ArticleNature genetics2006
A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice.
Article in Nature genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 69 citations in OpenAlex.
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- The effects of mutant Ras proteins on the cell signalome.Cancer metastasis reviews · 2020Review
- Capturing the primordial Kras mutation initiating urethane carcinogenesis.Nature communications · 2020Article
- A model for RAS mutation patterns in cancers: finding the sweet spot.Nature reviews. Cancer · 2018Review
- Widespread Selection for Oncogenic Mutant Allele Imbalance in Cancer.Cancer cell · 2018Article
- Oncogenic RAS isoforms show a hierarchical requirement for the guanine nucleotide exchange factor SOS2 to mediate cell transformation.Science signaling · 2018Article
- FBXW7 deletion contributes to lung tumor development and confers resistance to gefitinib therapy.Molecular oncology · 2018Article
- The parathyroid hormone regulates skin tumour susceptibility in mice.Scientific reports · 2017Article
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- The role of wild type RAS isoforms in cancer.Seminars in cell & developmental biology · 2016Review
- Genetic background determines if Stat5b suppresses or enhances murine hepatocarcinogenesis.Molecular carcinogenesis · 2015Article
- Identification of genetic loci that control mammary tumor susceptibility through the host microenvironment.Scientific reports · 2015Article
- Rare codons capacitate Kras-driven de novo tumorigenesis.The Journal of clinical investigation · 2015Article
- Mouse pulmonary adenoma susceptibility 1 locus is an expression QTL modulating Kras-4A.PLoS genetics · 2014Article
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- Emerging roles for intersectin (ITSN) in regulating signaling and disease pathways.International journal of molecular sciences · 2013Review
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6 authors at 3 institutions in 1 country.
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Abstract
Pulmonary adenoma susceptibility 1 (Pas1) is the major mouse lung cancer susceptibility locus on chromosome 6 (ref. 1). Kras2 is a common target of somatic mutation in chemically induced mouse lung tumors and is a candidate Pas1 gene. M. spretus mice (SPRET/Ei) carry a Pas1 resistance haplotype for chemically induced lung tumors. We demonstrate that the SPRET/Ei Pas1 allele is switched from resistance to susceptibility by fixation of the parental origin of the mutant Kras2 allele. This switch correlates with low expression of endogenous Kras2 in SPRET/Ei. We propose that the Pas1 modifier effect is due to Kras2, and that a sensitive balance between the expression levels of wild-type and mutant alleles determines lung tumor susceptibility. These data demonstrate that cancer predisposition should also be considered in the context of somatic events and could have major implications for the design of human association studies to identify cancer susceptibility genes.
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