ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2010
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.
Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2010. 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, 15 citations in OpenAlex.
- Article
- Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice.Methods in cell biology · 2021Article
- XPC protects against smoking- and carcinogen-induced lung adenocarcinoma.Carcinogenesis · 2019Article
- Multiplexed in vivo homology-directed repair and tumor barcoding enables parallel quantification of Kras variant oncogenicity.Nature communications · 2017Article
- Epiregulin is required for lung tumor promotion in a murine two-stage carcinogenesis model.Molecular carcinogenesis · 2017Article
- Inflammation as a driver and vulnerability of KRAS mediated oncogenesis.Seminars in cell & developmental biology · 2016Review
- Mutational status of synchronous and metachronous tumor samples in patients with metastatic non-small-cell lung cancer.BMC cancer · 2016Article
- Contrasting responses of non-small cell lung cancer to antiangiogenic therapies depend on histological subtype.EMBO molecular medicine · 2014Article
- Stimulation of neoplastic mouse lung cell proliferation by alveolar macrophage-derived, insulin-like growth factor-1 can be blocked by inhibiting MEK and PI3K activation.Molecular cancer · 2011Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHuman lung cancer patients exhibit different KRAS mutations depending on smoking status. In a mouse model of human cancer, A/J and BALB/cBy mice treated with the tobacco carcinogen, 3-methylcholanthrene (MCA), followed by butylated hydroxytoluene (BHT)-elicited chronic inflammation develop a high multiplicity of lung tumors.
methodsDNA was isolated from MCA-induced lung tumors in A/J and BALB/cByJ mice. Kras codon 12 sequences from these tumors were compared to those in human lung tumors from smokers and never-smokers.
resultsThe distribution of Kras codon 12 mutations in MCA-induced A/J lung tumors is strikingly similar to those found in adenocarcinomas from human smokers. In contrast, codon 12 mutations in BALB/cBy mice contain predominantly G --> D mutations, which is the most common mutation in never smokers.
conclusionsA single lung carcinogen induces different tumor initiating mutations in different strains of mice. This may be useful for investigating the role of specific KRAS mutations in adenocarcinoma pathogenesis in smokers versus never smokers, identifying mechanisms that select for certain KRAS mutations and developing new drugs that specifically target cells with different KRAS mutations.
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