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Series GSE19605 Query DataSets for GSE19605
Status Public on Dec 23, 2009
Title Specificity for the Nature of Inflammation in Lung Cancer Promotion in Mice
Organism Mus musculus
Experiment type Expression profiling by array
Summary A large amount of epidemiologic data supports a role for chronic inflammation in epithelial carcinogenesis. In the lung, several studies have found that smokers with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the airways and alveoli, have an increased risk of lung cancer (1.3 to 4.9 fold) compared to smokers without COPD. We have also shown that COPD-like airway inflammation induced by an aerosolized lysate of non-typeable Hemophilus influenzae (NTHi) promotes lung cancer in a Clara cell-targeted K-ras mutant mouse model (CC-LR) of lung cancer. In contrast, existing epidemiologic data suggest that allergic inflammation of the airways may be protective against lung cancer. We tested this association in a mouse model of allergic airway inflammation. CC-LR mice were sensitized to ovalbumin by intraperitoneal injection weekly for two weeks, then challenged for 30 min to an aerosol of ovalbumin in 0.9% saline weekly for eight weeks. This resulted in eosinophilic lung inflammation associated with increased levels of T helper 2 (Th2) cytokines and mucous metaplasia of airway epithelium, similar to what is seen in asthma patients. However, consistent with epidemiologic data, this type of inflammation did not result in any significant differences in lung surface tumor number (22 ± 3 in OVA exposed vs 26 ± 6 in control mice). We conclude that asthma-like (Th2) inflammation does not promote lung carcinogenesis in a Ras-initiated background, and demonstrate a clear specificity for the nature of inflammation in lung cancer promotion. These findings will assist in determination of the essential cells and signaling events in lung cancer promotion by inflammation.

Keywords: lung, chonic inflammation, microarray
Overall design Wildtype or CC-LR (a Clara cell-targeted K-ras mutant mouse model of lung cancer) mice were either challenged with an aerosol of an NTHi lysate or to an aerosol of ovalbumin for eight weeks, and microarray analysis was performed on whole lung homogenates from mice on the first day after the 8th exposure.
Contributor(s) Moghaddam SJ, Evans SE
Citation(s) 21098042
Submission date Dec 22, 2009
Last update date Jun 14, 2018
Contact name Scott E Evans
Organization name University of Texas-M.D. Anderson Cancer Center
Department Pulmonary Medicine - Box 403
Street address 1400 Holcombe Blvd
City Houston
State/province TX
ZIP/Postal code 77030
Country USA
Platforms (1)
GPL6885 Illumina MouseRef-8 v2.0 expression beadchip
Samples (24)
GSM489029 CH4-1
GSM489030 CH4-2
GSM489031 CH4-3
BioProject PRJNA122441

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SOFT formatted family file(s) SOFTHelp
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Supplementary file Size Download File type/resource
GSE19605_RAW.tar 3.1 Mb (http)(custom) TAR
GSE19605_RAW.txt.gz 2.5 Mb (ftp)(http) TXT
Raw data are available on Series record
Processed data included within Sample table

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