Background: Previous studies revealed that in gastric epithelial cell, CagA can inhibit progression of the cell cycle through activation of nuclear factor of activated T-cell (NFAT) and NFAT-dependent genes, such as p21. We recently reported that CagA and its signaling molecules, p-SHP-2, p-ERK, and Bcl-xL were associated with H. pylori (HP) dependence of gastric mucosa-associated lymphoid tissue lymphoma (MALToma). In this study, we further assessed if CagA and NFAT co-operatively participate in the lymphomagenesis of gastric MALToma. Methods: HP strains were cultured from patients with HP-dependent gastric MALToma. We co-cultured gastric epithelial cell, MA-1 cell (t(14;18)(q32;q21)/IGH-MALT1-positive B-cell lymphoma), and Pfeiffer cell (diffuse large B-cell lymphoma) with HP strains and further evaluated the expression pattern of CagA, CagA-signaling molecules and NFATc1 using western blotting...
Date:
2016-10
Relation:
Annals of Oncology. 2016 Oct;27(Suppl. 6):Meeting Abstract 933P.
