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Malignant pleural mesothelioma (MPM) is a cancer most often associated with the exposure to asbestos fibers. Although asbestos has been banned in most Western countries the incidence of MPM is still raising and asbestos-related diseases are still a major public health problem. In addition MPM incidence will also rise in countries, where asbestos has not been banned yet and where there are no stringent health protection policies. Of concern, mesothelioma could also be induced by man-made fibers (e.g. nanomaterials). Therefore, the investigation of molecular mechanisms of asbestos-induced carcinogenesis in a systemic approach should provide tools for molecular epidemiology in fiber-exposed individuals and will contribute to the understanding of inflammation-driven carcinogenesis.Our working hypothesis is that chronic inflammation/injury activates stem cell signaling and continuous stimulation of repair in an inflammatory setting leads to oncogenic events and escape from immune control.We use Nf2-/+ mice exposed to asbestos intraperitoneally since a recent study has validated this model as a useful model to study mesothelioma by showing common genomic alterations between murine and human MPM using genomic profiling . Our aim was to obtain a transcriptome profile, including protein-coding and non-protein coding RNA, in precancerous and cancer tissue collected from mice developing mesothelioma after exposure to asbestos and compare with sham exposed mice. |