Malignant pleural mesothelioma (MPM) is a highly lethal cancer of the lining of the chest cavity. To expand our understanding of MPM, we conducted a comprehensive integrated genomic study, including the most detailed analysis of BAP1 alterations to date. We identified histology-independent molecular prognostic subsets, and defined a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity. We also report strong expression of the immune checkpoint gene VISTA in epithelioid MPM, strikingly higher than in other solid cancers, with implications for the immune response to MPM and for its immunotherapy. Our findings highlight new avenues for further investigation of MPM biology and novel therapeutic options.

Background. Evidence of a possible role of viruses in cancer first emerged in the early 1900s and was confirmed after the discovery of Epstein-Barr virus (EBV) in Conclusions. Simian virus 40 (SV40) is a small DNA virus from the genus polyomavirus, closely related to human polyomaviruses John Cunningham virus (JCV) and BK virus (BKV) and is highly oncogenic for rodents. The virus accidentally entered the human population through contaminated early batches of polio vaccine in the 1960s. After the discovery of SV40-like

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RRM1 polymorphisms as well as haplotypes showed an association with gemcitabine treatment efficacy and toxicity; therefore, they should be validated as potential markers for the prediction of clinical outcome in patients with MM.