• Something wrong with this record ?

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,

. 2016 ; 469 (3) : 321-30. [pub] 20160623

Language English Country Germany

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc17013747
E-resources Online Full text

NLK ProQuest Central from 2003-01-01 to 1 year ago
Medline Complete (EBSCOhost) from 2011-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest) from 2003-01-01 to 1 year ago
Health & Medicine (ProQuest) from 2003-01-01 to 1 year ago

Links

PubMed 27339451
DOI 10.1007/s00428-016-1977-y
Knihovny.cz E-resources

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.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc17013747
003      
CZ-PrNML
005      
20170418105557.0
007      
ta
008      
170413s2016 gw f 000 0|eng||
009      
AR
024    7_
$a 10.1007/s00428-016-1977-y $2 doi
035    __
$a (PubMed)27339451
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a gw
100    1_
$a Agaimy, Abbas $u Institute of Pathology, University Hospital of Erlangen, Krankenhausstrasse 8-10, 91054, Erlangen, Germany. abbas.agaimy@uk-erlangen.de. $7 gn_A_00002061
245    10
$a Loss of expression of the SWI/SNF complex is a frequent event in undifferentiated/dedifferentiated urothelial carcinoma of the urinary tract / $c A. Agaimy, S. Bertz, L. Cheng, O. Hes, K. Junker, B. Keck, A. Lopez-Beltran, M. Stöckle, B. Wullich, A. Hartmann,
520    9_
$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.
650    _2
$a dospělí $7 D000328
650    _2
$a senioři $7 D000368
650    _2
$a senioři nad 80 let $7 D000369
650    _2
$a karcinom z přechodných buněk $x metabolismus $x patologie $7 D002295
650    _2
$a DNA-helikasy $x metabolismus $7 D004265
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a lidé $7 D006801
650    _2
$a imunohistochemie $x metody $7 D007150
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a lidé středního věku $7 D008875
650    _2
$a jaderné proteiny $x metabolismus $7 D009687
650    _2
$a rhabdoidní nádor $x diagnóza $x metabolismus $x patologie $7 D018335
650    _2
$a gen SMARCB1 $x metabolismus $7 D000071796
650    _2
$a transkripční faktory $x metabolismus $7 D014157
650    _2
$a močové ústrojí $x metabolismus $x patologie $7 D014551
650    _2
$a urologické nádory $x diagnóza $x metabolismus $x patologie $7 D014571
655    _2
$a časopisecké články $7 D016428
700    1_
$a Bertz, Simone $u Institute of Pathology, University Hospital of Erlangen, Krankenhausstrasse 8-10, 91054, Erlangen, Germany.
700    1_
$a Cheng, Liang $u Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
700    1_
$a Hes, Ondrej $u Sikl's Department of Pathology, Charles University, Medical Faculty Hospital, Pilsen, Czech Republic.
700    1_
$a Junker, Kerstin $u Department of Urology and Pediatric Urology, Saarland University, Homburg, Saar, Germany.
700    1_
$a Keck, Bastian $u Department of Urology, University Hospital of Erlangen, Erlangen, Germany.
700    1_
$a Lopez-Beltran, Antonio $u Department of Pathology, Champalimaud Clinical Center, Lisbon, Portugal.
700    1_
$a Stöckle, Michael $u Department of Urology and Pediatric Urology, Saarland University, Homburg, Saar, Germany.
700    1_
$a Wullich, Bernd $u Department of Urology, University Hospital of Erlangen, Erlangen, Germany.
700    1_
$a Hartmann, Arndt $u Institute of Pathology, University Hospital of Erlangen, Krankenhausstrasse 8-10, 91054, Erlangen, Germany.
773    0_
$w MED00004660 $t Virchows Archiv an international journal of pathology $x 1432-2307 $g Roč. 469, č. 3 (2016), s. 321-30
856    41
$u https://pubmed.ncbi.nlm.nih.gov/27339451 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20170413 $b ABA008
991    __
$a 20170418105905 $b ABA008
999    __
$a ok $b bmc $g 1200212 $s 974525
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2016 $b 469 $c 3 $d 321-30 $e 20160623 $i 1432-2307 $m Virchows Archiv $n Virchows Arch $x MED00004660
LZP    __
$a Pubmed-20170413

Find record

Citation metrics

Archiving options