ArticleBritish journal of cancer1996
Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas.
Article in British journal of cancer, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Network and data integration for biomarker signature discovery via network smoothed T-statistics.PloS one · 2013Article
- Article
- Genomic structure of chromosome 17 deletions in BRCA1-associated ovarian cancers.Cancer genetics and cytogenetics · 2008Article
- STRAD in Peutz-Jeghers syndrome and sporadic cancers.Journal of clinical pathology · 2005Article
- Article
- Allelotyping defines minimal imbalance at chromosomal region 17q25 in non-serous epithelial ovarian cancers.Oncogene · 2000Article
- Allelic Losses from Chromosome 17 in Human Osteosarcomas.Pathology oncology research : POR · 1997Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using a panel of ten polymorphic markers, we examined the frequency of loss of heterozygosity (LOH) on chromosome 17 in 55 sporadic ovarian tumours. LOH on 17p and 17q was observed to be 50% and 62% respectively. LOH at D17S5 was detected in 24/36 (67%) of malignant cases and in 19/43 (44%) at TP53; the marker D17S855 intragenic to the BRCA1 gene showed allele loss in 50% (20/40) cases. The data presented here suggest that loss of the whole chromosome 17 is a relatively frequent event (30%) in ovarian carcinomas and this observation is especially frequent for serous, transitional cell and anaplastic histological subtypes. Mucinous and endometrioid ovarian tumours showed only short interstitial deletions (4/11, 36%). The overall frequency of the short deletions was relatively low (7/43, 16%) in our panel of carcinomas. Amplification of c-erbB-2/neu oncogene was detected in 32% (11/34) of the carcinomas tested; the gene was amplified only in those histological subtypes in which high incidence of LOH on chromosome 17 was observed, and was associated with advanced stages of the disease. We conclude that different histological types of tumour may have different aetiological mechanisms, and tumour-suppressor genes on chromosome 17 might be associated specifically with serous and transitional cell ovarian carcinomas.
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