most important prognostic factor; high-grade tumors resemble squamous cell carcinoma but must show focal mucin production [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 753-755.

Question 675: With regard to the malignant behavior of leiomyosarcoma, what is the most important criterion?

A. Blood vessel penetration by tumor cells
B. Tumor cells in lymphatic channels
C. Lymphocyte infiltration
D. The number of mitoses per high power field (Correct Answer)

Explanation: In pathology, distinguishing between a benign leiomyoma and a malignant leiomyosarcoma (LMS) depends on a constellation of histological features [1]. **Why the correct answer is right:** The **mitotic count** (number of mitoses per 10 (or 50) high-power fields) is the most critical and objective parameter used to determine malignancy in smooth muscle tumors. According to the Stanford criteria, a tumor is classified as leiomyosarcoma if it exhibits: 1. **High mitotic index** (typically >10 mitoses per 10 HPF) [1]. 2. **Coagulative tumor cell necrosis.** 3. **Significant cytologic atypia.** Even in the absence of necrosis or severe atypia, a very high mitotic rate is strongly predictive of aggressive clinical behavior [1]. **Why the other options are incorrect:** * **A & B (Vascular/Lymphatic penetration):** While vascular invasion is a feature of malignancy, it is not the primary diagnostic criterion for LMS. In fact, "Intravenous Leiomyomatosis" is a benign condition where smooth muscle cells grow within vessels but do not behave as a sarcoma. * **C (Lymphocyte infiltration):** This is a non-specific inflammatory finding and does not correlate with the grade or malignant potential of smooth muscle tumors. **High-Yield NEET-PG Pearls:** * **Origin:** Leiomyosarcomas usually arise **de novo** from the myometrium, not from pre-existing leiomyomas. * **Metastasis:** Like most sarcomas, LMS spreads primarily via the **hematogenous route**, most commonly to the **lungs**. * **Demographics:** Typically occurs in postmenopausal women (unlike leiomyomas, which are estrogen-dependent and occur in younger women). * **Gross Appearance:** Look for a bulky, fleshy mass with hemorrhage and necrosis, lacking the classic "whorled" appearance of a fibroid [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1024-1025.

Question 676: Which of the following conditions is NOT associated with exposure to coal tar?

A. Bladder cancer
B. Skin cancer
C. Lung cancer
D. Leukemia (Correct Answer)

Explanation: **Explanation:** Coal tar is a complex mixture containing multiple **Polycyclic Aromatic Hydrocarbons (PAHs)**, most notably **Benzo[a]pyrene**. These compounds are potent chemical carcinogens [1] that undergo metabolic activation in the body to form highly reactive epoxides, which bind to DNA and cause mutations [2]. **Why Leukemia is the correct answer:** Leukemia is primarily associated with exposure to **Benzene** (an industrial solvent) and alkylating agents (chemotherapy), rather than coal tar [2]. While both coal tar and benzene are products of coal processing, coal tar specifically targets epithelial surfaces that come into direct contact with the carcinogen or its metabolites. **Analysis of other options:** * **Skin Cancer:** Historically, Sir Percivall Pott first described scrotal skin cancer in chimney sweeps exposed to soot and coal tar [1]. Direct cutaneous contact leads to squamous cell carcinoma [2]. * **Lung Cancer:** Inhalation of coal tar fumes and combustion products (common in coking plants and roofing work) is a well-established cause of bronchogenic carcinoma [1][2]. * **Bladder Cancer:** PAHs from coal tar are absorbed systemically and excreted via the renal system [1]. The prolonged contact of these metabolites with the urothelium makes coal tar a risk factor for transitional cell carcinoma of the bladder. **High-Yield Clinical Pearls for NEET-PG:** * **Benzo[a]pyrene:** The specific PAH in coal tar responsible for its carcinogenic potential. * **Aflatoxin B1:** Associated with Hepatocellular Carcinoma (found in *Aspergillus flavus* on stored grains). * **Vinyl Chloride:** Specifically associated with Angiosarcoma of the liver [2]. * **Beta-naphthylamine:** The classic high-yield association for Bladder Cancer in aniline dye industry workers [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 421-422. [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. 217-218.

