Project description:Transcriptomic comparison of FVB mouse strain lung Cells one week upon injecting mice intraperitoneally with either saline or Urethane. Mouse lung cell were also compared at the transcriptomic level with the mouse lung adenocarcinoma cell line FULA 1, which was established in our lab We injected 6 (3 males, 3 females) FVB mice 8 weeks old, with either saline or urethane. One week later we sacrificed and harvested their lungs. The dissected lungs were assayed to RNA extraction (via trizol) in order to identify their transcriptomic signature. Moreover we compared the gene expression of the mouse lung cells to the mouse lung adenocarcinoma cell line FULA 1.
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:We repeatedly injected FVB and C57BL/6 intraperitonealy with urethane. Mice developed lung tumours. We sacrificed the mice, harvested their lungs and cultured the tumour cells. After over 60 passages we established 3 novel mouse lung adenocarcinoma cell lines. The aim of this study os to compare their transcriptomic profile.
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:We estimated differences of urethane-induced tumors between Nrf2+/+ and Nrf2-/- ICR mouse. To identify Nrf2-regulated genes in tumors, we examined the mRNA expression profile both in tumor and non-tumor tissue of mouse 4 months after urethane administration. We performed microarray analyses using the comparable size of lung tumors (1.0 mm < tumor diameter < 1.5 mm) and intact non-tumor lung tissues derived either from Nrf2+/+ (n=8) or Nrf2–/–mice (n=8) at 16-weeks after urethane(1-g/kg body weight) treatment.
Project description:AIRmax and AIRmin mouse lines show a differential lung inflammatory response and differential lung tumor susceptibility after urethane treatment, thus constituting a good genetic model to investigate differences in gene expression profiles related to inflammatory response and lung tumor susceptibility. The transcript profile of ~24,000 known genes was analyzed in normal lung tissue of untreated and urethane-treated AIRmax and AIRmin mice. In lungs of untreated mice, inflammation associated genes involved in pathways such as “leukocyte transendothelial migration”, “cell adhesion” and “tight junctions” were differentially expressed in AIRmax versus AIRmin mice. Moreover, gene expression levels differed significantly in urethane-treated mice even at 21 days after treatment. In AIRmin mice, modulation of expression of genes involved in pathways associated with inflammatory response paralleled the previously observed persistent infiltration of inflammatory cells in the lung of these mice. In conclusion, a specific gene expression profile in normal lung tissue is associated with mouse line susceptibility or resistance to lung tumorigenesis and with different inflammatory response, and urethane treatment causes a long-lasting alteration of the lung gene expression profile that correlates with persistent inflammatory response of AIRmin mice.
Project description:Transcriptomic comparison of FVB mouse strain lung Cells one week upon injecting mice intraperitoneally with urethane and with the mouse lung adenocarcinoma cell line FULA 1
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:FVB, Balb/c, and C57BL/6 mice received the tobacco carcinogens urethane (Sigma Aldrich, U2500) intraperitoneally (1g/Kg in 100 μl phosphate-buffered saline) or diethylnitrosamine (200 mg/kg) (Sigma Aldrich, N0756). Carcinogen induced lung adenocarcinoma murine cell lines generation| Ten months post first carcinogen (urethane, DEN) exposure mice were sacrificed, lung tumours were dissected from surrounding healthy lung parenchyma under sterile conditions, were halved, one half was processed for histology and the other half was chopped into 1 mm pieces and seeded to cell culture dishes. Cells were cultured under standard conditions outlined below. When adenocarcinoma was diagnosed for a given tumour, its corresponding culture was passaged in vitro over a period of 18 months and 60 passages, whichever occurred first. After gene expression and mutational signature extraction, the signature were compared with human lung adenocarcinoma RNAseq results.
