Premium
Very frequent loss of heterozygosity throughout chromosome 17 in sporadic ovarian carcinoma
Author(s) -
Foulkes William D.,
Black Donald M.,
Solomon Ellen,
Trowsdale John,
Stamp Gordon W. H.
Publication year - 1993
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/ijc.2910540210
Subject(s) - loss of heterozygosity , biology , chromosome , locus (genetics) , chromosome 17 (human) , genetics , comparative genomic hybridization , cancer research , microbiology and biotechnology , gene , allele
Frequent loss of heterozygosity (LOH) on both arms of chromosome 17 has been described in ovarian carcinoma (OC) by a number of groups, and the recent fine mapping of an inherited breast‐ovarian cancer gene ( brc Al) to a small region at 17q 12–21 has focused interest on this area. We studied 28 sporadic OCs with 21 markers at 18 loci on chromosome 17 (5 on 17p and 13 on 17q). LOH on 17p was 78%, and always involved p53. In 86% of cases showing LOH, all informative markers on chromosome 17 showed reduction to homozygosity. Using 6 markers flanking the brc AI locus on 17q, LOH was 75%, but only one tumour showed LOH with telomeric retention. The data therefore suggest that small deletions on chromosome 17 are very uncommon in sporadic OC. No genomic rearrangements by Southern blotting were seen in the brc Al candidate gene estradiol 17β dehydrogenase 2 (1 7hsd 2), or in erb B2, prohibitin ( phb ) and nmel (previously nm23‐HI). LOH on chromosome 17 was more common in high‐grade, late‐stage carcinomas, and no LOH was seen in any benign or borderline tumour. This study has clearly demonstrated that LOH at any one site on chromosome 17 is most commonly explained by LOH over the whole of the chromosome. We consider possible reasons for the absence of small deletions on chromosome 17 in OC.