Abstract
Due to occupational asbestosis exposure, malignant pleural mesothelioma (MPM) incidence has increased continuously for the last 30 years, a plateau being anticipated around 2030. Molecular carcinogenesis of MPM involves NF2, WT1 RASSF1, p16, and BAP1 tumor-suppressor genes alterations, regulating apoptosis, cell invasion and motility, cell division, chromatin remodeling, and DNA repair control. In selected patients, debulking surgery (pleurectomy–decortication) provided unsatisfactory long-term results. First-line chemotherapy was based on a doublet of pemetrexed and cisplatin for 15 years. Addition of the monoclonal antibody bevacizumab (Avastin®), targeting vascular endothelial growth factor (VEGF), has been shown to improve overall survival (to nearly 19 months), without quality of life (QoL) alteration, in the French Intergroup-sponsored randomized Mesothelioma Avastin Cisplatin Pemetrexed Study (MAPS) phase 3 trial. The emergence of immune check-point inhibitors (ICI) in cancer treatment prompted to study whether (1) MPM could be considered as “hot” tumors regarding inflammatory infiltration, (2) ICI could play a role in MPM treatments, and (3) what could be the predictors of ICI efficacy in MPM. Convergent preliminary results currently support that, indeed, ICI could represent a major advance in future MPM standard care and are reviewed in this chapter.
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