ArticleOncotarget2017
Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Targeted therapy and immunotherapy for gastric cancer: rational strategies, novel advancements, challenges, and future perspectives.Molecular medicine (Cambridge, Mass.) · 2025Review
- Weipiling decoction alleviates N-methyl-N-nitro-N'-nitrosoguanidine-induced gastric precancerous lesions via NF-κB signalling pathway inhibition.Chinese medicine · 2022Article
- Brain metastasis from gastric adenocarcinoma: A large comprehensive population-based cohort study on risk factors and prognosis.Frontiers in oncology · 2022Article
- The deleterious association between proton pump inhibitors and prostate cancer-specific mortality - a population-based cohort study.Prostate cancer and prostatic diseases · 2020Article
- Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer.Oxidative medicine and cellular longevity · 2020Review
- Dietary Fat-Accelerating Leptin Signaling Promotes Protumorigenic Gastric Environment in Mice.Nutrients · 2019Article
- Inhibitory effects of isocryptotanshinone on gastric cancer.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate if oral omeprazole application induces cancers of fore and glandular stomach in mice.
methodsA total of 66 eligible male mice were randomly divided into 6 groups, which were treated with control reagent, low (6 mg/kg) and high dose omeprazole (30 mg/kg), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, 100 mg/L water), and MNNG plus low and high dose omeprazole, respectively. After 24 weeks, concentrations of acid phosphatase (ACP) and N-acetyl-β-D-glucosaminidase(NAG) in serum and spleen was examined, and p21 and mTOR levels in stomach were detected.
resultsThe mouse spleen weight index was smaller in the omeprazole group than the control group, and in the MNNG plus omeprazole groups than the MNNG group. In the fore-stomach, more carcinomas were observed in the MNNG plus omeprazole groups than in the MNNG group. In the glandular stomach, there existed more atypical hyperplasia cases in the MNNG plus omeprazole groups than the MNNG-treated group, and one carcinoma was induced in the MNNG plus high dose omeprazole group. Omeprazole alone caused minor gastric pathological changes. Omeprazole treatment lowered both serum and spleen ACP and NAG levels in both the non-MNNG-treated and MNNG-treated subgroups. In fore-stomach, there existed decreased p21 and mTOR levels in the omeprazole-treated groups than in the control group, and in the MNNG plus omeprazole groups than the MNNG-treated group.
conclusionOmeprazole promotes carcinogenesis of the mouse fore-stomach but not the glandular stomach following treatment with MNNG. Lysosomal hydrolase activity was inhibited and some cancer-associated proteins was dysregulated, which requires further explorations.
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