Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 151: Desmoplasia is defined as:

A. Increase in number of neoplastic cells
B. Benign tumors arising in fibrous tissue
C. Abundant collagenous stroma in a tumor (Correct Answer)
D. Benign cartilaginous tumors

Explanation: **Explanation:** **Desmoplasia** refers to the proliferation of non-neoplastic connective tissue (specifically an **abundant collagenous stroma**) induced by certain malignant tumors [1]. This reaction is triggered by the release of growth factors (like TGF-β) by tumor cells, which stimulate host fibroblasts to produce excessive collagen [1]. * **Why Option C is correct:** Desmoplasia is a characteristic stromal response where the tumor feels "stony hard" or "scirrhous" on palpation due to the dense fibrous tissue [1][2]. This is a hallmark of many invasive carcinomas. * **Why other options are incorrect:** * **Option A:** An increase in the number of neoplastic cells is simply termed **proliferation** or tumor growth. * **Option B:** A benign tumor arising from fibrous tissue is called a **Fibroma**. * **Option D:** A benign cartilaginous tumor is called a **Chondroma**. **NEET-PG High-Yield Pearls:** 1. **Classic Examples:** Desmoplasia is most characteristically seen in **Invasive Ductal Carcinoma (IDC) of the breast**, Adenocarcinoma of the **Pancreas**, and Prostate cancer [1]. 2. **Scirrhous Morphology:** When desmoplasia is extensive, the tumor is described as "scirrhous" (e.g., Linitis plastica in gastric cancer). 3. **Clinical Significance:** On clinical examination, desmoplasia is what causes the "fixed" and "hard" nature of malignant lumps [2]. On mammography, it contributes to the "stellate" or "spiculated" appearance of breast lesions. 4. **Mechanism:** It is a host response to the invading tumor, not the tumor cells themselves [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. 203-204. [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. 204-206.

Question 152: Psammoma bodies may be seen in all of the following conditions, except?

A. Follicular carcinoma of the thyroid (Correct Answer)
B. Papillary carcinoma of the thyroid
C. Meningioma
D. Serous cystadenocarcinoma of the ovary

Explanation: **Explanation:** Psammoma bodies are characteristic microscopic findings in pathology representing **dystrophic calcification**. They appear as concentric, laminated, basophilic (blue-purple) spherical structures. **1. Why Follicular Carcinoma of the Thyroid (Option A) is the Correct Answer:** Follicular carcinoma of the thyroid is characterized by the formation of follicles and a thick fibrous capsule with vascular or capsular invasion [1]. It **does not** typically form psammoma bodies [1]. In contrast, psammoma bodies are a hallmark feature of Papillary Thyroid Carcinoma (PTC) [1]. Their absence in follicular carcinoma is a key histological differentiator between these two types of thyroid cancer. **2. Analysis of Incorrect Options (Conditions where Psammoma bodies ARE seen):** * **Papillary Carcinoma of the Thyroid (Option B):** Psammoma bodies are found in approximately 40-50% of cases, usually located within the cores of the papillae [1]. * **Meningioma (Option C):** Specifically the psammomatous subtype of meningioma is rich in these calcifications. * **Serous Cystadenocarcinoma of the Ovary (Option D):** These tumors frequently exhibit psammoma bodies, which serve as a diagnostic clue for serous morphology. **Clinical Pearls for NEET-PG:** To remember the common conditions associated with Psammoma bodies, use the mnemonic **"PSaMMoma"**: * **P:** **P**apillary carcinoma of thyroid, **P**rolactinoma (rarely). * **S:** **S**erous cystadenocarcinoma of ovary, **S**omatostatinoma. * **M:** **M**eningioma, **M**esothelioma. **High-Yield Fact:** Psammoma bodies represent a process of single-cell necrosis followed by the deposition of calcium salts in concentric layers. They are a classic example of **dystrophic calcification** (calcification in dead/dying tissue with normal serum calcium levels). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1101.

Question 153: A 45-year-old woman presents with abdominal pain and vaginal bleeding. A hysterectomy is performed and shows a benign tumor of the uterus derived from a smooth muscle cell. What is the appropriate diagnosis?

