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Discovery of new DNA amplification loci in prostate cancer by comparative genomic hybridization *
Author(s) -
El Gedaily Ahmed,
Bubendorf Lukas,
Willi Niels,
Fu Wenting,
Richter Jan,
Moch Holger,
Mihatsch Michael J.,
Sauter Guido,
Gasser Thomas C.
Publication year - 2001
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 - 10.1002/1097-0045(20010215)46:3<184::aid-pros1022>3.0.co;2-8
Subject(s) - comparative genomic hybridization , prostate cancer , biology , prostate , gene duplication , cancer , chromoplexy , gene , dna sequencing , genetics , cancer research , dna , copy number analysis , genome , copy number variation , pca3
Abstract Background DNA sequence amplifications are involved in the progression of many tumor types, and have also been found in advanced prostate cancer. The aim of this study was to detect new loci of DNA amplifications in prostate cancer. Methods Comparative genomic hybridization (CGH) was used for whole genome screening of DNA sequence copy number alterations in 27 advanced prostate cancers. Results The most prevalent changes were losses of 8p, 13q (52%, each), 6q (48%), 18q (37%), 5q (30%), 2q, 4q and 16q (26%, each), and gains of 8q (48%), Xq (40%), and Xp (26%). In addition, 16 high‐level amplifications were found. These included Xq12 (five), 8q24 (two), and 11q13 (one) with known putative target genes (androgen receptor, MYC and Cyclin D1), and 1q21‐25 (three), 10q22 (two), 17q23‐24 (two), and 8q21 (one) where the target genes remain unknown. Conclusions High‐level amplifications at different chromosomal sites occur in advanced prostate cancer. The detection of amplified chromosomal regions may serve as a starting point to discover novel oncogenes involved in prostate cancer progression. Prostate 46:184–190, 2001. © 2001 Wiley‐Liss, Inc.