Evidence map›Paper›PMID 42249954›Full record

ArticleMedical molecular morphology2026

Significance of p53-binding protein 1 as an in situ DNA damage marker for ulcerative colitis.

Nazigul Zhumagazhiyeva, Miho Doo, Yerkezhan Sailaubekova, Yoshiyuki Matsumoto, Iori Fujisawa, Eri Yoshioka, Masanobu Ikeda, Keiichi Hasiguchi, Maiko Tabuchi, Yasuaki Shibata and 5 more

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Article in Medical molecular morphology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Nazigul Zhumagazhiyeva *Department of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Miho Doo *Department of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Yerkezhan SailaubekovaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Yoshiyuki MatsumotoDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Iori FujisawaDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Eri YoshiokaDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Masanobu IkedaDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Keiichi HasiguchiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Maiko TabuchiDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Yasuaki ShibataDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Takahiro MotoyamaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Yuki MatsuokaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Katsuya MatsudaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Hisamitsu MiyaakiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Yuko AkazawaDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. akazaway@nagasaki-u.ac.jp.

Funding

Japan Society for the Promotion of Science 23K06442
6 · The paper itself

Abstract

Ulcerative colitis is a chronic inflammatory bowel disease characterized by persistent inflammation of the colon. The extensive and persistent mucosal damage associated with ulcerative colitis (UC) can contribute to carcinogenesis, thereby underscoring the significant clinical interest in identifying an in situ marker. p53-binding protein (53BP1) is a DNA damage response (DDR) molecule that localizes at sites of double-strand breaks. Herein, we investigated the in situ DDR in UC by evaluating 53BP1 immunofluorescence. Our study revealed a significant increase in abnormal 53BP1 foci, defined as three or more foci and/or foci larger than 1 µm within the nucleus, in patients with UC compared to controls. Furthermore, the presence of abnormal 53BP1 foci in UC correlated with the severity of symptoms, endoscopic gradings, serological and histopathological inflammation. Of note, 53BP1 foci were observed in the colon mucosa of patients in remission, indicating that 53BP1 is a sensitive DDR marker. In addition, large 53BP1 foci, indicative of a severe DDR, were more prevalent in patients with colitic cancer than in controls. In conclusion, our findings suggest that 53BP1 may serve as a in situ marker reflecting the extent of the DDR in UC.

Indexed as

Colitis, UlcerativeDNA DamageTumor Suppressor p53-Binding Protein 1AdultAgedBiomarkersColonFemaleHumansIntestinal MucosaMaleMiddle AgedBiomarkersTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 153BP1Colitic cancerDNA double-strand breakDNA instabilityInflammationInflammatory bowel diseases

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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.