Abstract 1067: Characterization of DNA hypermethylation in two cases of peritoneal mesothelioma

Abstract Background: Malignant mesothelioma (MM) is a rare disease with a poor prognosis. Pleural mesothelioma, which is the most common type of MM, is considered to be caused by asbestos exposure and is increasing in incidence, with about 15,000 new cases diagnosed worldwide annually. On the other hand, peritoneal mesothelioma is a very rare type of MM; thus its pathogenesis is even less understood than pleural mesothelioma. Recent research on the pathogenesis of malignant pleural mesothelioma has indicated that both epigenetic and genetic alterations contribute to tumorigenesis. Here, we hypothesize that peritoneal mesothelioma also has an epigenetic alteration in the same genes (KAZALD1, TMEM30B and MAPK13). Our goal is to identify DNA methylation of these three candidate genes in two peritoneal mesothelioma cases. Methods: Laser capture microdissection (LCM) was used to separate diseased sections of formalin-fixed paraffin-embedded (FFPE) samples from one surgically resected tissue (epithelial type) and one autopsy tissue (sarcomatous type). Genomic DNA was subsequently extracted by the standard phenol chloroform method. The DNA was then treated with sodium bisulfite, and pyrosequencing analysis was used to quantitatively analyze the methylation of candidate genes reported to be hypermethylated in malignant pleural mesothelioma (KAZALD1, TMEM30B and MAPK13). Results: TMEM30B and MAPK13 were not methylated in either case. However, KAZALD1 was highly methylated in sarcomatoid type peritoneal mesothelioma. Discussion: We first report that the KAZALD1 gene was hypermethylated in sarcomatoid type malignant peritoneal mesothelioma. Citation Format: Ritsuko Oikawa, Yoshiyuki Watanabe, Ryota Hama, Hiroyuki Yamamoto, Fumio Itoh. Characterization of DNA hypermethylation in two cases of peritoneal mesothelioma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1067. doi:10.1158/1538-7445.AM2015-1067