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Molecular cytogenetic identification of cyclin D1 gene amplification in a renal pelvic tumor attributed to phenacetin abuse
Author(s) -
Lee Chyi Chia R.,
Wanibuchi Hideki,
Yamamoto Shinji,
Hirose Masao,
Hayashi Yutaro,
Fukushima Shoji
Publication year - 1999
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.1999.00902.x
Subject(s) - cyclin d1 , fluorescence in situ hybridization , biology , cancer research , immunohistochemistry , gene duplication , carcinoma , pathology , ploidy , chromosome , gene , microbiology and biotechnology , medicine , cell cycle , genetics
Despite extensive epidemiologic evidence of phenacetin abuse as a risk factor for renal pelvic carcinomas, genetic alterations in the resultant tumors remain largely unclear. In this report, a phenacetin‐associated renal pelvic carcinoma (histologically a transitional‐cell carcinoma) from an 80‐year‐old female patient was evaluated by molecular cytogenetic methods. Fluorescence in situ hybridization was used to identify chromosome gains or losses for the cyclin D1 , p53 , Rb and c‐myc genes and the ploidy of their respective chromosomes. Cyclin D1 gene amplification, but normal copy numbers of p53 , Rb and c‐myc , and normal ploidy of chromosomes 8, 11, 13 and 17 were observed. Expression of cyclin D1 protein was confirmed by immunohistochemistry. In the absence of p53 , Rb or c‐myc abnormalities, the results suggested that cyclin D1 gene amplification and its protein overexpression may be involved in the genesis of renal pelvic carcinomas associated with phenacetin abuse.