Detection of Endogenous DNA Double-strand Breaks in Oral Squamous Epithelial Lesions by P53-binding Protein 1.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Oct 2021
Historique:
received: 27 06 2021
revised: 24 07 2021
accepted: 24 08 2021
entrez: 1 10 2021
pubmed: 2 10 2021
medline: 9 10 2021
Statut: ppublish

Résumé

P53-binding protein 1 (53BP1) is one of the DNA damage response (DDR) molecules. This study aimed to assess 53BP1 expression by immunofluorescence (IF) as a biomarker to differentiate between oral squamous epithelial lesions (OSELs). We analyzed 129 archival oral biopsy samples, including 18 benign squamous lesions (BSLs), 37 low-grade dysplasias (LGDs), 22 high-grade dysplasias (HGDs), and 52 oral squamous cell carcinomas (OSCCs). 53BP1 and Ki-67 expressions were examined by double IF to assess the type of 53BP1 expression. We found that OSCC exhibited several 53BP1 nuclear foci, particularly high-DNA damage response (HDDR) and large focus (LF)-type, suggesting the presence of endogenous DNA double-strand breaks in the cancer genome, which could disrupt DDR and induce genomic injury. We also found a difference in 53BP1 expression between LGD and HGD, but not between BSL and LGD. Among the Ki-67-positive cells, HDDR- and LF-type expressions were higher in OSELs of higher grades. 53BP1 expression can be a valuable biomarker for OSELs to help estimate the grade of oral epithelial dysplasia.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
P53-binding protein 1 (53BP1) is one of the DNA damage response (DDR) molecules. This study aimed to assess 53BP1 expression by immunofluorescence (IF) as a biomarker to differentiate between oral squamous epithelial lesions (OSELs).
MATERIALS AND METHODS METHODS
We analyzed 129 archival oral biopsy samples, including 18 benign squamous lesions (BSLs), 37 low-grade dysplasias (LGDs), 22 high-grade dysplasias (HGDs), and 52 oral squamous cell carcinomas (OSCCs). 53BP1 and Ki-67 expressions were examined by double IF to assess the type of 53BP1 expression.
RESULTS RESULTS
We found that OSCC exhibited several 53BP1 nuclear foci, particularly high-DNA damage response (HDDR) and large focus (LF)-type, suggesting the presence of endogenous DNA double-strand breaks in the cancer genome, which could disrupt DDR and induce genomic injury. We also found a difference in 53BP1 expression between LGD and HGD, but not between BSL and LGD. Among the Ki-67-positive cells, HDDR- and LF-type expressions were higher in OSELs of higher grades.
CONCLUSION CONCLUSIONS
53BP1 expression can be a valuable biomarker for OSELs to help estimate the grade of oral epithelial dysplasia.

Identifiants

pubmed: 34593426
pii: 41/10/4771
doi: 10.21873/anticanres.15292
doi:

Substances chimiques

Biomarkers, Tumor 0
Ki-67 Antigen 0
TP53BP1 protein, human 0
Tumor Suppressor p53-Binding Protein 1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4771-4779

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Toshinobu Imaizumi (T)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Department of Diagnostic Pathology, Nagasaki University Hospital, Nagasaki, Japan.

Katsuya Matsuda (K)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Kei Tanaka (K)

Department of Diagnostic Pathology, Nagasaki University Hospital, Nagasaki, Japan.

Hisayoshi Kondo (H)

Biostatistics Section, Division of Scientific Data Registry, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.

Nozomi Ueki (N)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Hirokazu Kurohama (H)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Chieko Otsubo (C)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Yuki Matsuoka (Y)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Yuko Akazawa (Y)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Shiro Miura (S)

Department of Diagnostic Pathology, National Hospital Organization Nagasaki Medical Center, Nagasaki, Japan.

Masahiro Nakashima (M)

Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; moemoe@nagasaki-u.ac.jp.

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Classifications MeSH