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Loss of expression of the SWI/SNF complex is a frequent event in undifferentiated/dedifferentiated urothelial carcinoma of the urinary tract
A. Agaimy, S. Bertz, L. Cheng, O. Hes, K. Junker, B. Keck, A. Lopez-Beltran, M. Stöckle, B. Wullich, A. Hartmann,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články
NLK
ProQuest Central
od 2003-01-01 do Před 1 rokem
Medline Complete (EBSCOhost)
od 2011-01-01 do Před 1 rokem
Nursing & Allied Health Database (ProQuest)
od 2003-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2003-01-01 do Před 1 rokem
- MeSH
- DNA-helikasy metabolismus MeSH
- dospělí MeSH
- gen SMARCB1 metabolismus MeSH
- imunohistochemie metody MeSH
- jaderné proteiny metabolismus MeSH
- karcinom z přechodných buněk metabolismus patologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- močové ústrojí metabolismus patologie MeSH
- rhabdoidní nádor diagnóza metabolismus patologie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- transkripční faktory metabolismus MeSH
- urologické nádory diagnóza metabolismus patologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
Loss of the SWI/SNF chromatin remodeling complex has been recently implicated in the pathogenesis of dedifferentiated carcinomas from different organs, but its possible role in undifferentiated urothelial carcinoma (UC) has not been studied to date. In this study, we analyzed by immunohistochemistry 14 undifferentiated UCs (11 from bladder and 3 from renal pelvis) with a nondescript anaplastic or rhabdoid morphology, using commercially available antibodies against the SWI/SNF components SMARCB1 (INI1), SMARCA2, SMARCA4, SMARCC1, SMARCC2, and ARID1A. Patients were eight females and six males aged 40 to 84 years (median, 65). All tumors were muscle-invasive (9 were T3-4). A conventional UC component was seen in eight cases and varied from in situ to papillary. The undifferentiated component comprised 60-100 % of the tumors. Histologically, most tumors showed diffuse dyscohesive or pseudoalveolar growth of variably sized cells with frequent rhabdoid features. Transition from conventional to undifferentiated UC was abrupt, except in one case. The undifferentiated component almost always expressed pan-cytokeratin AE1/AE3 (13/14) and variably vimentin (8/14) and GATA3 (9/14). Complete loss of at least one SWI/SNF subunit limited to the undifferentiated component was detected in 10/14 cases (71 %). SMARCA2 was most frequently lost (six) followed by ARID1A (four), SMARCB1/INI1 (two), SMARCA4 (one), and SMARCC1 (one). This is the first study exploring SWI/SNF expression in undifferentiated UC of the urinary tract. Our results are in line with recent studies reporting involvement of the SWI/SNF complex in the dedifferentiation process of a variety of epithelial neoplasms in different organs, including the urinary tract, and association with aggressive clinical course.
Department of Pathology Champalimaud Clinical Center Lisbon Portugal
Department of Urology and Pediatric Urology Saarland University Homburg Saar Germany
Department of Urology University Hospital of Erlangen Erlangen Germany
Indiana University School of Medicine Indianapolis IN 46202 USA
Sikl's Department of Pathology Charles University Medical Faculty Hospital Pilsen Czech Republic
Citace poskytuje Crossref.org
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- $a Loss of the SWI/SNF chromatin remodeling complex has been recently implicated in the pathogenesis of dedifferentiated carcinomas from different organs, but its possible role in undifferentiated urothelial carcinoma (UC) has not been studied to date. In this study, we analyzed by immunohistochemistry 14 undifferentiated UCs (11 from bladder and 3 from renal pelvis) with a nondescript anaplastic or rhabdoid morphology, using commercially available antibodies against the SWI/SNF components SMARCB1 (INI1), SMARCA2, SMARCA4, SMARCC1, SMARCC2, and ARID1A. Patients were eight females and six males aged 40 to 84 years (median, 65). All tumors were muscle-invasive (9 were T3-4). A conventional UC component was seen in eight cases and varied from in situ to papillary. The undifferentiated component comprised 60-100 % of the tumors. Histologically, most tumors showed diffuse dyscohesive or pseudoalveolar growth of variably sized cells with frequent rhabdoid features. Transition from conventional to undifferentiated UC was abrupt, except in one case. The undifferentiated component almost always expressed pan-cytokeratin AE1/AE3 (13/14) and variably vimentin (8/14) and GATA3 (9/14). Complete loss of at least one SWI/SNF subunit limited to the undifferentiated component was detected in 10/14 cases (71 %). SMARCA2 was most frequently lost (six) followed by ARID1A (four), SMARCB1/INI1 (two), SMARCA4 (one), and SMARCC1 (one). This is the first study exploring SWI/SNF expression in undifferentiated UC of the urinary tract. Our results are in line with recent studies reporting involvement of the SWI/SNF complex in the dedifferentiation process of a variety of epithelial neoplasms in different organs, including the urinary tract, and association with aggressive clinical course.
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