Jie Lu1, Mark G Burnett1, Max Shpak2,3,4. 1. NeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas, TX, U.S.A. 2. NeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas, TX, U.S.A. shpak.max@gmail.com. 3. Center for Systems and Synthetic Biology, University of Texas, Austin, Texas, TX, U.S.A. 4. Fresh Pond Research Institute, Cambridge, MA, U.S.A.
Abstract
BACKGROUND: Familial cancers are those that co-occur among first-degree relatives without showing Mendelian patterns of inheritance. MATERIALS AND METHODS: In this analysis, we compare the genomic characteristics of familial and sporadic cancers, with a focus on low-grade gliomas (LGGs) using sequence and expression data from the Cancer Genome Atlas. RESULTS: Familial cancers show similar genomic and molecular biomarker profiles to sporadic cancers, consistent with the similarity in their clinical features. There are no statistically significant differences among somatic mutation, copy number variant, or gene expression patterns between familial and sporadic cancers; methylation profiles are the only class of molecular data to show significant differences. CONCLUSION: Familial cancers are likely driven by multiple, individually weak contributions to familiality (i.e. large numbers of alleles and/or shared environmental risks). Consequently, these risk factors tend to be obscured by stronger confounding variables such as clinical or molecular variation among cancer subtypes. Copyright
BACKGROUND:Familial cancers are those that co-occur among first-degree relatives without showing Mendelian patterns of inheritance. MATERIALS AND METHODS: In this analysis, we compare the genomic characteristics of familial and sporadic cancers, with a focus on low-grade gliomas (LGGs) using sequence and expression data from the Cancer Genome Atlas. RESULTS:Familial cancers show similar genomic and molecular biomarker profiles to sporadic cancers, consistent with the similarity in their clinical features. There are no statistically significant differences among somatic mutation, copy number variant, or gene expression patterns between familial and sporadic cancers; methylation profiles are the only class of molecular data to show significant differences. CONCLUSION:Familial cancers are likely driven by multiple, individually weak contributions to familiality (i.e. large numbers of alleles and/or shared environmental risks). Consequently, these risk factors tend to be obscured by stronger confounding variables such as clinical or molecular variation among cancer subtypes. Copyright
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