Abstract 1414P
Background
Anti-PD-1/PD-L1-based therapy is the standard of care for patients with advanced gastric cancer or esophagogastric junction cancer. Helicobacter pylori (H. pylori, Hp) chronic infection in the stomach mucosa was the major cause of most gastric cancers, and there is a lack of data regarding the association between the efficacy of ICIs and H. pylori infection. We therefore perform a retrospective multicenter study to address this clinically relevant issue.
Methods
Gastric cancer or esophagogastric junction cancer patients who had Hp status results before ICI treatment from January 2016 through July 2020 at our institutes (Beijing Cancer Hospital, Zhejiang Cancer Hospital, or Sun Yat-sen University Cancer Center) were retrospectively reviewed. The patients received regimens including anti-PD-1/PD-L1 mono-therapy, or anti-PD-1/PD-L1 in combination with chemotherapy or anti-angiogenic/ tyrosine kinase inhibitors (TKI). Parameters including age, gender, primary site, differentiation, MSI status, PD-L1, metastastic sites, regimens etc., were included in the analysis.
Results
Of 120 patients, the 55 (45.8%) who tested positive for H. pylori were more likely to have MSI-H tumors (P = 0.016). H. pylori positivity was associated with longer PFS (P = 0.004) and OS (P = 0.013) within the entire cohort regardless of therapeutic modalities. The Hp infection was independently correlated with longer PFS (P = 0.008) and OS (P = 0.005) in the multivariate analysis. In patients receiving ICI monotherapy, H. pylori infection was significantly associated with better survival than H. pylori-negative patients in both PFS (P = 0.023) and OS (P = 0.002). In patients who received ICIs as the first-line therapy, H. pylori was associated with longer PFS (P = 0.003) and a trend of longer OS (P = 0.022).
Conclusions
Although Patients with vs. without H. pylori infection demonstrated distinct clinicopathologic features, H. pylori infection was still independently associated with favorable survival outcomes after the adjustment for multiple variables. Underlying molecular and cellular mechanisms remain elusive and warrant further study.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Qing Wei.
Funding
Zhejiang Natural Science Funding No.LQ21H160005.
Disclosure
All authors have declared no conflicts of interest.