Tsuruta S, et al. - In order to gain knowledge on molecular subtypes of gastric hepatoid adenocarcinomas, researchers analyzed 52 hepatoid adenocarcinomas to determine the expression of surrogate markers of molecular subtypes (MLH1, p53, and EBER in situ hybridization) and some biomarkers (p21, p16, Rb, cyclin D1, cyclin E, β-catenin, Bcl-2, IMP3, ARID1A and HER2), and mutations of TP53, CTNNB1, KRAS, and BRAF. The control group included 36 solid-type poorly differentiated adenocarcinomas. Relatively frequent expressions of HER2 were displayed by hepatoid adenocarcinomas. Compared with the control group, shorter survival, more frequent overexpressions of p16 (67%) and IMP3 (98%) were shown by hepatoid adenocarcinomas. Except for one case each, KRAS or CTNNB-1 mutations were not found in any of hepatoid adenocarcinomas, and no hepatoid adenocarcinomas had BRAF mutation. Overall, gastric hepatoid adenocarcinomas were considered as a genetically heterogenous group. Most of these tumors showed chromosomal instability ("CIN") but findings also revealed the existence of a small number of microsatellite-instable (MSI) hepatoid adenocarcinomas.