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Gain of androgen receptor gene copies in primary prostate cancer due to X chromosome polysomy
Author(s) -
Röpke Albrecht,
Erbersdobler Andreas,
Hammerer Peter,
Palisaar Jüri,
John Kerstin,
Stumm Markus,
Wieacker Peter
Publication year - 2003
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/pros.10356
Subject(s) - polysomy , antiandrogen , prostate cancer , androgen receptor , prostate , androgen , medicine , androgen deprivation therapy , prostatectomy , cancer research , oncology , cancer , endocrinology , biology , chromosome , gene , genetics , hormone , fluorescence in situ hybridization
Abstract BACKGROUND Prostate cancer is an androgen dependent tumor. In advanced prostate cancers androgen deprivation has proved to be an effective therapy, but 25% show no response. In this study prostatectomy specimens from patients without preoperative therapy were analyzed to determine the possible mechanism of primary antiandrogen resistance. METHODS The number of androgen receptor (AR) gene copies and X‐centromeres were investigated from 80 prostate cancer specimens by FISH analysis. RESULTS In 9 out of 80 prostate cancers additional X‐chromosomes with the corresponding AR gene could be detected. Polysomy of the X‐chromosome correlates with pathological classification and tumor volume. CONCLUSIONS Additional AR genes due to polysomy of the X‐chromosome are present in a subgroup of primary prostate cancers prior to antiandrogen therapy. Because the growth of prostate cancers is androgen dependent, these specimens may have an advantage in low concentrations of androgens. This may be a factor for initial antiandrogen resistance. © 2003 Wiley‐Liss, Inc.