Evidence map›Paper›PMID 41162621›Full record

ArticleScientific reports2025

MUC1 promoter methylation pattern diversity and its association with TET3 expression and prognosis in cholangiocarcinoma.

Seiya Yokoyama, Ikumi Kitazono, Michiyo Higashi, Kei Matsuo, Taiji Hamada, Mari Kirishima, Hirotsugu Noguchi, Takashi Tasaki, Miki Murakami, Toshiaki Akahane and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

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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. Article
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

14 authors.

Seiya YokoyamaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Ikumi KitazonoDepartment of Surgical Pathology, Kagoshima University Hospital, 8-35-1, Sakuragaoka, Kagoshima, Japan.
Michiyo HigashiDepartment of Surgical Pathology, Kagoshima University Hospital, 8-35-1, Sakuragaoka, Kagoshima, Japan.
Kei MatsuoDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Taiji HamadaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Mari KirishimaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Hirotsugu NoguchiDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Takashi TasakiDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Miki MurakamiDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Toshiaki AkahaneDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Tatsuhiko FurukawaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Takao OhtsukaDepartment of Digestive Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, Japan.
Tomoyuki SugimotoDepartment of Information and Computer Sciences, Graduate School of Engineering Science, Osaka University, 1-3, Machikaneyama, Toyonaka, Osaka, Japan.
Akihide TanimotoDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan. akit09@m3.kufm.kagoshima-u.ac.jp.

Funding

a grant from Grants-in-Aid for Scientific Research on Scientific Research (C) 21K07222a grant from Grants-in-Aid for Scientific Research on Scientific Research (C) 25K19910Research Support Project for Life Science and Drug Discovery JP24ama121054
6 · The paper itself

Abstract

Cholangiocarcinoma (CC) is a highly lethal malignancy that urgently requires reliable prognostic biomarkers. Although MUC1 expression and promoter methylation have been implicated in CC, the clinical significance of promoter methylation pattern composition, beyond average methylation levels, remains unclear. Here, we investigated the relationship between MUC1 promoter methylation heterogeneity, MUC1 mRNA expression, and prognosis in CC. We analyzed bisulfite amplicon sequencing data and mRNA expression of MUC1, DNA methylation-related enzymes (TET1, TET2, TET3, Dnmt1, and Dnmt3a), and tumor microenvironment stress markers in 131 CC tissues. In the neoplastic region, high MUC1 mRNA expression was associated with poor overall survival (HR = 0.131, 95% CI: 0.02 to 0.95, p = 0.042) and correlated with the abundance of completely unmethylated promoter patterns (r = 0.386, p < 0.001). Among the enzymes analyzed, only TET3 expression significantly correlated with the abundance of completely unmethylated patterns in the neoplastic region (Cohen's f

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaDioxygenasesDNA MethylationMucin-1Promoter Regions, GeneticAgedBiomarkers, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedMixed Function OxygenasesPrognosisBiomarkers, TumorDioxygenasesMixed Function OxygenasesMUC1 protein, humanMucin-1TET3 protein, humanCholangiocarcinomaDiversityMucinPrognosisPromoter methylation

Identifiers

PMID41162621
PMCPMC12572258

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LicenceCC BY-NC-ND
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Registered trials

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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.