ArticleInternational journal of cancer2010
Epistatic interactions govern chemically-induced lung tumor susceptibility and Kras mutation site in murine C57BL/6J-ChrA/J chromosome substitution strains.
Article in International journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Tumour promotion through the lens of evolution.Nature · 2026Review
- Kras oncogene ablation prevents resistance in advanced lung adenocarcinomas.The Journal of clinical investigation · 2023Article
- Article
- Danger zone.eLife · 2021Article
- Article
- Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice.Methods in cell biology · 2021Article
- Capturing the primordial Kras mutation initiating urethane carcinogenesis.Nature communications · 2020Article
- The Atypical Receptor CCRL2 Is Essential for Lung Cancer Immune Surveillance.Cancer immunology research · 2019Article
- A model for RAS mutation patterns in cancers: finding the sweet spot.Nature reviews. Cancer · 2018Review
- Immune Surveillance by Natural IgM Is Required for Early Neoantigen Recognition and Initiation of Adaptive Immunity.American journal of respiratory cell and molecular biology · 2018Article
- WeSME: uncovering mutual exclusivity of cancer drivers and beyond.Bioinformatics (Oxford, England) · 2017Article
- Activation of liver X receptor inhibits the development of pulmonary carcinomas induced by 3-methylcholanthrene and butylated hydroxytoluene in BALB/c mice.Scientific reports · 2016Article
- Article
- Rare codons capacitate Kras-driven de novo tumorigenesis.The Journal of clinical investigation · 2015Article
- The error-prone DNA polymerase ι provides quantitative resistance to lung tumorigenesis and mutagenesis in mice.Oncogene · 2014Article
- The Kras mutational spectra of chemically induced lung tumors in different inbred mice mimics the spectra of KRAS mutations in adenocarcinomas in smokers versus nonsmokers.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2010Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer susceptibility results from interactions between sensitivity and resistance alleles. We employed murine chromosome substitution strains to study how resistance alleles affected sensitive alleles during chemically-induced lung carcinogenesis. The C57BL/6J-Chr#(A/J) strains, constructed by selectively breeding sensitive A/J and resistant C57BL/6J (B6) mice, each contain one pair of A/J chromosomes within an otherwise B6 genome. Pas1, the major locus responsible for this differential strain response to urethane carcinogenesis, resides on Chr 6, but C57BL/6J-Chr6(A/J) mice (hereafter CSS-6) developed few tumors following a single urethane injection, which demonstrates epistatic interactions with other B6 alleles. CSS6 mice developed dozens of lung tumors after chronic urethane exposure, however, indicating that these epistatic interactions could be overcome by repeated carcinogen administration. Unlike A/J, but similar to B6 mice, CSS6 mice were resistant to lung carcinogenesis induced by 3-methylcholanthrene (MCA). Tumor multiplicity increased if BHT administration followed urethane exposure, showing that a Chr 6 gene(s) regulates sensitivity to chemically-induced tumor promotion. Unlike A/J tumors (predominantly codon 61 A-->T transversions), Kras mutations in tumors induced by urethane in CSS-6 mice were similar to B6 tumors (codon 61 A-->G transitions). DNA repair genes not located on Chr 6 may determine the nature of Kras mutations. CSS-6 mice are a valuable resource for testing the ability of candidate genes to modulate lung carcinogenesis.
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