BACKGROUND: The 16q23 locus has been recently suggested in both breast and prostate cancer to contain a gene involved in disease progression. The breast cancer antiestrogen resistance 1 (BCAR1) gene, located at 16q23, contributes to many cellular processes including migration and survival, and interacts in vitro with the growth factor receptor EGFR and the metastasis suppressor KAI1. METHODS: BCAR1, EGFR, and KAI1 expression was studied by immunohistochemistry on a tissue microarray containing 100 localized prostate cancers (LPC), 15 hormone refractory prostate cancers (HRPC), and 15 lymph node metastasis (LNM). Forty eight of the LPC were also analyzed for 16q23 LOH status using microsatellite markers. RESULTS: BCAR1 staining was present in 25% of LPC, associated with higher Gleason score, and in 60% and 80% of, respectively, LNM and HRPC. BCAR1 expression was inversely correlated with 16q23 LOH status (P < 0.001), and was associated with high EGFR staining (P < 0.02), and negative KAI1 expression (P < 0.01). CONCLUSIONS: BCAR1 expression in LPC seems to be regulated at least in part by genetic events. The increased expression of BCAR1 with disease progression suggests a potential interest for both prognosis and treatment. (c) 2006 Wiley-Liss, Inc.
BACKGROUND: The 16q23 locus has been recently suggested in both breast and prostate cancer to contain a gene involved in disease progression. The breast cancer antiestrogen resistance 1 (BCAR1) gene, located at 16q23, contributes to many cellular processes including migration and survival, and interacts in vitro with the growth factor receptor EGFR and the metastasis suppressor KAI1. METHODS:BCAR1, EGFR, and KAI1 expression was studied by immunohistochemistry on a tissue microarray containing 100 localized prostate cancers (LPC), 15 hormone refractory prostate cancers (HRPC), and 15 lymph node metastasis (LNM). Forty eight of the LPC were also analyzed for 16q23 LOH status using microsatellite markers. RESULTS:BCAR1 staining was present in 25% of LPC, associated with higher Gleason score, and in 60% and 80% of, respectively, LNM and HRPC. BCAR1 expression was inversely correlated with 16q23 LOH status (P < 0.001), and was associated with high EGFR staining (P < 0.02), and negative KAI1 expression (P < 0.01). CONCLUSIONS:BCAR1 expression in LPC seems to be regulated at least in part by genetic events. The increased expression of BCAR1 with disease progression suggests a potential interest for both prognosis and treatment. (c) 2006 Wiley-Liss, Inc.
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