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Identification of a 1‐cM region of common deletion on 13q14 associated with human prostate cancer
Author(s) -
Ueda Takeshi,
Emi Mitsuru,
Suzuki Hiroyoshi,
Komiya Akira,
Akakura Koichiro,
Ichikawa Tomohiko,
Watanabe Masatoshi,
Shiraishi Taizo,
Masai Motoyuki,
Igarashi Tatsuo,
Ito Haruo
Publication year - 1999
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199903)24:3<183::aid-gcc2>3.0.co;2-j
Subject(s) - loss of heterozygosity , biology , prostate cancer , locus (genetics) , tumor suppressor gene , cancer research , cancer , prostate , primary tumor , ovarian cancer , breast cancer , pathology , allele , gene , metastasis , genetics , medicine , carcinogenesis
Frequent allelic losses on chromosome arm 13q are observed in carcinomas of the head and neck, breast, ovary, and pituitary gland. We analyzed 59 primary prostate tumors (stage B, 18 patients; C, 12 patients; D1, 4 patients; and endocrine therapy‐resistant cancer death, 25 patients), as well as 18 metastatic tissues from 14 of the 25 cancer death patients for loss of heterozygosity (LOH) using 35 microsatellite markers on chromosome arm 13q. Of the 59 primary tumors, 31 (53%) showed LOH involving at least one locus. Detailed deletion mapping identified a distinct commonly deleted region in the 1‐cM interval flanked by D13S153 and D13S273 on 13q14 and this region overlapped a part of the RB1 gene. Paired DNAs were available from both primary and metastatic tumors in the 14 cases of cancer death; among those pairs, we detected LOH on 13q in seven (50%) primary tumors, and in all metastatic foci (P = 0.0029). Moreover, the regions lost in metastatic tissues were more extensive than those seen in the corresponding primary tumors. These results suggest that inactivation of a putative tumor suppressor gene(s) including the RB1 gene on 13q14 plays an important role in human prostate cancer. Genes Chromosomes Cancer 24:183–190, 1999. © 1999 Wiley‐Liss, Inc.