Project description:AJ mouse is susceptible to lung carcinogenesis from urethane treatment and is a good model for human adenocarcinoma. We completed a study using microarray analysis of bronchoalveolar lavage cells from control or urethane treated mice. A unique macrophage expression signature in the lung tumor microenvironment was able to correctly classify the lavage samples. Keywords: AJ mouse control and urethane treatment carcinogenesis protocol
Project description:AJ mouse is susceptible to lung carcinogenesis from urethane treatment and is a good model for human adenocarcinoma. We completed a study using microarray analysis to identify a unique macrophage expression signature in the lung tumor microenvironment. Keywords: Urethane treatment time course
Project description:AJ mouse is susceptible to lung carcinogenesis from urethane treatment and is a good model for human adenocarcinoma. We completed a study using microarray analysis of bronchoalveolar lavage cells from control or urethane treated mice. A unique macrophage expression signature in the lung tumor microenvironment was able to correctly classify the lavage samples. Experiment Overall Design: RNA from bronchoalveolar lavage cells of age matched untreated AJ mice controls (C) or from urethane treated (T) AJ mice was prepared. Datasets were accurately classified using a unique macrophage gene expression signature derived from the tumor microenvironment.
Project description:AJ mouse is susceptible to lung carcinogenesis from urethane treatment and is a good model for human adenocarcinoma. We completed a study using microarray analysis to identify a unique macrophage expression signature in the lung tumor microenvironment. Experiment Overall Design: RNA from lung tissues of age matched untreated controls (Normal) from AJ mice were from two time points 24 to 26 weeks (N) or 42 weeks (N42) after saline injection. Datasets were compared to previously published adjacent to tumor lung tissues in Stearman et al Am J Path 167 1763 (2005).
Project description:This SuperSeries is composed of the following subset Series:; GSE7244: Expression data from AJ mouse control lung tissue; GSE7258: Expression data of bronchoalveolar lavage cells from control or urethane treated AJ mice Experiment Overall Design: Refer to individual Series
Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFβ-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions
Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFβ-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions Gene expression profile was analyzed in 11 individual lesions (8 adenomas and 3 adenocarcinomas) from the NDMA-silica treated mice and 5 lesions (2 adenomas, and 3 adenocarcinomas) from NDMA-only treated mice
