ArticleGut2017
Deletion of
Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Tumor count and risk of lymph node metastasis in multiple rectal neuroendocrine tumors: an individual-level pooled analysis.World journal of surgical oncology · 2026Article
- Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms.Molecular cancer · 2026Article
- TRIM6 ablation reverses ICB resistance in MSS gastric cancer by unleashing cGAS-STING-dependent antitumor immunity.Journal of experimental & clinical cancer research : CR · 2025Article
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Uncovering the role of traditional Chinese medicine in immune-metabolic balance of gastritis from the perspective of Cold and Hot: Jin Hong Tablets as a case study.Chinese medicine · 2024Article
- Menin in Cancer.Genes · 2024Review
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- Functional antagonism between CagA and DLC1 in gastric cancer.Cell death discovery · 2022Article
- New Mouse Model Suggests That Some Neuroendocrine Tumors May Originate From Neural Crest-Derived Cells.Cellular and molecular gastroenterology and hepatology · 2022Article
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- Genomics of High-Grade Neuroendocrine Neoplasms: Well-Differentiated Neuroendocrine Tumor with High-Grade Features (G3 NET) and Neuroendocrine Carcinomas (NEC) of Various Anatomic Sites.Endocrine pathology · 2021Review
- Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System.Frontiers in endocrinology · 2021Review
- Low Pepsinogen I/II Ratio and High Gastrin-17 Levels Typify Chronic Atrophic Autoimmune Gastritis Patients With Gastric Neuroendocrine Tumors.Clinical and translational gastroenterology · 2020Article
- Cyclooxygenase-2 up-regulates hepatic somatostatin receptor 2 expression.Scientific reports · 2018Article
- Gastroenteropancreatic neuroendocrine neoplasms: genes, therapies and models.Disease models & mechanisms · 2018Review
- Gastrin Induces Nuclear Export and Proteasome Degradation of Menin in Enteric Glial Cells.Gastroenterology · 2017Article
- Enteric Glia: The Origin of Duodenal Gastrinomas?Gastroenterology · 2017Article
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Pathophysiology of Gastric NETs: Role of Gastrin and Menin.Current gastroenterology reports · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGastric carcinoids are slow growing neuroendocrine tumours arising from enterochromaffin-like (ECL) cells in the corpus of stomach. Although most of these tumours arise in the setting of gastric atrophy and hypergastrinemia, it is not understood what genetic background predisposes development of these ECL derived tumours. Moreover, diffuse microcarcinoids in the mucosa can lead to a field effect and limit successful endoscopic removal.
objectiveTo define the genetic background that creates a permissive environment for gastric carcinoids using transgenic mouse lines.
designThe multiple endocrine neoplasia 1 gene locus (Men1) was deleted using Cre recombinase expressed from the Villin promoter (Villin-Cre) and was placed on a somatostatin null genetic background. These transgenic mice received omeprazole-laced chow for 6 months. The direct effect of gastrin and the gastrin receptor antagonist YM022 on expression and phosphorylation of the cyclin inhibitor p27
resultsThe combination of conditional Men1 deletion in the absence of somatostatin led to the development of gastric carcinoids within 2 years. Suppression of acid secretion by omeprazole accelerated the timeline of carcinoid development to 6 months in the absence of significant parietal cell atrophy. Carcinoids were associated with hypergastrinemia, and correlated with increased Cckbr expression and nuclear export of p27
conclusionsGastric carcinoids require threshold levels of hypergastrinemia, which modulates p27
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What OpenQuestion holds
Registered trials
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.