title: Bax-interacting factor-1 expression in prostate cancer.
abstract: BACKGROUND
  Bax-interacting factor (Bif)-1 protein is a member of the endophilin B family that binds to and activates the proapoptotic Bax protein in response to apoptotic signals. Loss of Bif-1 suppresses the intrinsic pathway of apoptosis and promotes tumorigenesis. We examined the expression levels of Bif-1 protein in human prostate cancer.
  
  
  METHODS
  Thirty-nine archival tissue specimens of human prostate cancer, and a human prostate cancer tissue microarray containing 19 samples of normal prostate, 26 samples of benign prostatic hyperplasias (BPHs), 30 samples of high-grade prostatic intraepithelial neoplasia (PIN), and 153 samples of prostate cancer, were selected for immunohistochemical staining with Bif-1 antibody. The slides were scored by 2 independent observers.
  
  
  RESULTS
  Nontissue microarray samples: moderate to strong Bif-1 staining was identified in 38 of 39 prostate cancer samples. In 32 cases, foci of PIN were identified adjacent to prostate cancer samples. Of these, 29 samples (90.6%) showed strong and diffuse Bif-1 staining. Benign prostatic hyperplasias, identified in 27 cases, was weakly Bif-1 positive in 88.9% of cases. Tissue microarray samples: 38.6% (59 of 153) of prostate cancer samples showed moderate to strong Bif-1 expression, and 21.6% (33 of 153) were Bif-1 negative. Bif-1 expression was moderate to strong in 76.7% (23 of 30) of PIN. Bif-1 was weak to moderate in 53.8% (14 of 26) of BPH and negative in 46.2% (12 of 26) of them. Low to moderate Bif-1 was seen in 89.5% of normal prostate samples.
  
  
  CONCLUSIONS
  The loss of Bif-1 expression in a subset of prostate cancer samples is in agreement with the proapoptotic function of Bif-1. The significance of the increased Bif-1 in a subgroup of prostate cancer samples and in PIN remains to be determined. It seems that Bif-1 has a role in prostate cancer, providing the rationale for using Bif-1 as a target for prostate anticancer therapy.
authors.affiliation: Department of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612-9497, USA. coppold@moffitt.usf.edu
authors.forename: Domenico
authors.initials: D
authors.lastname: Coppola
authors.forename: Cecilia
authors.initials: C
authors.lastname: Oliveri
authors.forename: Zena
authors.initials: Z
authors.lastname: Sayegh
authors.forename: David
authors.initials: D
authors.lastname: Boulware
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Julio
authors.initials: J
authors.lastname: Pow-Sang
authors.forename: Julie Y
authors.initials: JY
authors.lastname: Djeu
authors.forename: Hong-Gang
authors.initials: HG
authors.lastname: Wang
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism*; D000230:Adenocarcinoma / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000918:Antibody Specificity; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011470:Prostatic Hyperplasia / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000378:metabolism*; D046888:Tissue Array Analysis
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C429293:SH3GLB1 protein, human