Abstract
Diffuse malignant peritoneal mesothelioma (DMPM) is a rare malignant neoplasm with a poor survival. Although some advances in knowledge have been obtained for the pleural form, much less is known about DMPM. Advantages in terms of prognosis are still limited and strong efforts need to be made. The aim of our study was to correlate several histological and molecular factors with survival in a large cohort of 45 DMPMs. We evaluated histotype, nuclear grade, mitotic count, necrosis, inflammation, desmoplastic reaction, Ki67 percentage, WT-1 expression, p16 protein by immunohistochemistry and CDKN2A deletion by FISH. Our results showed that epithelioid histotype, nuclear grade 2, mitotic count ≤5 x mm2, absence of desmoplasia and p16/CDKN2A deletion, low Ki67 value, and high WT-1 expression were correlated with the most prolonged survival (p = 0.0001). Moreover, p16 loss in immunohistochemistry reflected CDKN2A deletion detected with FISH, and both were correlated with the worst survival (p = 0.0001). At multivariate analysis, Ki67 value, WT-1 expression and p16/CDKN2A deletion emerged as independent prognostic factors (p = 0.01, p = 0.0001 and p = 0.01, respectively). These parameters are easy to analyse at the time of DMPM diagnosis and may support better patient stratification, prediction of treatment effectiveness and therapeutic optimization.
Highlights
Malignant mesothelioma (MM) is a rare neoplasm that arises from mesothelial cells of serous cavities [1]
Forty-five Diffuse malignant peritoneal mesothelioma (DMPM) were evaluated. 35 male (77.8%) and 10 female (22.2%) patients with a mean age of 63.7 ± 11.5 years were included in the study
Mitotic count showed a mean of 7.6 ± 5.6 x mm2
Summary
Malignant mesothelioma (MM) is a rare neoplasm that arises from mesothelial cells of serous cavities [1]. The onset of MM is strictly related to asbestos exposure, and there is a long latency time prior to first manifestations. Based on the widespread employment of asbestos in the past years, the incidence is expected to drastically increase, reaching a peak between 2002–2050 [2]. MM remains a very aggressive and fatal disease. The five-year mortality rate is higher than 95% [3]. Therapeutic strategies are based on a multimodal approach, including surgery, radiation, and chemotherapy. Targeted therapy with biological agents (i.e., tyrosine kinase inhibitors, proteasome inhibitors) [4] and immunotherapy with immune checkpoint inhibitors (i.e., anti -programmed cell death 1-PD-1/anti -programmed cell death ligand 1 PD-L1 drugs) [5]
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