A. Angiomyolipoma
B. Leiomyoma (Correct Answer)
C. Leiomyosarcoma
D. Myxoma

Explanation: **Explanation:** The correct diagnosis is **Leiomyoma**. This is a classic presentation of the most common benign tumor of the female reproductive tract [1]. **Why Leiomyoma is correct:** The question describes a **benign** tumor derived from **smooth muscle cells** in the uterus. In medical terminology, "leio-" means smooth, "myo-" means muscle, and "-oma" denotes a benign neoplasm. Leiomyomas (commonly known as fibroids) are monoclonal tumors arising from the myometrium [1]. They are estrogen-dependent, often enlarging during pregnancy and regressing after menopause. **Why other options are incorrect:** * **Angiomyolipoma:** This is a benign tumor composed of blood vessels (angio), smooth muscle (myo), and fat (lipoma). It is most commonly associated with the **kidney** and is a classic feature of Tuberous Sclerosis. * **Leiomyosarcoma:** While this is a smooth muscle tumor, the suffix "-sarcoma" indicates a **malignant** neoplasm [1]. These typically arise *de novo* rather than from pre-existing leiomyomas and exhibit nuclear atypia, high mitotic index, and zonal necrosis [1]. * **Myxoma:** This is a benign connective tissue tumor characterized by a primitive "myxoid" (mucinous) stroma. The most common site is the **left atrium** of the heart, not the uterus. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Characterized by "intersecting bundles of spindle-shaped smooth muscle cells" with a **whorled (spiral) pattern** [1]. * **Degenerations:** The most common type is **Hyaline degeneration** [1]. **Red degeneration** (carneous degeneration) occurs due to rapid growth during pregnancy leading to infarction. * **Genetics:** Often associated with mutations in the **MED12** gene [1]. * **Key Distinction:** Unlike many other tumors, leiomyomas do *not* have a high risk of malignant transformation into leiomyosarcomas [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 154: Which of the following is NOT a familial breast cancer gene?

A. BRCA1
B. P53
C. P16 (Correct Answer)
D. PTEN

Explanation: ### Explanation The correct answer is **C. P16**. **Why P16 is the correct answer:** The **P16/INK4a** gene (located on chromosome 9p21) is a tumor suppressor gene that regulates the cell cycle by inhibiting Cyclin-Dependent Kinases (CDK4/6) [1]. While it is a critical gene in oncology, its germline mutations are primarily associated with **Familial Melanoma** and **Pancreatic Cancer**, not familial breast cancer [1]. In the context of breast pathology, P16 immunohistochemistry is more commonly used as a surrogate marker for HPV infection in cervical or oropharyngeal cancers, rather than a screening tool for hereditary breast syndromes. **Analysis of Incorrect Options:** * **BRCA1 (Option A):** The most common cause of familial breast cancer (Chromosome 17q). It is associated with a high risk of medullary carcinoma of the breast and serous ovarian carcinoma. * **P53 (Option B):** Germline mutations in *TP53* (Chromosome 17p) cause **Li-Fraumeni Syndrome**. Breast cancer is one of the "core" cancers in this syndrome, often occurring at a very young age. * **PTEN (Option D):** Germline mutations in *PTEN* (Chromosome 10q) lead to **Cowden Syndrome**. This syndrome is characterized by multiple hamartomas and a significantly increased risk of breast, thyroid (follicular), and endometrial cancers. **High-Yield Clinical Pearls for NEET-PG:** * **BRCA2:** Located on Chromosome 13q; associated with **male breast cancer** and prostatic/pancreatic cancers. * **STK11:** Associated with **Peutz-Jeghers Syndrome**, which carries an increased risk of breast cancer. * **CHEK2:** A cell cycle checkpoint gene also implicated in moderate-risk familial breast cancer. * **CDH1:** Mutations lead to **Hereditary Diffuse Gastric Cancer** and are specifically linked to **Lobular Carcinoma** of the breast. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-306.

Question 155: Which among the following is not a feature of follicular lymphoma?

