ArticleCancer genetics and cytogenetics2008
Genomic structure of chromosome 17 deletions in BRCA1-associated ovarian cancers.
Article in Cancer genetics and cytogenetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Endogenous and environmental factors that induce DNA replication defects and genomic instability in ER-negative heterozygous BRCA1 cells.Scientific reports · 2026Article
- Global characterization of extrachromosomal circular DNAs in advanced high grade serous ovarian cancer.Cell death & disease · 2022Article
- Germline HOXB13 mutation p.G84E do not confer an increased bladder or kidney cancer risk in polish population.Hereditary cancer in clinical practice · 2022Article
- BRCA1 intronic Alu elements drive gene rearrangements and PARP inhibitor resistance.Nature communications · 2019Article
- Loss of heterozygosity at BRCA1/2 loci in hereditary and sporadic ovarian cancers.Journal of applied genetics · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The aim of this study was to determine the genomic structure of the deletions on chromosome 17 in ovarian carcinomas from women with inherited BRCA1 mutations. Normal and tumor DNA from 14 ovarian tumors associated with inherited BRCA1 mutations were extracted and tested for loss of heterozygosity (LOH) at microsatellite markers along chromosome 17. Finer mapping using more microsatellite markers and single nucleotide polymorphisms helped further define the LOH margins. The genomic repeated elements within the LOH breakpoint regions were identified using the University of California Santa Cruz Genome Database, and the frequencies were compared to regions of equal GC percentages across the genome. Of the 14 ovarian tumors, 12 showed LOH of the entire chromosome 17. The other two tumors lost the distal end of the 17q arm. The breakpoints of these two tumors occurred in regions with significantly high frequencies of short interspersed nuclear elements (SINE), specifically Alu elements. Ovarian tumors of high grade and stage have large regions of LOH along chromosome 17, with most tumors showing loss of the entire chromosome. In those tumors with retention of part of chromosome 17, LOH margins suggest that a high Alu content may have a role in the deletions.
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Registered trials
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