Prostatic basal cell carcinoma is a malignant neoplasm composed of basaloid cells forming infiltrative nests and tubules, which may potentially be misdiagnosed as benign basal cell proliferations (i.e., florid basal cell hyperplasia or basal cell adenoma) and also closely resembles adenoid cystic carcinoma of the salivary gland. MYB-NFIB gene rearrangement occurs in 30-86% of salivary gland adenoid cystic carcinomas. We sought to further characterize MYB gene rearrangement in prostatic basal cell carcinoma and correlate MYB-NFIB fusion status with other clinicopathologic characteristics. To this end, FISH analysis for MYB-NFIB gene fusion using fusion probes was performed on formalin-fixed, paraffin-embedded tissue sections from prostatic basal cell carcinoma (n = 30), florid basal cell hyperplasia (n = 18), and basal cell adenoma (n = 4). Fourteen of 30 (47%) cases of basal cell carcinoma were positive for MYB-NFIB gene fusion FISH, and no cases of benign basal cell proliferations were positive (p < 0.05). FISH-positive patients (mean age = 63 years, range: 35-81) tended to be younger than FISH-negative patients (mean age = 70 years, range: 55-93). Most FISH-positive cases demonstrated adenoid cystic carcinoma-like morphology (57%), and most FISH-negative cases demonstrated nonadenoid cystic carcinoma-like morphology (93%); one case (FISH-positive) demonstrated areas with both adenoid cystic carcinoma-like and nonadenoid cystic carcinoma-like morphology. FISH-positive cases more frequently demonstrated perineural invasion (50% vs. 14%, p < 0.05) compared to FISH-negative cases. Conversely, tall basal cells (i.e., neoplastic cells at least two times taller than wide) were more frequent in FISH-negative cases than FISH-positive cases (93% vs. 36%, p < 0.05). Approximately, 50% of prostatic basal cell carcinoma harbor MYB-NFIB gene fusion. The majority of these cases were characterized by adenoid cystic carcinoma-like morphology, perineural invasion, and lack tall basal cells. Florid basal cell hyperplasia and basal cell adenoma are negative for MYB-NFIB gene fusion.

Department of Pathology and Laboratory Medicine and Henry Ford Cancer Institute Henry Ford Health System Detroit MI USA Departmentof Pathology Wayne State University School of Medicine Detroit MI USA

Department of Pathology and Laboratory Medicine Indiana University School of Medicine Indianapolis IN USA

Department of Pathology Charles University Hospital Plzeň Pilsen Czech Republic

Department of Pathology Cordoba University Faculty of Medicine Cordoba Spain Champalimaud Clinical Center Lisbon Portugal

Department of Pathology Medical College of Wisconsin Milwaukee WI USA

Department of Pathology Northwestern University Chicago IL USA

Departments of Pathology and Urology Emory University Atlanta GA USA

Institute of Pathological Anatomy and Histopathology School of Medicine Polytechnic University of the Marche Region and United Hospitals Ancona Italy

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$a Magers, Martin J $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

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$a MYB-NFIB gene fusion in prostatic basal cell carcinoma: clinicopathologic correlates and comparison with basal cell adenoma and florid basal cell hyperplasia / $c MJ. Magers, KA. Iczkowski, R. Montironi, DJ. Grignon, S. Zhang, SR. Williamson, X. Yang, M. Wang, AO. Osunkoya, A. Lopez-Beltran, O. Hes, JN. Eble, L. Cheng,

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$a Prostatic basal cell carcinoma is a malignant neoplasm composed of basaloid cells forming infiltrative nests and tubules, which may potentially be misdiagnosed as benign basal cell proliferations (i.e., florid basal cell hyperplasia or basal cell adenoma) and also closely resembles adenoid cystic carcinoma of the salivary gland. MYB-NFIB gene rearrangement occurs in 30-86% of salivary gland adenoid cystic carcinomas. We sought to further characterize MYB gene rearrangement in prostatic basal cell carcinoma and correlate MYB-NFIB fusion status with other clinicopathologic characteristics. To this end, FISH analysis for MYB-NFIB gene fusion using fusion probes was performed on formalin-fixed, paraffin-embedded tissue sections from prostatic basal cell carcinoma (n = 30), florid basal cell hyperplasia (n = 18), and basal cell adenoma (n = 4). Fourteen of 30 (47%) cases of basal cell carcinoma were positive for MYB-NFIB gene fusion FISH, and no cases of benign basal cell proliferations were positive (p < 0.05). FISH-positive patients (mean age = 63 years, range: 35-81) tended to be younger than FISH-negative patients (mean age = 70 years, range: 55-93). Most FISH-positive cases demonstrated adenoid cystic carcinoma-like morphology (57%), and most FISH-negative cases demonstrated nonadenoid cystic carcinoma-like morphology (93%); one case (FISH-positive) demonstrated areas with both adenoid cystic carcinoma-like and nonadenoid cystic carcinoma-like morphology. FISH-positive cases more frequently demonstrated perineural invasion (50% vs. 14%, p < 0.05) compared to FISH-negative cases. Conversely, tall basal cells (i.e., neoplastic cells at least two times taller than wide) were more frequent in FISH-negative cases than FISH-positive cases (93% vs. 36%, p < 0.05). Approximately, 50% of prostatic basal cell carcinoma harbor MYB-NFIB gene fusion. The majority of these cases were characterized by adenoid cystic carcinoma-like morphology, perineural invasion, and lack tall basal cells. Florid basal cell hyperplasia and basal cell adenoma are negative for MYB-NFIB gene fusion.

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$a Iczkowski, Kenneth A $u Department of Pathology, Medical College of Wisconsin, Milwaukee, WI, USA.

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$a Montironi, Rodolfo $u Institute of Pathological Anatomy and Histopathology, School of Medicine, Polytechnic University of the Marche Region and United Hospitals, Ancona, Italy.

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$a Grignon, David J $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

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$a Zhang, Shaobo $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

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$a Williamson, Sean R $u Department of Pathology and Laboratory Medicine and Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, USA. Departmentof Pathology, Wayne State University School of Medicine, Detroit, MI, USA.

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$a Yang, Ximing $u Department of Pathology, Northwestern University, Chicago, IL, USA.

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$a Wang, Mingsheng $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

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$a Osunkoya, Adeboye O $u Departments of Pathology and Urology, Emory University, Atlanta, GA, USA.

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$a Lopez-Beltran, Antonio $u Department of Pathology, Cordoba University Faculty of Medicine, Cordoba, Spain. Champalimaud Clinical Center, Lisbon, Portugal.

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$a Hes, Ondrej $u Department of Pathology, Charles University Hospital Plzeň, Pilsen, Czech Republic.

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$a Eble, John N $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

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$a Cheng, Liang $u Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA. liang_cheng@yahoo.com.

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$w MED00003380 $t Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc $x 1530-0285 $g Roč. 32, č. 11 (2019), s. 1666-1674

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