Skip to Main content Skip to Navigation
Journal articles

Mesotheliomas in Genetically Engineered Mice Unravel Mechanism of Mesothelial Carcinogenesis

Abstract : Malignant mesothelioma (MM), a rare and severe cancer, mainly caused as a result of past-asbestos exposure, is presently a public health concern. Current molecular studies aim to improve the outcome of the disease, providing efficient therapies based on the principles of precision medicine. To model the molecular profile of human malignant mesothelioma, animal models have been developed in rodents, wild type animals and genetically engineered mice harbouring mutations in tumour suppressor genes, especially selecting genes known to be inactivated in human malignant mesothelioma. Animals were either exposed or not exposed to asbestos or to other carcinogenic fibres, to understand the mechanism of action of fibres at the molecular level, and the role of the selected genes in mesothelial carcinogenesis. The aim of the manuscript was to compare mesothelioma models to human malignant mesothelioma and to specify the clue genes playing a role in mesothelial carcinogenesis. Collectively, MM models recapitulate the clinical features of human MM. At least two altered genes are needed to induce malignant mesothelioma in mice. Two pathways regulated by Cdkn2a and Trp53 seem independent key players in mesothelial carcinogenesis. Other genes and pathways appear as bona fide modulators of the neoplastic transformation.
Complete list of metadata

Cited literature [80 references]  Display  Hide  Download
Contributor : Didier Jean Connect in order to contact the contributor
Submitted on : Friday, February 14, 2020 - 1:48:24 AM
Last modification on : Wednesday, May 19, 2021 - 2:26:02 PM
Long-term archiving on: : Friday, May 15, 2020 - 12:38:14 PM


Publisher files allowed on an open archive



Didier Jean, Marie-Claude Jaurand. Mesotheliomas in Genetically Engineered Mice Unravel Mechanism of Mesothelial Carcinogenesis. International Journal of Molecular Sciences, MDPI, 2018, 19 (8), pp.2191. ⟨10.3390/ijms19082191⟩. ⟨inserm-02478607⟩



Record views


Files downloads