A. (11;14) translocation (Correct Answer)
B. BCL2 over expression
C. BCL6 rearrangement
D. CD5 negative

Explanation: **Explanation:** Follicular Lymphoma (FL) is a common low-grade B-cell non-Hodgkin lymphoma derived from germinal center B-cells [1]. **Why Option A is the Correct Answer:** The **t(11;14)** translocation is the hallmark of **Mantle Cell Lymphoma**, not Follicular Lymphoma [4]. This translocation involves the *CCND1* gene on chromosome 11 and the *IGH* gene on chromosome 14, leading to the overexpression of **Cyclin D1**, which promotes cell cycle progression [4]. **Analysis of Incorrect Options:** * **Option B (BCL2 overexpression):** This is the characteristic feature of FL [1]. It results from the **t(14;18)** translocation, which places the *BCL2* anti-apoptotic gene under the control of the immunoglobulin heavy chain promoter [1]. This leads to reduced apoptosis in B-cells [2]. * **Option C (BCL6 rearrangement):** While t(14;18) is the primary driver, approximately 5–10% of FL cases (especially Grade 3) show **BCL6** rearrangements at 3q27 [3]. BCL6 is essential for germinal center formation. * **Option D (CD5 negative):** FL expresses B-cell markers (CD19, CD20, CD10) but is typically **CD5 negative** and **CD23 negative**. This helps distinguish it from Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma, which are CD5 positive [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Characterized by a "back-to-back" follicular pattern; lacks tingible body macrophages (unlike reactive hyperplasia) [1]. * **Genetics:** t(14;18) is the most common cytogenetic abnormality [1]. * **Transformation:** FL can transform into a more aggressive **Diffuse Large B-Cell Lymphoma (DLBCL)**, known as Richter’s transformation (though this term is more commonly used for CLL). * **Grading:** Based on the number of **centroblasts** per high-power field (Mann and Berard criteria). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564. [4] 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. 610-612.

Question 156: Mutation in the p53 gene is associated with which malignancy?

A. Endometrial carcinoma type 1
B. Retinoblastoma
C. Colorectal carcinoma (Correct Answer)
D. Prostate cancer

Explanation: **Explanation:** **Mutation in the TP53 gene** (located on chromosome 17p) is the most common genetic alteration in human cancers. It acts as the "Guardian of the Genome" by regulating the cell cycle and inducing apoptosis in response to DNA damage [1]. **Why Colorectal Carcinoma is correct:** In the classic **Adenoma-Carcinoma sequence** (Vogelstein model), the loss of the p53 tumor suppressor gene is a critical "late event" that triggers the transition from a late-stage adenoma to an invasive carcinoma. While *APC* mutations initiate the process, the inactivation of p53 is what ultimately allows for uncontrolled cell proliferation and genomic instability [2]. **Analysis of Incorrect Options:** * **Endometrial Carcinoma Type 1:** This is the estrogen-dependent (endometrioid) type, primarily associated with **PTEN** mutations and microsatellite instability (MSI). *Note: p53 mutations are actually a hallmark of Type 2 (Serous) endometrial carcinoma.* * **Retinoblastoma:** This is classically associated with the **RB1 gene** mutation (Chromosome 13q14), the first tumor suppressor gene ever discovered (Knudson’s two-hit hypothesis) [3]. * **Prostate Cancer:** While p53 can be involved in advanced stages, the most characteristic early genetic changes involve **PTEN** loss and **TMPRSS2-ERG** gene fusions. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in TP53 leading to a high risk of diverse cancers (SBLA: Sarcoma, Breast, Leukemia, Adrenal gland). * **Mechanism:** p53 induces **p21**, which inhibits Cyclin/CDK complexes, causing cell cycle arrest in the **G1 phase** [1]. * **Aflatoxin B1:** Associated with a specific mutation in p53 (codon 249) leading to Hepatocellular Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [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. 226-227. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298.

Question 157: Which of the following genetic mutations is involved in breast carcinoma?

