Gastric Cancer Risk by eEF1A Dimethylation in Eradicated Mucosa

Eradication therapy for chronic Helicobacter pylori (H. pylori) infection reduces the risk for gastric cancer (GC), but does not remove it entirely, and markers for patients still at high risk for GC after eradication therapy are needed. Researchers investigated if eEF1A lysine 55 (eEF1AK55me2) dimethylation associated with H. pylori status, eradication therapy outcomes, and GC risk.

Dimethylation of eEF1A May Predict Gastric Cancer After Eradication Therapy

In their observational study, published in BMC Gastroenterology, the researchers found evidence that H. pylori infection drove eEF1A dimethylation in gastric mucosa. They also suggested that “accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori eradicated-gastric mucosa.”

The study retrospectively enrolled 115 patients who underwent upper gastrointestinal endoscopy, of which 11 were H. pylori-positive, 29 were H. pylori-negative, and 75 were post-eradication therapy. Researchers used immunofluorescent staining to measure eEF1A dimethyl levels in gastric mucosa cells.

According to the report, eEF1A dimethylation levels significantly increased in the surface (P=.0031) and basal (P=.0036) areas of H. pylori-positive gastric mucosa compared with negative mucosa. Of note, eEF1A dimethyl levels in the surface were significantly lowered after eradication therapy (P=.005), but levels in the basal area were not affected.

Further analyses showed that high dimethylation of eEF1A in the basal area was an independent predictive factor for occurence of GC (odds ratio, 3.6611; 95% CI, 1.350-12.949; P=.0441). In addition, the researchers identified a relationship between eEF1A dimethylation and expressions of 2 reprogramming factors, Oct4 and Nanog.

Ultimately, the study’s authors presented evidence that suggests a link between increased eEF1A dimethylation and H. pylori infection, which could increase risk for gastric cancer, even after H. pylori eradication therapy.

Related: New Insights into Biology, Origin of Deadly Stomach and Esophageal Cancers