ArticleCellular oncology (Dordrecht, Netherlands)2012
Genomic aberrations relate early and advanced stage ovarian cancer.
Article in Cellular oncology (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Apparent Diffusion Coefficient Histogram Analysis for Assessing Tumor Staging and Detection of Lymph Node Metastasis in Epithelial Ovarian Cancer: Correlation with p53 and Ki-67 Expression.Molecular imaging and biology · 2019Article
- Emerging diagnostic, prognostic and therapeutic biomarkers for ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2017Review
- Proteogenomic convergence for understanding cancer pathways and networks.Clinical proteomics · 2014Review
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18 authors.
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Abstract
backgroundBecause of the distinct clinical presentation of early and advanced stage ovarian cancer, we aim to clarify whether these disease entities are solely separated by time of diagnosis or whether they arise from distinct molecular events.
methodsSixteen early and sixteen advanced stage ovarian carcinomas, matched for histological subtype and differentiation grade, were included. Genomic aberrations were compared for each early and advanced stage ovarian cancer by array comparative genomic hybridization. To study how the aberrations correlate to the clinical characteristics of the tumors we clustered tumors based on the genomic aberrations.
resultsThe genomic aberration patterns in advanced stage cancer equalled those in early stage, but were more frequent in advanced stage (p = 0.012). Unsupervised clustering based on genomic aberrations yielded two clusters that significantly discriminated early from advanced stage (p = 0.001), and that did differ significantly in survival (p = 0.002). These clusters however did give a more accurate prognosis than histological subtype or differentiation grade.
conclusionThis study indicates that advanced stage ovarian cancer either progresses from early stage or from a common precursor lesion but that they do not arise from distinct carcinogenic molecular events. Furthermore, we show that array comparative genomic hybridization has the potential to identify clinically distinct patients.
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