Transcriptome of normal lung distinguishes mouse lines with different susceptibility to inflammation and to lung tumorigenesis

被引：8

作者：

De Franco, Marcelo ^{[1
]}

Colombo, Francesca ^{[2
]}

Galvan, Antonella ^{[2
]}

De Cecco, Loris ^{[2
]}

Spada, Elena ^{[3
]}

Milani, Silvano ^{[3
]}

Ibanez, Olga M. ^{[1
]}

Dragani, Tommaso A. ^{[2
]}

机构：

[1] Inst Butantan, Lab Imunogenet, BR-05503900 Sao Paulo, Brazil

[2] Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Labs, I-20133 Milan, Italy

[3] Univ Milan, Ist Stat Med & Biometria GA Maccacaro, Milan, Italy

来源：

CANCER LETTERS | 2010年 / 294卷 / 02期

基金：

巴西圣保罗研究基金会;

关键词：

Microarray; mRNA profile; Inflammatory response; Animal models; GENE-EXPRESSION; PAS1; LOCUS; MICE; PREDISPOSITION; CANCER; CARCINOGENESIS; TRANSMIGRATION; SEMAPHORINS; METABOLISM; ACTIVATION;

D O I：

10.1016/j.canlet.2010.01.038

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

AIRmax and AIRmin mouse lines show a differential lung inflammatory response and differential lung tumor susceptibility after urethane treatment. The transcript profile of similar to 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. Moreover, gene expression levels differed significantly in urethane-treated mice: 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. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

引用

页码：187 / 194

页数：8

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