ArticleG3 (Bethesda, Md.)2012
Mapping six new susceptibility to colon cancer (Scc) loci using a mouse interspecific backcross.
Article in G3 (Bethesda, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Allele-specific imbalance mapping at human orthologs of mouse susceptibility to colon cancer (Scc) loci.International journal of cancer · 2015Article
- Sex disparity in colonic adenomagenesis involves promotion by male hormones, not protection by female hormones.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- A strategy to identify dominant point mutant modifiers of a quantitative trait.G3 (Bethesda, Md.) · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) has a complex etiology resulting from the combination of multiple genetic and environmental factors, each with small effects. Interactions among susceptibility modifier loci make many of the loci difficult to detect in human genome-wide association studies. Previous analyses in mice have used classical inbred strains, which share large portions of their genomes due to common ancestry. Herein, we used an interspecific backcross between the Mus musculus strain A/J and the Mus spretus strain SPRET/EiJ to map 6 additional CRC modifier loci (Scc16-21) and 2 suggestive loci. Three loci modify the location of tumors along the proximal-distal axis of the colon. Six CRC modifiers previously mapped in intraspecific crosses were also replicated. This work confirms genetic models suggesting that CRC is caused by many small effect alleles and brings the catalog of reported CRC modifier loci to 23 spread across 13 chromosomes. Furthermore, this work provides the foundation for large population-level epistatic interaction tests to identify combinations of low effect alleles that may have large effects on CRC susceptibility.
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Registered trials
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