Evidence map›Paper›PMID 40522380›Full record

ArticleInternational journal of clinical oncology2025

Characteristics of gut microbiota in high-methylated colorectal cancer.

Tatsushi Saito, Hideaki Karasawa, Kota Ouchi, Tomoyuki Ono, Taiki Kajiwara, Atsushi Kohyama, Wakako Ikeda-Ohtsubo, Shinji Fukuda, Fumiyoshi Fujishima, Yohei Ozawa and 7 more

Abstract read
In one paragraph

Article in International journal of clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Gut Microbial Metabolism in Colorectal Cancer.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Tatsushi SaitoDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Hideaki KarasawaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan. hideaki.karasawa.e1@tohoku.ac.jp.ORCID http://orcid.org/0000-0003-0358-3398
Kota OuchiDepartment of Oncology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Tomoyuki OnoDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Taiki KajiwaraDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Atsushi KohyamaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Wakako Ikeda-OhtsuboFood and Feed Immunology Group, Laboratory of Animal Food Function, Graduate School of Agricultural Science, Tohoku University, Sendai, 980-8572, Japan.
Shinji FukudaInstitute for Advanced Biosciences, Keio University, 246-2 Kakuganji, Mizukami, Tsuruoka, 997-0052, Japan.
Fumiyoshi FujishimaDepartment of Pathology, Tohoku University Hospital, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Yohei OzawaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Hideyuki SuzukiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Kazuhiro WatanabeDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Chikashi IshiokaDepartment of Oncology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Takashi KameiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Shinobu OhnumaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.
Takaaki AbeDepartment of Biomedical Engineering Regenerative and Biomedical Engineering Medical Science, Tohoku University Graduate School of Biomedical Engineering, 6-6 Aoba, Aoba-Ku, Sendai, 980-8579, Japan.
Michiaki UnnoDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, 980-8574, Japan.

Funding

Japan Agency for Medical Research and Development (AMED) JP22ek0210133Japan Agency for Medical Research and Development (AMED) JP23zf0127001Japan Society for the Promotion of Science (JSPS) KAKENHI 24K11819Japan Society for the Promotion of Science (JSPS) KAKENHI JP23fk0108655
6 · The paper itself

Abstract

backgroundEpigenetic alterations, including DNA methylation, significantly contribute to colorectal cancer (CRC); the gut microbiota is also involved. However, studies on the possible role of microbiota in DNA methylation are limited. This study investigates the association between gut microbiota composition and high-methylated CRC (HMCC).

methodsFecal and tumor tissue samples were collected from 86 patients with sporadic CRC. HMCC was defined based on the methylation status of 16 CpG sites of tumor-derived genomic DNA. 16S rRNA gene sequencing was performed to reveal the composition of the gut microbiota. The load of Fusobacterium nucleatum (F. nucleatum) in tumor tissues was assessed using quantitative polymerase chain reaction (qPCR).

resultsHMCC was identified in 21 patients, whereas 65 were classified as having low-methylated CRC (LMCC). HMCC was significantly associated with proximal location, large diameter, undifferentiated histology, and high frequency of BRAF mutation. In gut microbial analyses, the relative abundances of 84 bacteria, including F. nucleatum, were significantly different between HMCC and LMCC. The load of F. nucleatum in CRC specimens was significantly correlated with its relative abundance in fecal samples and tended to be enriched in HMCC tissues.

conclusionsThis study characterizes the gut microbiota profile in HMCC and suggests that bacteria, such as F. nucleatum, may contribute to HMCC pathogenesis through DNA methylation. Further studies are needed to determine whether the microbiome acts as a promoter or bystander in HMCC development.

Indexed as

Colorectal NeoplasmsDNA MethylationGastrointestinal MicrobiomeAdultAgedAged, 80 and overCpG IslandsFecesFemaleFusobacterium nucleatumHumansMaleMiddle AgedProto-Oncogene Proteins B-rafRNA, Ribosomal, 16SBRAF protein, humanProto-Oncogene Proteins B-rafRNA, Ribosomal, 16SColorectal cancerCpG island methylator phenotypeFusobacterium nucleatumHigh-methylated colorectal cancer

Identifiers

PMID40522380
PMCPMC12378490

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.