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Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas
Objective: Sarcomatoid carcinomas of the lung are a group of aggressive tumors. It has been reported that losses of SMARCA4 and SMARCA2, which play a role in the repair and remodeling of chromatin, contribute to the initiation, progression, and differentiation of neoplasms. The aim of our study was...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Federation of Turkish Pathology Societies
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518200/ https://www.ncbi.nlm.nih.gov/pubmed/36178285 http://dx.doi.org/10.5146/tjpath.2022.01590 |
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author | Urer, Halide Nur Unver, Nurcan Fener, Neslihan |
author_facet | Urer, Halide Nur Unver, Nurcan Fener, Neslihan |
author_sort | Urer, Halide Nur |
collection | PubMed |
description | Objective: Sarcomatoid carcinomas of the lung are a group of aggressive tumors. It has been reported that losses of SMARCA4 and SMARCA2, which play a role in the repair and remodeling of chromatin, contribute to the initiation, progression, and differentiation of neoplasms. The aim of our study was to examine SMARCA4 and SMARCA2 profiles in sarcomatoid carcinomas of the lung. Material and Method: We screened pleomorphic carcinomas (PCs), carcinosarcomas (CSs), and pulmonary blastomas (PBs). The loss of SMARCA4 and SMARCA2 expression in the tumors was evaluated using immunohistochemical methods. The tumors were also examined to determine immunophenotype, histological tumor diagnosis, surgical resection, tumor histological component, largest tumor diameter, and lymph node metastasis status. Results: Sixty-nine cases were screened, of which 84% were PCs, 13% were CSs, and 2.8% were PBs. In PCs components, 84.4% were biphasic and 15.5% were monophasic. The PCs showed the most frequent loss of SMARCA4 (25.8%) and SMARCA2 (44.8%). A loss of SMARCA4 and SMARCA2, respectively, was detected in 14.2% and 24.4% in both components of biphasic PCs; 12.2% and 14.2% in the sarcoma component of biphasic PCs; 0% and 8.1% in the carcinoma component of biphasic PCs; 22.2% and 33.3% in monophasic PCs; 0% and 22.2% in both components of CSs; and 0% and 22.2% in the sarcoma component of CSs. Conclusion: These findings demonstrate a loss of expression of SMARCA4 and SMARCA2 in pulmonary sarcomatoid carcinomas. Loss of the SMARCA complex may be caused by the heterogeneous morphological profile of sarcomatoid carcinomas, independent of tumor histopathological parameters. |
format | Online Article Text |
id | pubmed-10518200 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Federation of Turkish Pathology Societies |
record_format | MEDLINE/PubMed |
spelling | pubmed-105182002023-09-25 Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas Urer, Halide Nur Unver, Nurcan Fener, Neslihan Turk Patoloji Derg Original Article Objective: Sarcomatoid carcinomas of the lung are a group of aggressive tumors. It has been reported that losses of SMARCA4 and SMARCA2, which play a role in the repair and remodeling of chromatin, contribute to the initiation, progression, and differentiation of neoplasms. The aim of our study was to examine SMARCA4 and SMARCA2 profiles in sarcomatoid carcinomas of the lung. Material and Method: We screened pleomorphic carcinomas (PCs), carcinosarcomas (CSs), and pulmonary blastomas (PBs). The loss of SMARCA4 and SMARCA2 expression in the tumors was evaluated using immunohistochemical methods. The tumors were also examined to determine immunophenotype, histological tumor diagnosis, surgical resection, tumor histological component, largest tumor diameter, and lymph node metastasis status. Results: Sixty-nine cases were screened, of which 84% were PCs, 13% were CSs, and 2.8% were PBs. In PCs components, 84.4% were biphasic and 15.5% were monophasic. The PCs showed the most frequent loss of SMARCA4 (25.8%) and SMARCA2 (44.8%). A loss of SMARCA4 and SMARCA2, respectively, was detected in 14.2% and 24.4% in both components of biphasic PCs; 12.2% and 14.2% in the sarcoma component of biphasic PCs; 0% and 8.1% in the carcinoma component of biphasic PCs; 22.2% and 33.3% in monophasic PCs; 0% and 22.2% in both components of CSs; and 0% and 22.2% in the sarcoma component of CSs. Conclusion: These findings demonstrate a loss of expression of SMARCA4 and SMARCA2 in pulmonary sarcomatoid carcinomas. Loss of the SMARCA complex may be caused by the heterogeneous morphological profile of sarcomatoid carcinomas, independent of tumor histopathological parameters. Federation of Turkish Pathology Societies 2023-05-15 /pmc/articles/PMC10518200/ /pubmed/36178285 http://dx.doi.org/10.5146/tjpath.2022.01590 Text en Copyright © 2023 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open-access article published by Federation of Turkish Pathology Societies under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is properly cited. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Original Article Urer, Halide Nur Unver, Nurcan Fener, Neslihan Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title | Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title_full | Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title_fullStr | Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title_full_unstemmed | Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title_short | Analysis of SMARCA4 and SMARCA2 Loss in Lung Sarcomatoid Carcinomas |
title_sort | analysis of smarca4 and smarca2 loss in lung sarcomatoid carcinomas |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518200/ https://www.ncbi.nlm.nih.gov/pubmed/36178285 http://dx.doi.org/10.5146/tjpath.2022.01590 |
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