ArticlePloS one2009
Complex segregation analysis of pedigrees from the Gilda Radner Familial Ovarian Cancer Registry reveals evidence for mendelian dominant inheritance.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Whole-Genome Sequencing IdentifiesCancers · 2022Article
- Familial Segregation of Venous Thromboembolism in Sweden: A Nationwide Family Study of Heritability and Complex Segregation Analysis.Journal of the American Heart Association · 2021Article
- Whole-exome sequencing of ovarian cancer families uncovers putative predisposition genes.International journal of cancer · 2020Article
- Hereditary association between testicular cancer and familial ovarian cancer: A Familial Ovarian Cancer Registry study.Cancer epidemiology · 2018Article
- Paternal lineage early onset hereditary ovarian cancers: A Familial Ovarian Cancer Registry study.PLoS genetics · 2018Article
- Complex Segregation Analysis Provides Evidence for Autosomal Dominant Transmission in the Chinese Han Families with Ankylosing Spondylitis.BioMed research international · 2017Article
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Authors and funding
9 authors.
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Abstract
backgroundFamilial component is estimated to account for about 10% of ovarian cancer. However, the mode of inheritance of ovarian cancer remains poorly understood. The goal of this study was to investigate the inheritance model that best fits the observed transmission pattern of ovarian cancer among 7669 members of 1919 pedigrees ascertained through probands from the Gilda Radner Familial Ovarian Cancer Registry at Roswell Park Cancer Institute, Buffalo, New York. METHODOLOGY/PRINCIPAL
findingsUsing the Statistical Analysis for Genetic Epidemiology program, we carried out complex segregation analyses of ovarian cancer affection status by fitting different genetic hypothesis-based regressive multivariate logistic models. We evaluated the likelihood of sporadic, major gene, environmental, general, and six types of Mendelian models. Under each hypothesized model, we also estimated the susceptibility allele frequency, transmission probabilities for the susceptibility allele, baseline susceptibility and estimates of familial association. Comparisons between models were carried out using either maximum likelihood ratio test in the case of hierarchical models, or Akaike information criterion for non-nested models. When assessed against sporadic model without familial association, the model with both parent-offspring and sib-sib residual association could not be rejected. Likewise, the Mendelian dominant model that included familial residual association provided the best-fitting for the inheritance of ovarian cancer. The estimated disease allele frequency in the dominant model was 0.21. CONCLUSIONS/SIGNIFICANCE: This report provides support for a genetic role in susceptibility to ovarian cancer with a major autosomal dominant component. This model does not preclude the possibility of polygenic inheritance of combined effects of multiple low penetrance susceptibility alleles segregating dominantly.
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