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Allelic loss on chromosomes 8p, 22q and 18q (DCC) in human prostate cancer
Author(s) -
Crundwell Malcolm C.,
Chughtai Shaheen,
Knowles Margaret,
Takle Lindsay,
Luscombe Mike,
Neoptolemos John P.,
Morton Dion G.,
Phillips Stewart M. A.
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960822)69:4<295::aid-ijc10>3.0.co;2-5
Subject(s) - loss of heterozygosity , locus (genetics) , biology , prostate cancer , allele , cancer research , carcinogenesis , tumor suppressor gene , prostate , chromosome , metastasis , hyperplasia , genetics , gene , cancer , endocrinology
Previous studies have suggested the involvement of tumour‐suppressor genes on chromosomes 8p, 22q and 18q ( DCC ) in prostate cancer. The aim of this study was to further characterize these regions. We investigated 20 polymorphic regions on the 3 chromosome arms in 43 cancers and 10 cases of benign prostatic hyperplasia (BPH). Allelic loss was observed in 72% of cancers on 8p, 16% on 22q and 24% at DCC . For BPH, loss was observed in 20% on 8p and in 12% at DCC . The low incidence of LOH on 22q implies that this locus has no significant role in prostate carcinogenesis. At DCC , although the overall incidence was low, tumours with LOH were mostly of high grade or had metastases, suggesting a role for this gene in prostate cancer progression. On chromosome 8p, 29% of cancers had deletions at the LPL locus on 8p22 and 60% had deletions within a region flanked by the markers D8S339 and ANKI on 8p11.1‐p21.1. Within this region, 2 distinct areas of allelic loss were observed, at one or both ANKI and D8S255, and in the region defined by the markers D8S259‐D8S505. For the regions 8p22 and ANKI ‐D8S255, tumours with metastases had a greater frequency of LOH compared to non‐metastasizing tumours, suggesting the presence of putative metastasis‐suppressor genes in these regions. © 1996 Wiley‐Liss, Inc.