Morphological features of TMPRSS2–ERG gene fusion prostate cancer No conflicts of interest were declared.
dc.contributor.author | Mosquera, J-M. | en_US |
dc.contributor.author | Perner, Sven | en_US |
dc.contributor.author | Demichelis, F. | en_US |
dc.contributor.author | Kim, R. | en_US |
dc.contributor.author | Hofer, M. D. | en_US |
dc.contributor.author | Mertz, K. D. | en_US |
dc.contributor.author | Paris, P. L. | en_US |
dc.contributor.author | Simko, J. | en_US |
dc.contributor.author | Collins, C. | en_US |
dc.contributor.author | Bismar, T. A. | en_US |
dc.contributor.author | Chinnaiyan, Arul M. | en_US |
dc.contributor.author | Rubin, Mark A. | en_US |
dc.date.accessioned | 2007-09-20T18:41:04Z | |
dc.date.available | 2008-09-08T14:25:14Z | en_US |
dc.date.issued | 2007-05 | en_US |
dc.identifier.citation | Mosquera, J-M; Perner, S; Demichelis, F; Kim, R; Hofer, MD; Mertz, KD; Paris, PL; Simko, J; Collins, C; Bismar, TA; Chinnaiyan, AM; Rubin, MA (2007)."Morphological features of TMPRSS2–ERG gene fusion prostate cancer No conflicts of interest were declared. ." The Journal of Pathology 212(1): 91-101. <http://hdl.handle.net/2027.42/56053> | en_US |
dc.identifier.issn | 0022-3417 | en_US |
dc.identifier.issn | 1096-9896 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/56053 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17385188&dopt=citation | en_US |
dc.description.abstract | The TMPRSS2–ETS fusion prostate cancers comprise 50–70% of the prostate-specific antigen (PSA)-screened hospital-based prostate cancers examined to date, making it perhaps the most common genetic rearrangement in human cancer. The most common variant involves androgen-regulated TMPRSS2 and ERG , both located on chromosome 21. Emerging data from our group and others suggests that TMPRSS2–ERG fusion prostate cancer is associated with higher tumour stage and prostate cancer-specific death. The goal of this study was to determine if this common somatic alteration is associated with a morphological phenotype. We assessed 253 prostate cancer cases for TMPRSS2–ERG fusion status using an ERG break-apart FISH assay. Blinded to gene fusion status, two reviewers assessed each tumour for presence or absence of eight morphological features. Statistical analysis was performed to look for significant associations between morphological features and TMPRSS2–ERG fusion status. Five morphological features were associated with TMPRSS2–ERG fusion prostate cancer: blue-tinged mucin, cribriform growth pattern, macronucleoli, intraductal tumour spread, and signet-ring cell features, all with p -values < 0.05. Only 24% ( n = 30/125) of tumours without any of these features displayed the TMPRSS2–ERG fusion. By comparison, 55% ( n = 38/69) of cases with one feature (RR = 3.88), 86% ( n = 38/44) of cases with two features (RR = 20.06), and 93% ( n = 14/15) of cases with three or more features (RR = 44.33) were fusion positive ( p < 0.001). To our knowledge, this is the first study that demonstrates a significant link between a molecular alteration in prostate cancer and distinct phenotypic features. The strength of these findings is similar to microsatellite unstable colon cancer and breast cancer involving BRCA1 and BRCA2 mutations. The biological effect of TMPRSS2–ERG overexpression may drive pathways that favour these common morphological features that pathologists observe daily. These features may also be helpful in diagnosing TMPRSS2–ERG fusion prostate cancer, which may have both prognostic and therapeutic implications. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. | en_US |
dc.format.extent | 931794 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | John Wiley & Sons, Ltd. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cancer Research, Oncology and Pathology | en_US |
dc.title | Morphological features of TMPRSS2–ERG gene fusion prostate cancer No conflicts of interest were declared. | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Pathology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Departments of Pathology and Urology, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA ; University of Ulm, Department of Pathology, Ulm, Germany | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA ; ITC-irst, SRA Division, Bioinformatics Group, Povo, Trento, Italy | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA | en_US |
dc.contributor.affiliationother | Comprehensive Cancer Center, University of California, San Francisco, CA, USA | en_US |
dc.contributor.affiliationother | Comprehensive Cancer Center, University of California, San Francisco, CA, USA | en_US |
dc.contributor.affiliationother | Comprehensive Cancer Center, University of California, San Francisco, CA, USA | en_US |
dc.contributor.affiliationother | Departments of Pathology and Oncology, McGill University Faculty of Medicine, Montreal, QC, Canada | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA ; Harvard Medical School, Boston, MA, USA ; Broad Institute of MIT and Harvard Medical School, Cambridge, MA, USA ; Dana Farber Harvard Comprehensive Cancer Center, Boston, MA, USA ; Department of Pathology, Brigham and Women's Hospital/Harvard Medical School, 221 Longwood Avenue, EBRC 442A, Boston, MA 02115-6110, USA. | en_US |
dc.identifier.pmid | 17385188 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/56053/1/2154_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/path.2154 | en_US |
dc.identifier.source | The Journal of Pathology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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