FIGURE 4.

Sensitivity to H. pylori eradication therapy is correlated with active gastritis; resistance to H. pylori eradication therapy is correlated with phosphorylated S6K1. (A) The resistant group had higher levels of miR‐155 and lower levels of DEPTOR and TLR5 than the sensitive group. From left to right: X‐axis: sensitive and resistant groups; Y‐axis: dCT of U6‐miR‐155, actin‐DEPTOR, and actin‐TLR5. (B) Representative histopathology of active and chronic gastritis and immunohistochemistry of pS6K1 in gastric diffuse large B‐cell lymphomas. Upper: lymphoma cells surrounding a destroyed foveolar gland with intraluminal neutrophils and debris (left), lymphoma cells in a vascular‐rich stroma with intravascular accumulation of neutrophils (middle), and weak pS6K1 expression (right). Lower: crushed lymphoma cells in a fibrotic stroma and a foveolar gland with intestinal metaplasia (left) and interstitial plasmacytosis (middle), and strong pS6K1 expression on lymphoma cells (right). H/E and immunoperoxidase stains on formalin‐fixed paraffin‐embedded tissue sections (all 1000×, except for the lower left at 400×). (C) The sensitive group is associated with active gastritis; the resistant group is associated with the expression of phosphorylated S6K1. Left: X‐axis: sensitive and resistant groups; Y‐axis: case numbers with active, mixed, chronic gastritis. Right: X‐axis: sensitive and resistant groups; Y‐axis: percentages of phosphorylated S6K1+ cells by immunohistochemistry, mean ± SE. (D) Overall survival (OS) and progression‐free survival (PFS) for the sensitive group are similar to that of the resistant group secondarily treated with chemotherapy. The 5‐year OS is 95.2% (95% CI, 90.6%–99.8%) for 21 sensitive cases and 76.3% (95% CI, 57.7%–97.9%) for 23 resistant cases that also received chemotherapy after failure to H. pylori eradication therapy (p = 0.33). The 5‐year PFS is 95.2% (95% CI, 90.6%–99.8%) for the sensitive group and 68.2% (95% CI, 48.6%–87.8%) for the resistant group (p = 0.15)