PMID- 23661613 OWN - NLM STAT- MEDLINE DCOM- 20131030 LR - 20211021 IS - 1097-0045 (Electronic) IS - 0270-4137 (Print) IS - 0270-4137 (Linking) VI - 73 IP - 13 DP - 2013 Sep TI - Immunohistochemical expression of ERG in the molecular epidemiology of fatal prostate cancer study. PG - 1371-7 LID - 10.1002/pros.22684 [doi] AB - BACKGROUND: Gene fusions between the ERG transcription factor and the androgen-regulated gene TMPRSS2 occur in a subset of prostate cancers and contribute to transformation of prostatic epithelial cells. Prior reports have used fluorescence in situ hybridization (FISH) or quantitative PCR (QPCR) to determine the presence of TMPRSS2-ERG fusions or ERG expression, respectively. Recently, several groups have reported on immunohistochemistry (IHC) to measure ERG expression, which is much more readily performed in clinical practice. However, the prior studies examining ERG expression by IHC had small sample sizes or they failed to clarify the association of ERG protein expression with important clinico-pathological features or prostate cancer-specific mortality. METHODS: To address these deficits, we evaluated ERG expression by IHC in 208 radical prostatectomy samples from the Kaiser Permanente Molecular Epidemiology of Fatal Prostate Cancer (MEFPC) study, a case-control study of prostate cancer-specific mortality. RESULTS: Nuclear ERG expression was seen in neoplastic prostate epithelia in 49 of the samples (23.7%). ERG expression in tumor cells was associated with higher tumor stage (OR = 2.0, 95% confidence interval 1.0-4.0, P value = 0.04). ERG immunoreactivity was positively associated with prostate cancer-specific mortality, although the confidence interval was wide (OR = 1.9, 95% confidence interval 0.88-4.0, P value = 0.10). CONCLUSIONS: Our results demonstrate that ERG protein expression is readily quantifiable with an existing commercial antibody. Evaluating ERG protein expression may improve our ability to identify the subset of more aggressive, invasive prostate cancers. CI - (c) 2013 Wiley Periodicals, Inc. FAU - Weinmann, Sheila AU - Weinmann S AD - The Center for Health Research, Kaiser Permanente Northwest, Portland, Oregon 97227, USA. Sheila.Weinmann@kpchr.org FAU - Van Den Eeden, Stephen K AU - Van Den Eeden SK FAU - Haque, Reina AU - Haque R FAU - Chen, Chuhe AU - Chen C FAU - Richert-Boe, Kathryn AU - Richert-Boe K FAU - Schwartzman, Jacob AU - Schwartzman J FAU - Gao, Lina AU - Gao L FAU - Berry, Deborah L AU - Berry DL FAU - Kallakury, Bhaskar V S AU - Kallakury BV FAU - Alumkal, Joshi J AU - Alumkal JJ LA - eng GR - KL2 RR024141/RR/NCRR NIH HHS/United States GR - R01 CA100743/CA/NCI NIH HHS/United States GR - UL1 RR024140/RR/NCRR NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20130509 PL - United States TA - Prostate JT - The Prostate JID - 8101368 RN - 0 (ERG protein, human) RN - 0 (Oncogene Proteins, Fusion) RN - 0 (TMPRSS2-ERG fusion protein, human) RN - 0 (Trans-Activators) RN - 0 (Transcriptional Regulator ERG) SB - IM MH - Adult MH - Aged MH - Case-Control Studies MH - Humans MH - Immunohistochemistry MH - Male MH - Middle Aged MH - Oncogene Proteins, Fusion/*metabolism MH - Prostate/*metabolism/pathology/surgery MH - Prostatectomy MH - Prostatic Neoplasms/*metabolism/*mortality/pathology MH - Trans-Activators/*metabolism MH - Transcriptional Regulator ERG PMC - PMC3745520 MID - NIHMS469395 OTO - NOTNLM OT - biomarker OT - case-control OT - lethal prostate cancer COIS- Conflict of Interest Statement: There are no conflicts of interest to disclose. EDAT- 2013/05/11 06:00 MHDA- 2013/10/31 06:00 PMCR- 2014/09/01 CRDT- 2013/05/11 06:00 PHST- 2012/11/21 00:00 [received] PHST- 2013/04/08 00:00 [accepted] PHST- 2013/05/11 06:00 [entrez] PHST- 2013/05/11 06:00 [pubmed] PHST- 2013/10/31 06:00 [medline] PHST- 2014/09/01 00:00 [pmc-release] AID - 10.1002/pros.22684 [doi] PST - ppublish SO - Prostate. 2013 Sep;73(13):1371-7. doi: 10.1002/pros.22684. Epub 2013 May 9.