Analysis of molecular mechanism underlying de novo colorectal tumorigenesis pathway

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04299
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Sapporo Medical University
• Principal Investigator: Suzuki Hiromu 札幌医科大学, 医学部, 教授 (20381254)
• Co-Investigator(Kenkyū-buntansha): 山本 英一郎 札幌医科大学, 医学部, 講師 (60567915) ; 甲斐 正広 札幌医科大学, 医学部, 講師 (80260777) ; 丸山 玲緒 札幌医科大学, 医学部, 研究員 (60607985)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 大腸がん / エピゲノム / DNAメチル化 / 遺伝子変異

Outline of Final Research Achievements

Recent advances in the cancer genome study revealed molecular alterations in colorectal cancer (CRC). However, mechanisms underlying the colorectal tumorigenesis in pathways other than the conventional adenoma-carcinoma sequence are not fully understood. To address this issue, we focused on early colorectal lesions with superficial or laterally spreading morphologies and those in the serrated neoplastic pathway. Through performing genetic and epigenetic analysis in a large number of primary colorectal tumors, we identified NTSR1, DKGK, SMOC1 and ZNF582-AS1 as novel CRC-related genes. We found that methylation of NTSR1 is associated with lateral and noninvasive growth of colorectal tumors while methylation of SMOC1 is associated with the development of traditional serrated adenomas. Surface microstructures of early colorectal tumors are associated with genetic and epigenetic alterations, and are associated with the malignant potential.

Free Research Field

分子腫瘍学