In a recent publication in the Journal of the American Medical Association Network Open, over a long-term follow-up period, the use of H pylori treatments was associated with a diminished risk of gastric cancer (GC) among individuals with a high genetic risk, suggesting that primary prevention could be personalized to genetic risk for more effective prevention.

The authors wrote, “Helicobacter pylori treatment and nutrition supplementation may protect against gastric cancer (GC), but whether the beneficial effects only apply to potential genetic subgroups and whether high genetic risk may be counteracted by these chemoprevention strategies remains unknown.”

Using follow-up data from the Shandong Intervention Trial (SIT) and China Kadoorie Biobank (CKB), the researchers explored the genetic variants associated with the development of gastric lesions and GC risk and evaluated the clinical benefits associated with H pylori treatment and nutrition supplementation according to degree of genetic risk.

The researchers first conducted a longitudinal genome-wide association study (GWAS) to detect genetic variants for gastric lesion progression. The analyses included 2,816 participants (mean [SD] age, 46.95 [9.12] years; 1,429 [50.75%] women) in SIT and 100,228 participants (mean [SD] age, 53.69 [11.00] years; 57,357 [57.23%] women) in CKB.

For external validation of polygenic risk score (PRS) associated with the risk of GC was employed with a cohort of 1,394 participants (mean age 54.54 years, 37.8% women), including 702 with GC and 692 controls. The results revealed that during a 27.1-year follow-up period, researchers identified 147 and 825 cases of GC in the SIT and CKB cohorts, respectively.

According to the results, a PRS of 12 independent signals of genomic loci was linked with GC risk in the CKB cohort (highest vs. lowest decile of PRS: hazard ratio [HR] = 2.54; 95% CI, 1.8-3.57). The researchers further described a noteworthy association between the PRS and GC risk in the validation cohort, in which the odds of gastric cancer augmented 1.83-fold (95% CI, 1.11-3.05) for the highest versus lowest PRS decile.

Moreover, the results revealed that H pylori treatment was only linked with a diminished risk of GC among individuals with high genetic risk, not for those individuals with low genetic risk. The results also demonstrated that such effect adjustment was not discovered for vitamin or garlic supplementation.

Based on their results, the authors concluded that among those with high genetic risk, appropriate primary prevention of GC may be correlated with a lesser risk of GC, signifying that chemoprevention strategies should be personalized according to genetic risk for effective GC prevention.

The authors wrote, “Integrating host and genetic characteristics for fine risk stratification and, ideally, with tailored regimen selection, would be warranted in future endeavors for optimized primary prevention of GC.”

The content contained in this article is for informational purposes only. The content is not intended to be a substitute for professional advice. Reliance on any information provided in this article is solely at your own risk.