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Chromosome 16q24 deletion and decreased E‐cadherin expression: Possible association with metastatic potential in prostate cancer
Author(s) -
Pan Yi,
Matsuyama Hideyasu,
Wang Naining,
Yoshihiro Satoru,
Häggarth Lars,
Li Chunde,
Tribukait Bernhard,
Ekman Peter,
Bergerheim Ulf S.R.
Publication year - 1998
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19980615)36:1<31::aid-pros5>3.0.co;2-e
Subject(s) - prostate cancer , medicine , cadherin , prostate , cancer research , chromosome , oncology , biology , cancer , gene , pathology , genetics , cell
BACKGROUND Deletion of chromosome 16q is a frequent aberration in prostatic carcinoma, indicating the existence of candidate tumor suppressor genes involved in the pathogenesis of prostate cancer. METHODS Chromosome 16 numerical aberration and loss of 16q were studied by fluorescence in situ hybridization in 31 primary and 22 metastatic tumors from 53 patients. The results were compared with E‐cadherin expression, tumor grade and stage, and DNA ploidy. RESULTS Numerical chromosome 16 aberrations, 16q deletion, and loss of E‐cadherin expression were found in 29%, 35%, and 29% of the primary tumors, respectively, and in 73%, 73%, and 73% of the metastases, respectively. High tumor grade and DNA aneuploidy were also found to have significant correlation with metastases. CONCLUSIONS Deletion of chromosome 16q24 and/or loss of the E‐cadherin function appears in a high frequency in metastases of prostate cancer. The strong correlations suggest that they may be important risk factors, contributing to the metastatic potential of the tumor. Prostate 36:31–38, 1998. © 1998 Wiley‐Liss, Inc.