In this article, transcriptional deregulation, mediated by inactivation of the nuclear deubiquitinase BAP1, is implicated in the pathogenesis of mesothelioma.  The two most common known genetic alterations in mesotheliomas are 9p21 deletions on CDKN2A and 22q deletions causing NF2 loss. The authors show that another gene with a high rate of non-synonymous mutations is BAP1 (encoding BRCA1-associated protein 1).  Somatic mutations were found in 23% of mesotheliomas.  The study also shows that other common tumor suppressors, such as PTEN and p53, showed few or no mutations, confirming data from previous …

Here is an article recently published by the Asian/Pacific Society of Respirology analyzing the increase of asbestos use and occurence of asbestos-related disease in Asia.

The proportion of global asbestos use attributed to Asia has been steadily increasing over the years from 14% (1920–1970) to 33% (1971–2000) to 64% (2001–2007).

Asbestos use in Asia has now reached formidable levels in terms of per capita use and absolute volumes and a surge of asbestos-related diseases should be anticipated in the coming decades.

Here is a paper by Deborah Altomare analyzing Ink4A and Arf role in mesothelioma pathogenesis.
p16(INK4A) and p14(ARF) are frequently co-deleted in human malignant mesothelioma and the authors here find that in vivo both CDKN2A/ARF gene products suppress asbestos carcinogenicity. Furthermore, while the inactivation of Arf appears to be crucial for mesothelioma pathogenesis, the inactivation of both p16(INK4A) and p19(ARF) cooperate to accelerate asbestos-induced tumorigenesis.

Here is a paper analyzing the intriguing possibility that epigenetic drugs may increase the immunogenic profile of mesothelioma, thereby enhancing the ability of an immune response to target the tumor. 
HDAC inhibitors and demethylating agents open the chromatin into a conformation that facilitates transcription not only of tumor suppressors but also of tumor antigens, such as NY-ESO-1, MAGE-A1 and MAGE-A3.