A. APC
B. BRCA (Correct Answer)
C. HbAc
D. RB gene

Explanation: **Explanation:** **Correct Answer: B. BRCA** The **BRCA1 and BRCA2** genes are tumor suppressor genes involved in the repair of double-stranded DNA breaks via homologous recombination [1]. Mutations in these genes lead to genomic instability, significantly increasing the risk of **hereditary breast and ovarian cancer syndromes** [1]. BRCA1 is specifically associated with "triple-negative" breast cancers, while BRCA2 is linked to male breast cancer and prostatic carcinoma [1]. **Analysis of Incorrect Options:** * **A. APC (Adenomatous Polyposis Coli):** This is a tumor suppressor gene associated with the Wnt signaling pathway. Mutations are primarily linked to **Familial Adenomatous Polyposis (FAP)** and colorectal carcinoma, not breast cancer. * **C. HbAc:** This is a distractor. It likely refers to HbA1c (Glycated Hemoglobin), which is a clinical marker for long-term glucose control in Diabetes Mellitus, having no role in oncogenesis. * **D. RB Gene:** The Retinoblastoma (RB) gene is the "governor of the cell cycle" (regulating the G1-S checkpoint). While it is mutated in various cancers, its primary associations are **Retinoblastoma** and **Osteosarcoma**. **High-Yield NEET-PG Pearls:** * **BRCA1 Location:** Chromosome 17q21. * **BRCA2 Location:** Chromosome 13q12.3. * **Li-Fraumeni Syndrome:** Another hereditary cause of breast cancer involving the **TP53** mutation (the "guardian of the genome") [1]. * **HER2/neu (ERBB2):** A proto-oncogene (tyrosine kinase receptor) amplified in ~15-20% of breast cancers, serving as a target for Trastuzumab [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1060.

Question 158: Regarding the phyllodes tumor, all of the following statements are true, except:

A. Intralobular stromal tumor
B. Overexpression of HOXB13 is associated with more aggressive clinical behavior
C. Most of these tumors are high grade (Correct Answer)
D. Metastasis of only the non-epithelial/stromal component

Explanation: **Explanation:** Phyllodes tumors are fibroepithelial neoplasms of the breast that arise from the **intralobular stroma** [1]. Understanding their grading and behavior is crucial for NEET-PG. **Why Option C is the correct answer (False statement):** The majority of phyllodes tumors (approximately 60–75%) are **low-grade (benign)** [1]. Only a small percentage are classified as borderline or high-grade (malignant). Grading is based on stromal cellularity, mitotic rate, nuclear pleomorphism, and the nature of the tumor borders. **Analysis of other options:** * **Option A (True):** Unlike common fibroadenomas which can be interlobular, phyllodes tumors specifically arise from the **intralobular stroma** [1]. * **Option B (True):** Recent molecular studies have identified that the **overexpression of HOXB13** (a homeobox gene) is a significant biomarker for increased stromal proliferation and is associated with higher grades and more aggressive clinical behavior. * **Option D (True):** Phyllodes tumors are biphasic (epithelial and stromal). However, the malignant potential resides solely in the **stromal component** [1]. Consequently, when these tumors metastasize (most commonly to the lungs via hematogenous spread), the deposits consist only of the sarcomatous stromal elements, not the epithelium [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Characterized by "leaf-like" (phyllodes) projections of stroma covered by epithelium [1]. * **Age:** Typically occurs in the 6th decade (older than fibroadenoma patients). * **Treatment:** Wide local excision with 1cm margins is preferred over simple enucleation to prevent local recurrence [1]. * **Distinction:** Unlike fibroadenomas, phyllodes tumors show increased stromal cellularity and "stromal overgrowth" [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1072-1074.

Question 159: All of the following are examples of a round cell tumor, except?

