The chemoprevention of esophageal carcinogenesis with chronic inflammation by the suppression of lipoxygenase

• Project/Area Number: 15K10090
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Kanazawa University
• Principal Investigator: Oyama Katsunobu 金沢大学, 附属病院, 助教 (70460350)
• Co-Investigator(Kenkyū-buntansha): 伏田 幸夫 金沢大学, 医学系, 准教授 (10301194)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000); Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
• Keywords: 食道発癌 / 炎症発癌 / ラットモデル / LOX / Lipoxygenase

Outline of Final Research Achievements

The incidence of Barrett’s epithelium in control group was 94%, in pranlukast group; 69%, the incidence of esophageal adenocarcinoma in control group; 69%, pranlukast group; 15%. Both of Barrett’s epithelium and esophageal adenocarcinoma generation were significantly suppressed by pranlukast administration. Pranlukast administration suppressed tissue growth activity and increased apoptosis. Infiltrating macrophages were reduced by pranlukast administration.
The administration of pranlukast suppressed the generation of Barrett's epithelium and· esophageal adenocarcinoma. Suppression of chronic inflammatory condition by LOX inhibition lead to suppression of carcinogenesis. Moreover, infiltration of macrophages was particularly suppressed among inflammatory cells. Excessive stimulation of tissue growth by macrophages was considered to be one of carcinogenic factors.