Evidence map›Paper›PMID 39272845›Full record

ArticleCancers2024

Significance of P53-Binding Protein 1 as a Novel Molecular Histological Marker for Hypopharyngeal Squamous Neoplasms.

Hiroko Kawasaki-Inomata, Maiko Tabuchi, Kiyuu Norimatsu, Tetsuro Honda, Katsuya Matsuda, Keiichi Hashiguchi, Naoyuki Yamaguchi, Hideaki Nishi, Yoshihiko Kumai, Masahiro Nakashima and 3 more

Abstract read
In one paragraph

Article in Cancers, 2024. 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. 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

13 authors.

Hiroko Kawasaki-InomataDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.ORCID 0000-0001-8902-4217
Maiko TabuchiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Kiyuu NorimatsuDepartment of Rheumatology, National Hospital Organization Ureshino Medical Center, Saga 843-0393, Japan.
Tetsuro HondaMedical Education Development Center, Nagasaki University Hospital, Nagasaki 852-8501, Japan.
Katsuya MatsudaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0000-0001-7345-2014
Keiichi HashiguchiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.ORCID 0000-0003-4071-9653
Naoyuki YamaguchiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Hideaki NishiDepartment of Otolaryngology, Head and Neck Surgery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Yoshihiko KumaiDepartment of Otolaryngology, Head and Neck Surgery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Masahiro NakashimaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0000-0002-9036-8735
Hisamitsu MiyaakiDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Kazuhiko NakaoDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Yuko AkazawaDepartment of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.

Funding

Network-type Joint Usage/Research Center for Radiation Disaster Medical Science JYU1-26
6 · The paper itself

Abstract

The DNA damage response protein p53-binding protein 1 (53BP1) accumulates and forms foci at double-strand DNA breaks, indicating the extent of DNA instability. However, the potential role of 53BP1 as a molecular biomarker for hypopharyngeal squamous cell carcinoma (HPSCC) diagnosis remains unknown. Here, we evaluated the potential of immunofluorescence-based analysis of 53BP1 expression to differentiate the histology of hypopharyngeal neoplasms. A total of 125 lesions from 39 surgically or endoscopically resected specimens from patients with HPSCC was histologically evaluated. 53BP1 expression in the nucleus was examined using immunofluorescence. The number of 53BP1 nuclear foci increased with the progression from non-tumorous to low-grade dysplasia, high-grade dysplasia, and squamous cell carcinoma. Unstable 53BP1 expression served as an independent factor for distinguishing lesions that required intervention. Colocalization of 53BP1 foci in proliferating cells, as assessed by Ki67, was increased in tumors ≥ 1000 µm in depth compared to those <1000 µm in depth at the tumor surface. Hence, the expression patterns of nuclear 53BP1 foci were associated with the progression of hypopharyngeal neoplasms. These findings suggest that 53BP1 could serve as an ancillary marker to support histological diagnosis and predict the factors that influence prognosis in patients with HPSCC.

Indexed as

DNA double-strand breakgenomic instabilityhypopharyngeal squamous cell carcinomap53-binding protein 1

Identifiers

PMID39272845
PMCPMC11394016

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.