A. Neuroblastoma
B. Ewing's sarcoma
C. Medulloblastoma
D. Haemangioblastoma (Correct Answer)

Explanation: **Explanation:** Small Round Blue Cell Tumors (SRBCTs) are a group of highly malignant neoplasms characterized histologically by small, round, undifferentiated cells with high nuclear-to-cytoplasmic ratios and intense basophilic (blue) staining on H&E. **Why Haemangioblastoma is the correct answer:** Haemangioblastoma is **not** a round cell tumor [3]. It is a benign (WHO Grade 1), highly vascular tumor typically found in the cerebellum. Histologically, it is characterized by two main components: a dense network of thin-walled **capillaries** and large, polygonal **"stromal cells"** with clear, vacuolated cytoplasm (due to lipid content) [3]. It lacks the primitive, hyperchromatic round cells seen in SRBCTs. **Analysis of Incorrect Options:** * **Neuroblastoma:** A classic pediatric SRBCT derived from neural crest cells [1]. It often shows **Homer-Wright rosettes**. * **Ewing’s Sarcoma:** A primitive neuroectodermal tumor (PNET) characterized by uniform small round cells that often contain **glycogen** (PAS positive). It is associated with the t(11;22) translocation. * **Medulloblastoma:** The most common malignant brain tumor in children, located in the cerebellum [4]. It is a primitive embryonal tumor composed of densely packed small round cells, often forming **Homer-Wright rosettes** [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for SRBCTs:** "**MEN** **W**ill **L**ove **R**eal **S**ports" — **M**edulloblastoma, **E**wing’s Sarcoma, **N**euroblastoma, **W**ilms tumor, **L**ymphoma/Leukemia, **R**habdomyosarcoma [2], **S**mall cell carcinoma of lung. * **Haemangioblastoma Association:** Frequently associated with **von Hippel-Lindau (VHL) syndrome** and can produce erythropoietin, leading to secondary polycythemia [3]. * **Rosette Identification:** Homer-Wright rosettes (pseudorosettes with a central fibrillar tangles) are seen in Neuroblastoma and Medulloblastoma, whereas Flexner-Wintersteiner rosettes (true lumens) are characteristic of Retinoblastoma. **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. 211-212. [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. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 726-727. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315.

Question 160: Cancer cells derive nutrition from:

A. Glycolysis (Correct Answer)
B. Oxidative phosphorylation
C. Increase in mitochondria
D. From a fast food joint

Explanation: **Explanation:** The correct answer is **Glycolysis**. This phenomenon is known as the **Warburg Effect** (Aerobic Glycolysis) [3]. **1. Why Glycolysis is correct:** Even in the presence of ample oxygen, cancer cells shift their glucose metabolism away from the energy-efficient oxidative phosphorylation toward **aerobic glycolysis** [3]. While glycolysis produces significantly less ATP per glucose molecule (2 ATP vs. 36 ATP) [2], it provides the rapidly dividing tumor cells with metabolic intermediates (like carbon skeletons) necessary for the synthesis of cellular components such as nucleic acids, proteins, and lipids [1]. This metabolic reprogramming is a hallmark of cancer [3]. **2. Why the other options are incorrect:** * **Oxidative phosphorylation:** Although more efficient at producing ATP [2], cancer cells downregulate this pathway to prioritize the production of biosynthetic precursors needed for rapid growth [3]. * **Increase in mitochondria:** Cancer cells often exhibit mitochondrial dysfunction or alterations. They do not rely on an increased number of mitochondria for nutrition; rather, they rely on increased glucose uptake via upregulated **GLUT1 transporters** [3]. * **From a fast food joint:** This is a distractor and has no clinical relevance to cellular metabolism. **3. NEET-PG High-Yield Pearls:** * **Warburg Effect:** The clinical application of this effect is **PET Scanning (Positron Emission Tomography)**. Patients are injected with **18F-fluorodeoxyglucose (FDG)**, a glucose analogue. Because tumor cells have an insatiable "hunger" for glucose, they take up the FDG, allowing the primary tumor and metastases to be visualized. * **Key Driver:** The shift to aerobic glycolysis is often driven by signaling pathways like **PI3K/AKT** and the upregulation of transcription factors like **MYC** and **HIF-1̱** [1]. * **Autophagy:** In nutrient-deprived states, cancer cells may also use autophagy ("self-eating") to survive. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 308-310. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 56-57. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 26-27.

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