Evidence map›Paper›PMID 31111570›Full record

ArticleHelicobacter2019

CHAC1 overexpression in human gastric parietal cells with Helicobacter pylori infection in the secretory canaliculi.

Tomohisa Ogawa, Yuriko Wada, Kosuke Takemura, Philip G Board, Keisuke Uchida, Keisuke Kitagaki, Tomoki Tamura, Takashige Suzuki, Yutaka Tokairin, Yasuaki Nakajima and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Helicobacter, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.2field-weighted citation impact, top 6% of its field
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

13 citing papers in PubMed, 37 citations in OpenAlex.

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  6. High levels of unfolded protein response component CHAC1 associates with cancer progression signatures in malignant breast cancer tissues.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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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

11 authors at 4 institutions in 2 countries.

Tomohisa OgawaDepartment of Human Pathology, Graduate School and Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Yuriko WadaDepartment of Human Pathology, Graduate School and Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Kosuke TakemuraDepartment of Urology, Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital, Tokyo, Japan.
Philip G BoardThe ACRF Department of Cancer Biology and Therapeutics, Group of Molecular Genetics, The John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia.
Keisuke UchidaDivision of Surgical Pathology, Tokyo Medical and Dental University Hospital, Tokyo, Japan.
Keisuke KitagakiDivision of Surgical Pathology, Tokyo Medical and Dental University Hospital, Tokyo, Japan.
Tomoki TamuraDivision of Surgical Pathology, Tokyo Medical and Dental University Hospital, Tokyo, Japan.
Takashige SuzukiDepartment of Human Pathology, Graduate School and Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Yutaka TokairinDepartment of Gastrointestinal Surgery, Tokyo Medical and Dental University, Tokyo, Japan.
Yasuaki NakajimaDepartment of Gastrointestinal Surgery, Tokyo Medical and Dental University, Tokyo, Japan.
Yoshinobu EishiDepartment of Human Pathology, Graduate School and Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0521-1670
Tokyo Medical and Dental University · JPTokyo Medical and Dental University Hospital · JPAustralian National University · AUTokyo Metropolitan Komagome Hospital · JP

Funding

Japan Agency for Medical Research and Development Practical Research for Innovative Cancer ControlJapan Society for the Promotion of Science 16K19077
6 · The paper itself

Abstract

backgroundCation transport regulator 1 (CHAC1), a newly discovered enzyme that degrades glutathione, is induced in Helicobacter pylori (H. pylori)-infected gastric epithelial cells in culture. The CHAC1-induced decrease in glutathione leads to an accumulation of reactive oxygen species and somatic mutations in TP53. We evaluated the possible correlation between H. pylori infection and CHAC1 expression in human gastric mucosa. MATERIALS AND

methodsBoth fresh-frozen and formalin-fixed paraffin-embedded tissue samples of gastric mucosa with or without H. pylori infection were obtained from 41 esophageal cancer patients that underwent esophago-gastrectomy. Fresh samples were used for real-time polymerase chain reaction for H. pylori DNA and CHAC1 mRNA, and formalin-fixed samples were used for immunohistochemistry with anti-CHAC1 and anti-H. pylori monoclonal antibodies. Double-enzyme or fluorescence immunohistochemistry and immuno-electron microscopy were used for further analysis.

resultsSignificant CHAC1 overexpression was detected in H. pylori-infected parietal cells that expressed the human proton pump/H,K-ATPase α subunit, whereas a constitutively low level of CHAC1 mRNA expression was observed in the other samples regardless of the H. pylori infection status, reflecting the weak CHAC1 expression detected by immunohistochemistry in the fundic-gland areas. Immuno-electron microscopy revealed intact H. pylori cells in the secretory canaliculi of infected parietal cells. Some parietal cells exhibited positive nuclear signals for Ki67 in the neck zone of the gastric fundic-gland mucosa with H. pylori infection.

conclusionCation transport regulator 1 overexpression in H. pylori-infected parietal cells may cause the H. pylori-induced somatic mutations that contribute to the development of gastric cancer.

Indexed as

gamma-GlutamylcyclotransferaseGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansParietal Cells, GastricCHAC1 protein, humangamma-Glutamylcyclotransferasecation transport regulator 1gastric cancerHelicobacter pyloriparietal cellssecretary canaliculi

Identifiers

PMID31111570
PMCPMC6618068
OpenAlexW2946121352

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.