ArticlePloS one2012
Identity by descent mapping of founder mutations in cancer using high-resolution tumor SNP data.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Haplotype-resolved germline and somatic alterations in renal medullary carcinomas.Genome medicine · 2021Article
- Pediatric adrenocortical tumors: what they can tell us on adrenal development and comparison with adult adrenal tumors.Frontiers in endocrinology · 2015Review
- PIGS: improved estimates of identity-by-descent probabilities by probabilistic IBD graph sampling.BMC bioinformatics · 2015Article
- Extensive characterization of sphere models established from colorectal cancer cell lines.Cellular and molecular life sciences : CMLS · 2013Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dense genotype data can be used to detect chromosome fragments inherited from a common ancestor in apparently unrelated individuals. A disease-causing mutation inherited from a common founder may thus be detected by searching for a common haplotype signature in a sample population of patients. We present here FounderTracker, a computational method for the genome-wide detection of founder mutations in cancer using dense tumor SNP profiles. Our method is based on two assumptions. First, the wild-type allele frequently undergoes loss of heterozygosity (LOH) in the tumors of germline mutation carriers. Second, the overlap between the ancestral chromosome fragments inherited from a common founder will define a minimal haplotype conserved in each patient carrying the founder mutation. Our approach thus relies on the detection of haplotypes with significant identity by descent (IBD) sharing within recurrent regions of LOH to highlight genomic loci likely to harbor a founder mutation. We validated this approach by analyzing two real cancer data sets in which we successfully identified founder mutations of well-characterized tumor suppressor genes. We then used simulated data to evaluate the ability of our method to detect IBD tracts as a function of their size and frequency. We show that FounderTracker can detect haplotypes of low prevalence with high power and specificity, significantly outperforming existing methods. FounderTracker is thus a powerful tool for discovering unknown founder mutations that may explain part of the "missing" heritability in cancer. This method is freely available and can be used online at the FounderTracker website.
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