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NF1 and KRAS mutations in pancreatic cancer secondary to alcoholic chronic pancreatitis

村瀨 貴昭 近畿大学

2022.02.28

概要

The risk of developing pancreatic cancer is significantly higher in the patients with chronic pancreatitis than in those without chronic pancreatitis (CP). However, the genetic mechanisms for this increased risk remain unclear. We hypothesized that different genetic mechanisms may exist in the process of carcinogenesis secondary to CP. We included patients with pancreatic cancer who underwent pancreatectomy between 2012 and 2016 at Kindai University Hospital. Among them, 3 patients had alcoholic CP for more than 2 years. We examined 3 types of tissue samples from each patient: cancerous, CP, and normal tissues. We extracted DNA from each tissue type and used next-generation sequencing (NGS) to detect mutations. We found genomic comutation of KRAS and NF1 in 1 patient. There were no mutations in normal tissues, but mutations occurred in CP tissues. The rate of dissection of pancreatic ductal adenocarcinoma (PDAC) from cancerous tissues was approximately 30%, and the variant frequency of NF1 and KRAS was 34% and 32%, respectively. The rate of dissection of pancreatic ductal tissue from CP tissues was approximately 20%, and the variant frequency of NF1 and KRAS was 19% and 21%, respectively. Comutation of NF1 and KRAS may be a carcinogenic mechanism of pancreatic cancer in patients with alcoholic CP. NF1 and KRAS mutations may be a therapeutic target in patients with pancreatic cancer secondary to CP.

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