Assessment of the Changes in Mitochondrial Gene Polymorphism in Ulcerative Colitis and the Etiology of Ulcerative Colitis-associated Colorectal Cancer.


Journal

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

Informations de publication

Date de publication:
Jan 2020
Historique:
received: 10 11 2019
revised: 19 11 2019
accepted: 20 11 2019
entrez: 2 1 2020
pubmed: 2 1 2020
medline: 15 1 2020
Statut: ppublish

Résumé

Mitochondria are energy-producing organelles, and dysfunction in these organelles causes various types of disease. Although several studies have identified mutations in nuclear DNA that are associated with the etiology of ulcerative colitis (UC), information regarding mitochondrial DNA (mtDNA) in UC is limited. This study aimed to investigate the mitochondrial DNA polymorphism underlying the etiology of UC and UC-associated colorectal cancer. Next-generation sequencing was performed to assess mitochondrial DNA mutations in 12 patients with UC-associated cancer. The mtDNA mutations in the non-neoplastic mucosa, tumor tissues, and healthy controls were compared. The incidence of mutations of nicotinamide adenine dinucleotide phosphate ubiquinone oxidase subunit, ATP synthetase, and tRNA was higher in non-neoplastic mucosa in those with UC compared with the healthy controls. However, no statistically significant differences were observed in mutations between the tumor tissues and non-neoplastic mucosa in UC. Significant mutations in mtDNA were observed in the non-neoplastic mucosa of patients with UC-associated cancer.

Sections du résumé

BACKGROUND BACKGROUND
Mitochondria are energy-producing organelles, and dysfunction in these organelles causes various types of disease. Although several studies have identified mutations in nuclear DNA that are associated with the etiology of ulcerative colitis (UC), information regarding mitochondrial DNA (mtDNA) in UC is limited. This study aimed to investigate the mitochondrial DNA polymorphism underlying the etiology of UC and UC-associated colorectal cancer.
MATERIALS AND METHODS METHODS
Next-generation sequencing was performed to assess mitochondrial DNA mutations in 12 patients with UC-associated cancer. The mtDNA mutations in the non-neoplastic mucosa, tumor tissues, and healthy controls were compared.
RESULTS RESULTS
The incidence of mutations of nicotinamide adenine dinucleotide phosphate ubiquinone oxidase subunit, ATP synthetase, and tRNA was higher in non-neoplastic mucosa in those with UC compared with the healthy controls. However, no statistically significant differences were observed in mutations between the tumor tissues and non-neoplastic mucosa in UC.
CONCLUSION CONCLUSIONS
Significant mutations in mtDNA were observed in the non-neoplastic mucosa of patients with UC-associated cancer.

Identifiants

pubmed: 31892558
pii: 40/1/101
doi: 10.21873/anticanres.13931
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101-107

Informations de copyright

Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Toshiaki Tanaka (T)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan toshi-t@venus.dti.ne.jp.

Takashi Kobunai (T)

Translational Research Laboratory, Taiho Pharmaceutical Co., Ltd., Tokyo, Japan.

Yoko Yamamoto (Y)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Koji Murono (K)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Shigenbu Emoto (S)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Masaya Hiyoshi (M)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Manabu Kaneko (M)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Kazuhito Sasaki (K)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Yasutaka Shuno (Y)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Takeshi Nishikawa (T)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Keisuke Hata (K)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Kazushige Kawai (K)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Hiroaki Nozawa (H)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

Soichiro Ishihara (S)

Department of Surgical Oncology, the University of Tokyo, Tokyo, Japan.

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Classifications MeSH