Exploration for the mechanism by which metabolic syndrome contributes to the carcinogenesis of non-B non-C hepatocellular carcinoma

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K15239
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 50010:Tumor biology-related
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Iida Hiroya 滋賀医科大学, 医学部, 准教授 (30733901)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: Proinsulin産生骨髄由来細胞

Outline of Final Research Achievements

Thirty-four cases of NASH related hepatocellular carcinoma (HCC) that underwent initial resection from April 2014 to December 2018 were investigated. Immunostaining of PI-BMDCs at the tumor site were examined. Clinicopathological factors of PI-BMDCs positive group (n = 19) and PI-BMDCs negative group (n = 15) were compared. Age, presence or absence of diabetes, tumor staging, and tumor markers were similar between the two groups. The recurrence-free survival was 17.9 months in the positive group and 7.9 months in the negative group, which had a significant difference (p = 0.034). The survival rate tended to be favorable in the positive group, but no significant difference was observed (p = 0.07).

Free Research Field

消化器外科学

Academic Significance and Societal Importance of the Research Achievements

肝炎ウイルス患者の減少により、ウイルス由来肝癌は減少している。逆に非アルコール性脂肪肝炎 (NASH) 由来の肝癌は増加している。Proinsulin産生骨髄由来細胞(PI-BMDCs)は、糖尿病患者において肝細胞に発現し、炎症性サイトカインを放出することを我々のグループは見出した。今回、PI-BMDCsの発現がNASH肝癌の予後に与える影響を検討し、PI-BMDCsは、 NASH由来肝癌の予後を予測する新たなバイオマーカーとなる可能性が示唆された。