Fig. 5

Omic regulated Hypergastrinemic transformation of the ECL cells to GNETs Type 1. The loss of parietal cell function (chronic atrophic gastritis [CAG], pernicious anemia, or other autoimmune diseases) is associated with a low acid state, gastric pH increase and consequent hypergastrinemia with G cell hyperplasia. Since gastrin is a trophic agent for ECL cell proliferation, sustained hypergastrinemia results in ECL cell transformation from hyperplasia to dysplasia, and thereafter neoplastic transformation to a Type 1 GNET (insets right: endoscopy (superior) and H&E microscopy (inferior)). The canonical molecular drivers of neuroendocrine tumorigenesis (red central circle) include a number of omes, e.g. proliferome, growth factor signalome, metabolome, apoptome, etc. The NETest is a multigene assay designed to measure the individual “omes” and identify their expression in blood. Endoscopic and histological images adapted with permission from Lanke et al. [51]