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Association of Fusobacterium nucleatum with clinical and molecular features in colorectal serrated pathway
Author(s) -
Ito Miki,
Kanno Shinichi,
Nosho Katsuhiko,
Sukawa Yasutaka,
Mitsuhashi Kei,
Kurihara Hiroyoshi,
Igarashi Hisayoshi,
Takahashi Taiga,
Tachibana Mami,
Takahashi Hiroaki,
Yoshii Shinji,
Takenouchi Toshinao,
Hasegawa Tadashi,
Okita Kenji,
Hirata Koichi,
Maruyama Reo,
Suzuki Hiromu,
Imai Kohzoh,
Yamamoto Hiroyuki,
Shinomura Yasuhisa
Publication year - 2015
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.29488
Subject(s) - fusobacterium nucleatum , microsatellite instability , colorectal cancer , pathology , medicine , hepatology , hyperplastic polyp , gastroenterology , cancer research , biology , colonoscopy , cancer , genetics , gene , microsatellite , allele , periodontitis , porphyromonas gingivalis
Human gut microbiota is being increasingly recognized as a player in colorectal cancers (CRCs). Evidence suggests that Fusobacterium nucleatum ( F. nucleatum ) may contribute to disease progression and is associated with CpG island methylator phenotype (CIMP) and microsatellite instability (MSI) in CRCs; however, to date, there are no reports about the relationship between F. nucleatum and molecular features in the early stage of colorectal tumorigenesis. Therefore, we investigated the presence of F. nucleatum in premalignant colorectal lesions. In total, 465 premalignant lesions (343 serrated lesions and 122 non‐serrated adenomas) and 511 CRCs were studied. We determined the presence of F. nucleatum and analyzed its association with molecular features including CIMP, MSI and microRNA‐31 status. F. nucleatum was detected in 24% of hyperplastic polyps, 35% of sessile serrated adenomas (SSAs), 30% of traditional serrated adenomas (TSAs) and 33% of non‐serrated adenomas. F. nucleatum was more frequently detected in CIMP‐high premalignant lesions than in CIMP‐low/zero lesions ( p = 0.0023). In SSAs, F. nucleatum positivity increased gradually from sigmoid colon to cecum ( p = 0.042). F. nucleatum positivity was significantly higher in CRCs (56%) than in premalignant lesions of any histological type ( p < 0.0001). In conclusion, F. nucleatum was identified in premalignant colorectal lesions regardless of histopathology but was more frequently associated with CIMP‐high lesions. Moreover, F. nucleatum positivity increased according to histological grade, suggesting that it may contribute to the progression of colorectal neoplasia. Our data also indicate that F. nucleatum positivity in SSAs may support the “colorectal continuum” concept.