Evidence map›Paper›PMID 42323373›Full record

ArticleScientific reports2026

Genome-wide DNA methylation profiling during metabolic dysfunction-associated steatohepatitis-related hepatocarcinogenesis in patients in Japan and the United States.

Junko Kuramoto, Eri Arai, Mao Fujimoto, Hiroki Muramoto, Hidenori Ojima, Yosuke Seki, Kazunori Kasama, Nobuaki Funahashi, Haruhide Udagawa, Takao Nammo and 5 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Junko KuramotoDepartment of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan. j-kuramoto@keio.jp.
Eri AraiDepartment of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Mao FujimotoDepartment of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Hiroki MuramotoDepartment of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Hidenori OjimaDivision of Molecular Pathology, Tochigi Cancer Center, Utsunomiya, 320-0834, Japan.
Yosuke SekiWeight Loss and Metabolic Surgery Center, Yotsuya Medical Cube, Tokyo, 102-0084, Japan.
Kazunori KasamaWeight Loss and Metabolic Surgery Center, Yotsuya Medical Cube, Tokyo, 102-0084, Japan.
Nobuaki FunahashiSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, 226-8501, Japan.
Haruhide UdagawaDepartment of Registered Dietitians, Faculty of Health and Nutrition, Bunkyo University, Chigasaki, 253-8550, Japan.
Takao NammoDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, 565-0871, Japan.
Kazuki YasudaDepartment of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, 181-8611, Japan.
Nobuyoshi HiraokaDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, 104-0045, Japan.
Teruhiko YoshidaDepartment of Genetic Medicine and Services, National Cancer Center Hospital, Tokyo, 104-0045, Japan.
Kimberley Jane EvasonDepartment of Pathology, and Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, 84112, USA.
Yae KanaiDepartment of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.

Funding

he Miyakawa Memorial Research Foundation Grant-in-Aid, 2025the Japan Agency for Medical Research and Development AMED no.JP25fk0210150h0002the Japan Society for the Promotion of Science (JSPS) KAKENHI Grant Number 22K15415
6 · The paper itself

Abstract

This study aimed to compare ethnicity-related differences in DNA methylation profiles during metabolic dysfunction-associated steatohepatitis (MASH)-related hepatocarcinogenesis in patients from Japan and the United States (US). Genome-wide DNA methylation analysis using the Infinium assay was performed in 36, 148 and 36 samples of normal liver tissue (NLT), non-cancerous liver tissue showing MASH, and MASH-related hepatocellular carcinoma (HCC), respectively (220 samples in total), from the Japan and US cohorts. Principal component analysis revealed that MASH had a distinct DNA methylation profile differing from that of NLT, and that the MASH profiles in the two cohorts differed from each other. DNA methylation alterations of cancer-related genes in MASH were inherited by or strengthened in MASH-related HCC itself, resulting in expression alterations. DNA methylation alterations of FGFR2, FUT4, B3GNT5 and MOSC1 in the precancerous MASH stage were shared by the two cohorts, suggesting that such genes are commonly associated with MASH-related hepatocarcinogenesis. On the other hand, it was suggested that DNA methylation alterations of ZNF611 and SAMD10, and those of SHC1, are involved specifically in MASH-related hepatocarcinogenesis in the Japan and the US cohorts, respectively. These findings suggest that DNA methylation alterations, which may reflect race and lifestyle, are associated with MASH-related hepatocarcinogenesis.

Indexed as

CarcinogenesisCarcinoma, HepatocellularDNA MethylationFatty LiverLiver NeoplasmsAgedFemaleGene Expression Regulation, NeoplasticGenome-Wide Association StudyHumansJapanMaleMiddle AgedUnited StatesGenome-wide DNA methylation analysisHepatocellular carcinomaJapanMetabolic dysfunction-associated steatohepatitisThe United States

Identifiers

PMID42323373
PMCPMC13558654

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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.