Netazepide, a gastrin/cholecystokinin‐2 receptor antagonist, can eradicate gastric neuroendocrine tumours in patients with autoimmune chronic atrophic gastritis

Abstract

A gastrin/cholecystokinin 2 receptor antagonist is a potential medical and targeted treatment for type 1 gastric NETs, and an alternative to regular gastroscopy or surgery. Treatment should be continuous because the tumours will regrow if it is stopped. Progress can be monitored by CgA in blood or biomarkers in mucosal biopsies.

Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use

“…One hundred gastric biopsy samples in 5 different groups were selected from a cohort of 1400 prospectively recruited patients who underwent diagnostic upper gastrointestinal endoscopy at Royal Liverpool University Hospital[ 37 ] and from 8 patients with type I gastric NETs who had been recruited to a clinical trial[ 38 , 39 ] ( Table 1 ). The patients in the 1400 cohort had the following characteristics: Females 57.5%, median age 60 years with an interquartile range 48–70 years and 98.4% were Caucasian.…”

Comparison of the human gastric microbiota in hypochlorhydric states arising as a result ofHelicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use

“…One hundred gastric biopsy samples in 5 different groups were selected from a cohort of 1400 prospectively recruited patients who underwent diagnostic upper gastrointestinal endoscopy at Royal Liverpool University Hospital[14] and from 8 patients with type I gastric NETs who had been recruited to a clinical trial[15, 16] (Table 1).…”

Correct Identification of Cell of Origin May Explain Many Aspects of Cancer: The Role of Neuroendocrine Cells as Exemplified from the Stomach

“…Moreover, the gastrin receptor is localized to the ECL cell and probably not the parietal cell [12]. Gastrin has a specific positive trophic effect on the ECL cell as well as having a general trophic effect on the oxyntic mucosa [13]. Whether the general trophic effect is a direct one, mediated by a hitherto not recognized gastrin receptor on the stem cell, or indirect one by signal substances released from the ECL cell, including histamine [14] and Reg protein [15], is not solved.…”