PMID- 22024950
OWN - NLM
STAT- MEDLINE
DCOM- 20120709
LR  - 20120511
IS  - 1097-0045 (Electronic)
IS  - 0270-4137 (Linking)
VI  - 72
IP  - 9
DP  - 2012 Jun 15
TI  - Prognostic relevance of Bcl-2 overexpression in surgically treated prostate 
      cancer is not caused by increased copy number or translocation of the gene.
PG  - 991-7
LID - 10.1002/pros.21504 [doi]
AB  - BACKGROUND: Overexpression of anti-apoptotic Bcl-2 plays a role in prostate 
      cancer progression, particularly in transformation to androgen-independent 
      disease. Androgen-independent prostate cancers have been shown to harbor Bcl-2 
      gene copy number gains frequently suggesting that this genetic alteration might 
      play a role in Bcl-2 overexpression. The relation of Bcl-2 overexpression and 
      copy number gains or translocation of the BCL-2 gene in prostate cancer under 
      hormone-naive conditions is unknown. METHODS: Prostate cancers of 3,261 
      hormone-naive patients undergoing radical prostatectomy were arrayed in a TMA 
      with one tissue core (diameter 0.6 mm) per tumor. Bcl-2 immunohistochemistry, 
      analyzed for Bcl-2 expression level (negative, low, and high), was correlated 
      with clinical, histopathological and molecular (Ki67, p53) tumor features, and 
      biochemical failure. Cancers with high-level Bcl-2 expression were evaluated for 
      genetic aberrations by fluorescence in situ hybridization (FISH). RESULTS: Bcl-2 
      expression was significantly up-regulated in tumors with aggressive phenotype as 
      indicated by high Gleason score (P < 0.0001), advanced stage (P < 0.0001), and 
      high proliferation index (P = 0.0114). The different Bcl-2 expression levels 
      translated into significantly different survival curves showing better outcome 
      for patients with lower Bcl-2 levels. The prognostic information obtained from 
      the anti-apoptotic Bcl-2 was independent from the proliferation index (Ki67) of 
      the cancer. FISH analysis detected no copy number gains or translocation of the 
      Bcl-2 gene. CONCLUSION: Bcl-2 overexpression in prostate cancers under 
      hormone-naive conditions is not associated with increased copy numbers of the 
      gene. This suggests that these frequently detected genetic alterations in 
      androgen-independent tumors occur late in prostate cancer progression.
CI  - Copyright (c) 2011 Wiley Periodicals, Inc.
FAU - Fleischmann, A
AU  - Fleischmann A
AD  - Department of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, 
      Germany. achim.fleischmann@pathology.unibe.ch
FAU - Huland, H
AU  - Huland H
FAU - Mirlacher, M
AU  - Mirlacher M
FAU - Wilczak, W
AU  - Wilczak W
FAU - Simon, R
AU  - Simon R
FAU - Erbersdobler, A
AU  - Erbersdobler A
FAU - Sauter, G
AU  - Sauter G
FAU - Schlomm, T
AU  - Schlomm T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111024
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
SB  - IM
MH  - Aged
MH  - Disease Progression
MH  - Gene Dosage/*genetics
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Prostatic Neoplasms/*genetics/metabolism/*surgery
MH  - Proto-Oncogene Proteins c-bcl-2/*biosynthesis/*genetics/physiology
MH  - Translocation, Genetic/*physiology
EDAT- 2011/10/26 06:00
MHDA- 2012/07/10 06:00
CRDT- 2011/10/26 06:00
PHST- 2011/07/26 00:00 [received]
PHST- 2011/09/29 00:00 [accepted]
PHST- 2011/10/26 06:00 [entrez]
PHST- 2011/10/26 06:00 [pubmed]
PHST- 2012/07/10 06:00 [medline]
AID - 10.1002/pros.21504 [doi]
PST - ppublish
SO  - Prostate. 2012 Jun 15;72(9):991-7. doi: 10.1002/pros.21504. Epub 2011 Oct 24.