Increased PD‐1 expression on CD4+ and CD8+ T cells is involved in immune evasion in gastric cancer

Abstract

Upregulation of PD-1 on both CD4+ and CD8+ T cells may be, in part, responsible for immune evasion in gastric cancer patients.

Programmed cell death protein 1 expression is an independent prognostic factor in gastric cancer after curative resection

“…and CD8 ? T cells was involved in immune evasion [15]. Another study examined PD-L1, cytotoxic T-lymphocyte-associated antigen 4, and indolamine 2,3-dioxygenase expression by immunohistochemistry, and showed that PD-L1 positivity and a high-CD3 microenvironment were related to favorable survival outcomes [14].…”

CRISPR-Cas9-mediated disruption of PD-1 on human T cells for adoptive cellular therapies of EBV positive gastric cancer

“…28 In recent years, a number of studies confirmed PD-L1 expression on the surface of gastric cancer cells 29,30 ; PD-1 expression in peripheral circulating blood lymphocytes, tumor-infiltrating lymphocytes, and its ligands; and PD-L1 in serum and tumor tissue. 31 The expression of PD-L1 and PD-1 was closely related with tumor progression, invasion, …”

Beyond HER2: recent advances and future directions in targeted therapies in esophagogastric cancers

“…Preclinical and translational studies suggest that PD-1 may be an important and promising therapy in gastric cancers, as gastric cancers and infiltrating T cells have higher levels of PD-1 and PD-L1 than adjacent non-tumorous gastric tissue, and the peripheral blood (35). This buttresses the hypothesis that tumor expression of PD-L-1 may result in the recruitment of T cells, and their subsequent persistent activation and exhaustion, perhaps contributing to carcinogenesis and progression.…”

“…While there was no clear difference in outcomes between the two treatment arms in the primary endpoint, progression free survival or objective response rate, there was a significant difference in overall survival, favoring paclitaxel/olaparib, both in the overall population (HR =0.56), and in particular in the low ATM population (HR =0. 35). This has led to the development of a phase III study in patients with low ATM expression gastric cancers (43).…”