Abstract
The diagnosis of mesothelioma is not always straightforward, despite known immunohistochemical markers and other diagnostic techniques. One reason for the difficulty is that extrapleural tumors resembling mesothelioma may have several possible etiologies, especially in cases with no meaningful history of amphibole asbestos exposure. When the diagnosis of mesothelioma is based on histologic features alone, primary mesotheliomas may resemble various primary or metastatic cancers that have directly invaded the serosal membranes. Some of these metastatic malignancies, particularly carcinomas and sarcomas of the pleura, pericardium and peritoneum, may undergo desmoplastic reaction in the pleura, thereby mimicking mesothelioma, rather than the primary tumor. Encasement of the lung by direct spread or metastasis, termed pseudomesotheliomatous spread, occurs with several other primary cancer types, including certain late-stage tumors from genetic cancer syndromes exhibiting chromosomal instability. Although immunohistochemical staining patterns differentiate most carcinomas, lymphomas, and mestastatic sarcomas from mesotheliomas, specific genetic markers in tumor or somatic tissues have been recently identified that may also distinguish these tumor types from asbestos-related mesothelioma. A registry for genetic screening of mesothelioma cases would help lead to improvements in diagnostic criteria, prognostic accuracy and treatment efficacy, as well as improved estimates of primary mesothelioma incidence and of background rates of cancers unrelated to asbestos that might be otherwise mistaken for mesothelioma. This information would also help better define the dose-response relationships for mesothelioma and asbestos exposure, as well as other risk factors for mesothelioma and other mesenchymal or advanced metastatic tumors that may be indistinguishable by histology and staining characteristics.
Highlights
By far, the most extensively investigated cause of mesothelioma is asbestos exposure (Sporn and Roggli, 2004)
Some epidemiologic observations suggest that the incidence of mesothelioma caused by asbestos exposure peaked between about 1990 and 2010, because the highly potent amphibole exposures were largely curtailed in the 1960s and the typical latency period of 20–40 years since first exposure has transpired (Hemminki and Li, 2003; Hillard et al, 2003; Price and Ware, 2004; Weill et al, 2004; Burdorf et al, 2007; Teta et al, 2008; Harding and Darnton, 2010)
Further research is recommended to examine the incidence of malignant mesothelioma among individuals with various forms and severity of congenital heart disease, and perhaps in relation to rheumatic heart disease
Summary
The most extensively investigated cause of mesothelioma is asbestos exposure (Sporn and Roggli, 2004). Germline mutations in nuclear deubiquitinase BRCA1-associated protein 1 (BAP1) have been observed in familial clusters of mesothelioma not necessarily linked to asbestos (Testa et al, 2011) and in a fraction of pleural mesotheliomas in other case series (Bott et al, 2011; Jean et al, 2012; Tallet et al, 2013) These more recent associations are all tied into loss of normal cell signaling that occurs in a variety of cancer types, but further investigations may provide more specific genetic markers to help better distinguish mesothelioma diagnosis, treatment, and prognoses in the future (Bott et al, 2011; Jean et al, 2012; Gocha et al, 2013). The basis for genetic testing that may distinguish specific cancer types probably unrelated to asbestos exposure is reviewed, and the utility of a registry-based research program to enhance medical knowledge regarding the etiology of general and specific subtypes of mesothelioma is explored
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