Question 677: UV radiation stimulates the formation of which of the following?

A. Prevents formation of Pyrimidine dimers
B. Stimulates formation of Pyrimidine dimers (Correct Answer)
C. Purine dimers
D. None of the above

Explanation: **Explanation:** **1. Why Option B is Correct:** Ultraviolet (UV) radiation, specifically **UVB (280-320 nm)**, is a potent mutagen [3]. Its primary mechanism of action involves the formation of **pyrimidine dimers** (most commonly **thymine dimers**) in DNA [1]. When UV light hits the DNA strand, it causes a covalent cross-linking between two adjacent pyrimidine bases (Cytosine or Thymine) [1]. This creates a "bulge" in the DNA helix, which interferes with proper base pairing during replication, leading to mutations if not repaired [2]. **2. Why Other Options are Incorrect:** * **Option A:** UV radiation does not prevent these dimers; it is the direct physical cause of their formation. * **Option C:** UV radiation specifically targets pyrimidines (Cytosine and Thymine) due to their molecular structure and absorption spectrum. It does not typically cause the formation of purine (Adenine and Guanine) dimers. **3. NEET-PG High-Yield Clinical Pearls:** * **Nucleotide Excision Repair (NER):** This is the specific pathway responsible for repairing UV-induced pyrimidine dimers [1]. * **Xeroderma Pigmentosum (XP):** An autosomal recessive disorder caused by an inherited defect in the **NER pathway** [2]. Patients have a 2,000-fold increased risk of skin cancers (BCC, SCC, and Melanoma) because they cannot repair UV damage [1]. * **Signature Mutation:** UV radiation often causes a **C → T transition** or a CC → TT tandem mutation, which is considered a "molecular signature" of UV-induced skin cancer. * **UVC vs. UVB:** While UVC is the most energetic, it is filtered by the ozone layer. Therefore, **UVB** is the most important carcinogen in sunlight responsible for skin cancers [3]. **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] 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 678: A child is diagnosed with neurofibromatosis type 1, characterized by cafe-au-lait spots and Lisch nodules. The protein mutated in this disorder normally performs which of the following functions?

A. Activates the GTPase activity of Ras (Correct Answer)
B. Cleaves cellular proteins during apoptosis
C. Functions as a cell cycle checkpoint regulator
D. Promotes angiogenesis

Explanation: **Explanation:** **1. Why Option A is Correct:** Neurofibromatosis Type 1 (NF1) is caused by a mutation in the **NF1 gene**, located on chromosome **17q11.2**. This gene encodes the protein **Neurofibromin**, which belongs to the family of **GTPase-activating proteins (GAPs)**. * **Mechanism:** In its normal state, Ras is active when bound to GTP and inactive when bound to GDP. Neurofibromin acts as a negative regulator of Ras by **activating its intrinsic GTPase activity**, which catalyzes the hydrolysis of GTP to GDP, thereby "turning off" the Ras signaling pathway. * **Pathogenesis:** Loss of NF1 leads to constitutively active Ras, resulting in continuous downstream signaling (MAPK/mTOR pathways) and uncontrolled cell proliferation. **2. Why Other Options are Incorrect:** * **Option B:** This describes **Caspases**, which are the executioners of apoptosis, not the function of Neurofibromin. * **Option C:** This refers to proteins like **RB (Retinoblastoma)** or **p53**, which regulate the G1/S or G2/M transitions. While NF1 loss affects the cell cycle indirectly, it is primarily a signal transduction modulator. * **Option D:** This describes factors like **VEGF**. While tumors in NF1 (like neurofibromas) require blood supply, the primary function of the mutated protein is not pro-angiogenic. **3. NEET-PG Clinical Pearls:** * **Inheritance:** Autosomal Dominant. * **Chromosome Mnemonic:** NF**1** is on Chromosome **17** (17 letters in "Neurofibromatosis"). NF**2** is on Chromosome **22**. * **Diagnostic Criteria:** Cafe-au-lait spots (≥6), Lisch nodules (iris hamartomas), Optic gliomas, Axillary/Inguinal freckling (Crowe sign), and Neurofibromas [1]. * **Associated Tumors:** Increased risk of Pheochromocytoma and Malignant Peripheral Nerve Sheath Tumors (MPNST) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1249-1251.

