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Loss of heterozygosity on chromosome 2 in Japanese patients with prostate cancer
Author(s) -
Ueda Takeshi,
Komiya Akira,
Suzuki Hiroyoshi,
Shimbo Masaki,
Sakamoto Shinichi,
Imamoto Takashi,
Akakura Koichiro,
Shiraishi Taizo,
Ichikawa Tomohiko
Publication year - 2005
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.20228
Subject(s) - loss of heterozygosity , locus (genetics) , prostate cancer , biology , pathology , cancer research , microsatellite , chromosome , cancer , deletion mapping , prostate , primary tumor , allele , metastasis , genetics , gene , medicine
BACKGROUND Loss of heterozygosity (LOH) on chromosome 2 is thought to occur only occasionally in prostate cancer (PCa), but allelic losses in this region are frequent in other types of human cancer, such as lung, thyroid, head and neck, and cervix. Here, we show a high‐resolution deletion map of markers on chromosome 2 in Japanese patients with PCa. METHODS Tissue samples were obtained from 66 patients with PCa. DNA from normal, tumor, or metastatic tissue was used as the template for polymerase chain reaction amplification for LOH using 24 microsatellite markers on human chromosome 2. RESULTS Nineteen of the 66 cases (29%) showed LOH for at least one locus on chromosome 2. LOH on 2p was observed more frequently in cancer death cases than in organ confined and regional diseases ( P < 0.001). Paired DNAs were available from both primary and metastatic tumors in the eight cases of cancer death; among those pairs, we detected LOH on 2p in four primary tumors, and in all metastatic foci ( P < 0.05). Detailed deletion mapping in these tumors identified four distinct commonly deleted regions on 2p16.3, 2p12‐cent, 2q21.3, and 2q23.1‐2q32.1. CONCLUSIONS These results suggest that inactivation of putative tumor suppressor genes on chromosome 2 that may play an important role in the progression of Japanese patients with PCa. © 2005 Wiley‐Liss, Inc.