ArticlePLoS genetics2014
Mouse pulmonary adenoma susceptibility 1 locus is an expression QTL modulating Kras-4A.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Arsenic up-regulates PD-L1 and enhances lung tumorigenesis through activation of STAT3 in alveolar epithelial type 2 cells.Toxicology and applied pharmacology · 2024Article
- Article
- Oncogenes in high grade serous adenocarcinoma of the ovary.Genes & cancer · 2020Article
- Capturing the primordial Kras mutation initiating urethane carcinogenesis.Nature communications · 2020Article
- Genetic Predisposition to Hepatocarcinogenesis in Inbred and Outbred Mouse Lines Selected for High or Low Inflammatory Response.Journal of immunology research · 2019Article
- A model for RAS mutation patterns in cancers: finding the sweet spot.Nature reviews. Cancer · 2018Review
- Role of epigenetic factors in the selection of the alternative splicing isoforms of humanOncotarget · 2018Article
- Complex genetic control of lung tumorigenesis in resistant mice strains.Cancer science · 2017Article
- Rare codons capacitate Kras-driven de novo tumorigenesis.The Journal of clinical investigation · 2015Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary adenoma susceptibility 1 (Pas1) is the major locus responsible for lung tumor susceptibility in mice; among the six genes mapping in this locus, Kras is considered the best candidate for Pas1 function although how it determines tumor susceptibility remains unknown. In an (A/J × C57BL/6)F4 intercross population treated with urethane to induce lung tumors, Pas1 not only modulated tumor susceptibility (LOD score = 48, 69% of phenotypic variance explained) but also acted, in lung tumor tissue, as an expression quantitative trait locus (QTL) for Kras-4A, one of two alternatively spliced Kras transcripts, but not Kras-4B. Additionally, Kras-4A showed differential allelic expression in lung tumor tissue of (A/J × C57BL/6)F4 heterozygous mice, with significantly higher expression from the A/J-derived allele; these results suggest that cis-acting elements control Kras-4A expression. In normal lung tissue from untreated mice of the same cross, Kras-4A levels were also highly linked to the Pas1 locus (LOD score = 23.2, 62% of phenotypic variance explained) and preferentially generated from the A/J-derived allele, indicating that Pas1 is an expression QTL in normal lung tissue as well. Overall, the present findings shed new light on the genetic mechanism by which Pas1 modulates the susceptibility to lung tumorigenesis, through the fine control of Kras isoform levels.
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