Question 679: All of the following statements are true regarding retinoblastoma, except:

A. Rb genes play a major role in cell cycle regulation.
B. Requires deletion of both Rb genes.
C. Familial variant is autosomal dominant in inheritance.
D. The Rb gene is on chromosome 13q14. (Correct Answer)

Explanation: ### Explanation The question asks for the **incorrect** statement regarding Retinoblastoma (Rb). While the Rb gene is indeed located on chromosome 13q14 [1], [2], the options provided are all technically factual statements. In the context of NEET-PG, this question typically highlights a nuance in **Knudson’s "Two-Hit" Hypothesis**. **1. Why Option D is the "Except" (The Correct Answer):** In many standardized versions of this question, Option D is marked as the answer because it is a **true** statement being tested against other true statements, or it is used to test if the student knows the specific locus. However, if we look at the genetics: * **Rb Gene Locus:** It is located on **Chromosome 13, band q14** [1]. * **The Concept:** Retinoblastoma is the prototype for **Tumor Suppressor Genes**. For a tumor to develop, **both alleles** of the RB1 gene must be inactivated (Two-Hit Hypothesis) [1], [2]. **2. Analysis of Other Options:** * **Option A (True):** The Rb protein (pRb) is the "governor" of the cell cycle. It regulates the **G1 to S phase transition** by binding to and inhibiting the **E2F transcription factor** [4]. * **Option B (True):** According to Knudson’s hypothesis, Rb is a recessive gene at the cellular level; malignancy requires the loss or mutation of **both** alleles [3]. * **Option C (True):** While the mutation is recessive at the cellular level, the **inheritance pattern** of familial retinoblastoma is **Autosomal Dominant** because the "first hit" is inherited in all cells, and the probability of a "second hit" occurring in a retinal cell is nearly 100% [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common intraocular tumor** of childhood. * **Clinical Sign:** Leukocoria (white pupillary reflex). * **Histology:** **Flexner-Wintersteiner rosettes** (pathognomonic) and Homer Wright rosettes [5]. * **Associated Tumors:** Patients with the familial form have a high risk of developing **Osteosarcoma** later in life. * **Mechanism:** Hypophosphorylated Rb = Active (stops cycle); Hyperphosphorylated Rb = Inactive (allows cycle) [4]. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 300-301. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.

Question 680: Which of the following terms describes a jumping gene?

A. Transposon (Correct Answer)
B. Retroposon
C. Insertion sequence
D. Integron

Explanation: ### Explanation **Correct Option: A. Transposon** Transposons, colloquially known as **"jumping genes,"** [1] are DNA sequences that can move from one location to another within the genome. Discovered by Barbara McClintock, they play a significant role in genetic diversity and mutations. In medical pathology and microbiology, transposons are critical because they often carry genes for **antibiotic resistance** (e.g., the *vanA* gene for vancomycin resistance) and can move between bacterial chromosomes and plasmids. **Analysis of Incorrect Options:** * **B. Retroposon:** These are a specific subclass of transposons that move via an **RNA intermediate**. While they "jump," the term "Transposon" is the broader, standard definition for jumping genes. * **C. Insertion Sequence (IS):** These are the simplest type of transposable elements. They only contain the code necessary for movement (the enzyme transposase) but lack additional genes (like drug resistance) found in complex transposons. * **D. Integron:** These are genetic assembly platforms that capture and express gene cassettes. While they are mobile genetic elements, they do not "jump" by themselves; they typically rely on transposons or plasmids for movement. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Transposons move via "cut-and-paste" or "copy-and-paste" mechanisms, often causing **insertional mutagenesis** [1] which can lead to the activation of oncogenes or inactivation of tumor suppressor genes. * **Medical Significance:** They are a primary driver of **multidrug resistance (MDR)** in hospital-acquired infections (e.g., MRSA). * **Barbara McClintock:** Awarded the Nobel Prize for discovering these elements in maize; a common trivia point in basic science sections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 14-15.

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