ArticleCarcinogenesis2005
Conditional expression of the mutant Ki-rasG12C allele results in formation of benign lung adenomas: development of a novel mouse lung tumor model.
Article in Carcinogenesis, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways.Cells · 2024Review
- Double knock-in pig models with elements of binary Tet-On and phiC31 integrase systems for controllable and switchable gene expression.Science China. Life sciences · 2022Article
- Precision drugging of the MAPK pathway in head and neck cancer.NPJ genomic medicine · 2022Review
- Models of pancreatic ductal adenocarcinoma.Cancer metastasis reviews · 2021Review
- Effects of low dose and low dose rate low linear energy transfer radiation on animals - review of recent studies relevant for carcinogenesis.International journal of radiation biology · 2021Review
- Roles of DNA repair enzyme OGG1 in innate immunity and its significance for lung cancer.Pharmacology & therapeutics · 2019Review
- Management of KRAS-Mutant Non-Small Cell Lung Cancer in the Era of Precision Medicine.Current treatment options in oncology · 2018Review
- Homoharringtonine induced immune alteration for an Efficient Anti-tumor Response in Mouse Models of Non-small Cell Lung Adenocarcinoma Expressing Kras Mutation.Scientific reports · 2018Article
- Epidermal growth factor receptor as a novel molecular target for aggressive papillary tumors in the middle ear and temporal bone.Oncotarget · 2015Article
- Rapamycin prevents the development and progression of mutant epidermal growth factor receptor lung tumors with the acquired resistance mutation T790M.Cell reports · 2014Article
- Endotoxin induces proliferation of NSCLC in vitro and in vivo: role of COX-2 and EGFR activation.Cancer immunology, immunotherapy : CII · 2013Article
- A gated-7T MRI technique for tracking lung tumor development and progression in mice after exposure to low doses of ionizing radiation.Radiation research · 2012Article
- Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome.Journal of the National Cancer Institute · 2012Article
- A technique for murine irradiation in a controlled gas environment.Biomedical sciences instrumentation · 2012Article
- Cancer-prone mice expressing the Ki-rasG12C gene show increased lung carcinogenesis after CT screening exposures.Radiation research · 2011Article
- Conditional expression of oncogenic C-RAF in mouse pulmonary epithelial cells reveals differential tumorigenesis and induction of autophagy leading to tumor regression.Neoplasia (New York, N.Y.) · 2011Article
- Interaction between MYC and MCL1 in the genesis and outcome of non-small-cell lung cancer.Cancer research · 2011Article
- RAS Mutations and Oncogenesis: Not all RAS Mutations are Created Equally.Frontiers in genetics · 2011Article
- Angiotensin-(1-7) reduces fibrosis in orthotopic breast tumors.Cancer research · 2010Article
- MYC Inactivation Elicits Oncogene Addiction through Both Tumor Cell-Intrinsic and Host-Dependent Mechanisms.Genes & cancer · 2010Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
To determine the effects of expression of mutant Ki-ras on lung tumorigenesis, we developed a bitransgenic mouse model that expresses the human Ki-ras(G12C) allele in alveolar type II and/or Clara cells in a tetracycline-inducible, lung-specific manner. Expression of Ki-ras(G12C) caused multiple, small lung tumors over a 12-month time period. Although tumor multiplicity increased upon continued Ki-ras expression, most lung lesions were hyperplasias or well-differentiated adenomas. This is in contrast to the more severe phenotypes observed in other transgenic mouse models in which different mutant Ki-ras alleles were expressed in the lung. Expression of Ki-ras(G12C) was associated with a 2-fold increase in the activation of the Ras and Ral signaling pathways and increased phosphorylation of Ras downstream effectors, including Erk, p90 ribosomal S6 kinase, ribosomal S6 protein, p38 and MAPKAPK-2. In contrast, expression of the transgene had no effect on the activation of the JNK and Akt signaling pathways. Withdrawal of doxycycline for 1 month resulted in almost a complete absence of proliferative pulmonary lesions, suggesting tumor regression in the absence of Ki-ras expression. Mutant Ki-ras(G12C) expression was sufficient for initial lung tumor transformation, required for maintenance of tumor phenotype, and induced transformation of lung epithelial cells by the activation of multiple effector pathways. These results describe a novel mouse lung tumor model demonstrating benign tumor development in the absence of tumor progression, which will provide a new tool for understanding the early stages of lung tumor pathogenesis.
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