English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Open

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Despite multidisciplinary treatment for patients with advanced gastric cancer, their prognosis remains poor. Therefore, the development of novel therapeutic strategies is urgently needed, and immunotherapy utilizing anti‐programmed death 1/‐programmed death ligand‐1  mA b is an attractive approach. However, as there is limited information on how programmed death ligand‐1 is upregulated on tumor cells within the tumor microenvironment, we examined the mechanism of programmed death ligand‐1 regulation with a particular focus on interferon gamma in an in vitro setting and in clinical samples. Our in vitro findings showed that interferon gamma upregulated programmed death ligand‐1 expression on solid tumor cells through the  JAK ‐signal transducer and activator of transcription pathway, and impaired the cytotoxicity of tumor antigen‐specific  CTL  against tumor cells. Following treatment of cells with anti‐programmed death ligand‐1  mA b after interferon gamma‐pre‐treatment, the reduced anti‐tumor  CTL  activity by interferon gamma reached a higher level than the non‐treatment control targets. In contrast, programmed death ligand‐1 expression on tumor cells also significantly correlated with epithelial‐mesenchymal transition phenotype in a panel of solid tumor cells. In clinical gastric cancer samples, tumor membrane programmed death ligand‐1 expression significantly positively correlated with the presence of  CD 8‐positive T cells in the stroma and interferon gamma expression in the tumor. The results suggest that gastric cancer patients with high  CD 8‐positive T‐cell infiltration may be more responsive to anti‐programmed death 1/‐programmed death ligand‐1  mA b therapy.

PD ‐L1 expression is mainly regulated by interferon gamma associated with JAK ‐ STAT pathway in gastric cancer