%0 Journal Article
%T Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines
%A Penny Nymark
%A Pamela M Lindholm
%A Mikko V Korpela
%A Leo Lahti
%A Salla Ruosaari
%A Samuel Kaski
%A Jaakko Hollm¨¦n
%A Sisko Anttila
%A Vuokko L Kinnula
%A Sakari Knuutila
%J BMC Genomics
%D 2007
%I BioMed Central
%R 10.1186/1471-2164-8-62
%X We recognized a large number of previously known as well as new potential asbestos-associated genes and biological processes, and identified chromosomal regions enriched with genes potentially contributing to common responses to asbestos in these cell lines. These include genes such as the thioredoxin domain containing gene (TXNDC) and the potential tumor suppressor, BCL2/adenovirus E1B 19kD-interacting protein gene (BNIP3L), GO-terms such as "positive regulation of I-kappaB kinase/NF-kappaB cascade" and "positive regulation of transcription, DNA-dependent", and chromosomal regions such as 2p22, 9p13, and 14q21. We present the complete data sets as Additional files.This study identifies several interesting targets for further investigation in relation to asbestos-associated diseases.Asbestos causes DNA double strand breaks [1], chromosomal aberrations, and abnormal chromosome segregation [2]. Asbestos fibre-induced genotoxicity has been proposed to be caused by both a direct interaction with the genetic material and also indirect effects via production of reactive oxygen species (ROS) [3]. The respiratory diseases linked to asbestos exposure include fibrotic lung disease, mesothelioma, and lung cancer. The pathogenesis and histopathology of asbestosis resemble that of idiopathic pulmonary fibrosis. Some specific genes contributing to the development of asbestosis and asbestos-related cancer have been described, as reviewed in [4]. However, the exact molecular mechanisms behind asbestos-associated carcinogenesis and fibrosis/asbestosis are thought to be very complex and involve several parallel pathways [4,5] that remain to be clarified.Asbestos exposure has been reported to alter the expression of several genes involved in integrin-mediated signaling pathways, MAPK pathways, and NFKB/IKB pathways [6]. A recent study in a model for asbestos-induced oncogenesis demonstrated that the tumor necrosis factor, TNF-¦Á, triggered by macrophages, induced activation of the NFKB
%U http://www.biomedcentral.com/1471-2164/8/62