ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2020
A genetic origin for acid-base imbalance triggers the mitochondrial damage that explains the autoimmune response and drives to gastric neuroendocrine tumours.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Pyroptosis in gastric mucosal injury‑related diseases (Review).International journal of molecular medicine · 2025Review
- Genetically engineered mouse models in gastric precancerous lesions research.World journal of gastrointestinal surgery · 2025Review
- The persistent risk of secondary malignancies in gastric neuroendocrine tumor survivors: a population-based analysis.Clinical and experimental medicine · 2025Article
- The role of mitochondrial biogenesis, mitochondrial dynamics and mitophagy in gastrointestinal tumors.Cancer cell international · 2025Review
- Gastric neuroendocrine neoplasms.Nature reviews. Disease primers · 2024Review
- Remodeling of the gastric environment inmSystems · 2024Article
- IL-17A in gastric carcinogenesis: good or bad?Frontiers in immunology · 2024Review
- Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis.Current issues in molecular biology · 2023Review
- Mitochondrial Function in Health and Disease: Responses to Helicobacter pylori Metabolism and Impact in Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Review
- New Developments in Gastric Neuroendocrine Neoplasms.Current oncology reports · 2022Review
- Article
- Transcriptome profiling implicated in beneficiary actions of kimchi extracts againstJournal of clinical biochemistry and nutrition · 2021Article
- Metabolomic Study of Zuojin Pill in Relieving 1-Methyl-3-nitro-1-nitrosoguanidine-Induced Chronic Atrophic Gastritis.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Case Report: CMV Infection and Same Mechanism-Originated Intestinal Inflammation Compatible With Bowel/Crohn's Disease Is Suggested in ATP4A Mutated-Driven Gastric Neuroendocrine Tumors.Frontiers in medicine · 2021Article
- Clinicopathological characteristics and prognosis of 77 cases with type 3 gastric neuroendocrine tumours.World journal of gastrointestinal oncology · 2020Article
- Clinicopathological Features of Gastroesophageal Neuroendocrine Neoplasms.Current gastroenterology reports · 2020Review
- Identification of an Individualized Prognostic Signature Based on the RWSR Model in Early-Stage Bladder Carcinoma.BioMed research international · 2020Article
- The Altered Metabolic Molecular Signatures Contribute to the RAD001 Resistance in Gastric Neuroendocrine Tumor.Frontiers in oncology · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundType I gastric neuroendocrine tumors (gNETs) arise from hypergastrinemia in patients with autoimmune chronic atrophic gastritis. According to the classical model, the gastric H+/K+ ATPase was the causative autoantigen recognized by CD4+ T cells in chronic autoimmune scenario that secretes IL-17 and correlates with parietal cell (PC) atrophy, which drives to gastric achlorhydria and increases the risk for gastric neoplasms. However, the mechanism by which the inflammatory response correlates with PC atrophy is not clearly defined.
methodsRecently, we found that the ATP4A
resultsThe ATP4A
conclusionsA genetic origin that drives mitochondria alteration would initiate the gastric chronic inflammation instead of the classical IL-17 secretion-mediated mechanism explanation. Gastric euchlorhydria restoration is suggested to be indicated for mitochondrial recover. Our results open a new window to understand gastric neoplasms formation but also the inflammatory mechanisms and autoimmune disorders conducted by genetic origin that composes a premalignant scenario.
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