EBV⁺ and MSI Gastric Cancers Harbor High PD-L1/PD-1 Expression and High CD8⁺ Intratumoral Lymphocytes
Both EBV⁺ and MSI gastric cancers (GCs) have high lymphoid infiltration which is rare in MSS/EBV cancers. PD-L1/PD-1 interaction leads to a down-regulated immune response and it is one of the most promising targets for gastric cancer immunotherapy. PD-L1/PD-1 and CD8 expression were immunohistochemi...
Saved in:
Published in: | Cancers Vol. 10; no. 4; p. 102 |
---|---|
Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
MDPI AG
01-04-2018
MDPI |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Both EBV⁺ and MSI gastric cancers (GCs) have high lymphoid infiltration which is rare in MSS/EBV
cancers. PD-L1/PD-1 interaction leads to a down-regulated immune response and it is one of the most promising targets for gastric cancer immunotherapy. PD-L1/PD-1 and CD8 expression were immunohistochemically investigated in a series of 169 FFPE GCs, including 33 EBV⁺, 59 MSI and 77 MSS/EBV
cases. PD-L1 membrane immunoreactivity in more than 5% of tumor cells was present in 31/169 GCs and was associated with high levels of CD8 intraepithelial lymphocytes (TILs;
< 0.001). PD-L1⁺ cases were mainly poorly differentiated (71%), intestinal type (85%) and high lymphoid response (HLR; 90%) tumors. PD-L1 expression was only present in EBV⁺ (46%), MSI (24%) and rare MSS/EBV
(3%) GCs with high CD8⁺ TILs (
< 0.001). Despite being associated with a better prognosis both in the whole series (
< 0.05) and in the MSI subset, PD-L1 is not an independent prognostic factor. PD-L1 gene amplification was detected in 3/17 cases, including 2/7 EBV⁺ and 1/8 MSI GC. PD-1⁺ TILs were significantly higher in EBV⁺ than MSI and MSS/EBV
cases. PD-L1/PD-1 pathway is selectively activated in HLR GCs and could be considered an emerging therapeutic target, particularly for EBV and MSI GCs. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2072-6694 2072-6694 |
DOI: | 10.3390/cancers10040102 |