Journal
GASTRIC CANCER
Volume 24, Issue 5, Pages 983-989Publisher
SPRINGER
DOI: 10.1007/s10120-021-01215-3
Keywords
Epstein-Barr virus-positive gastric cancer; ARID1A mutations; CD274 copy-number amplification; PD-L1 overexpression; EBV-encoded microRNAs
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Funding
- JSPS KAKENHI [20K09083, 21K08675]
- Grants-in-Aid for Scientific Research [20K09083, 21K08675] Funding Source: KAKEN
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Epstein-Barr virus-positive gastric cancer (EBV (+) GC) is a subtype of GC associated with EBV infection, exhibiting unique genomic and clinicopathological features compared to other subtypes. Noncoding RNAs derived from EBV-infected cells play crucial roles in oncogenesis and tumor progression in EBV (+) GC. Recent studies focus on genetic mutations and protein overexpression in EBV (+) GC, proposing potential targeted therapies for this subtype.
Epstein-Barr virus-positive gastric cancer [EBV (+) GC] is associated with EBV infection and is one of the GC subtypes defined by the Cancer Genome Atlas. EBV (+) GC has several distinct genomic or epigenomic features and clinicopathological characteristics compared with other molecular subtypes of GC. Here, we summarize the unique features of EBV (+) GC including the clinical and histopathological features, and discuss associated genetic and epigenetic aberrations. We also discuss noncoding RNAs [EBV-encoded RNAs and EBV-encoded microRNAs (miRNAs)] derived from EBV-infected cells, which have not been described in detail previously. These noncoding RNAs are defined by their roles; for example, EBV-encoded miRNAs play pivotal roles in oncogenesis and tumor progression in EBV (+) GC. We also discuss recent advances in therapeutic modalities for EBV (+) GC, as well as the potential of EBV infection as a predictive biomarker of the response to anti-PD-1 therapy with immune checkpoint inhibitors. We introduce our recent studies focusing on AT-rich interactive domain 1A gene mutations and programmed death ligand-1 overexpression/CD274 copy-number amplification, which are recurrently identified in EBV (+) GC. Finally, based on those findings, we propose potential therapeutic options using candidate-targeted therapies against EBV (+) GC.
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