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Differences in the Tumor Microenvironment of EBV-Associated Gastric Cancers Revealed Using Single-Cell Transcriptome

Mikhail Y Salnikov1, Gregory J Fonseca2,3,4, Joe S Mymryk1,5,6,7

  • 1Department of Microbiology and Immunology, Western University, London, ON N6A 3K7, Canada.

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Summary

Epstein-Barr virus-associated gastric cancers (EBVaGCs) show distinct immune cell populations in their tumor microenvironment. These include proliferating T and B cells, suggesting a heightened inflammatory response unique to EBVaGCs.

Keywords:
Epstein–Barr virusTCGAbiphenotypic B cellsfollicular T helper cellsgastric cancergene expressioninterferonlymphocyte infiltrationsingle-cell RNA sequencingtumor immunologytumor microenvironment (TME)

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Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Epstein-Barr virus (EBV) is linked to approximately 10% of gastric cancers (GCs).
  • EBV-associated GCs (EBVaGCs) exhibit distinct molecular, histopathological, and clinical characteristics compared to EBV-negative GCs (EBVnGCs).
  • Viral proteins in EBVaGCs may elicit stronger immune responses due to their foreign antigen nature.

Purpose of the Study:

  • To identify and molecularly characterize distinct cellular subpopulations within the tumor microenvironment (TME) of EBVaGCs.
  • To analyze gene expression patterns across these subpopulations.
  • To compare the TME of EBVaGCs with EBV-negative GCs.

Main Methods:

  • Utilized bulk and single-cell RNA sequencing data.
  • Identified consistently expressed genes in EBVaGCs.
  • Analyzed gene expression across identified cellular subpopulations.

Main Results:

  • EBVaGCs demonstrate significant lymphocytic infiltration.
  • Three unique immune cell subpopulations were identified: proliferating T cells, proliferating B cells, and B cells with T cell features.
  • The proliferating T cell cluster expressed markers consistent with follicular T helper cells, indicating a heightened inflammatory response.

Conclusions:

  • EBVaGCs possess a unique TME composition characterized by specific immune cell subpopulations and increased inflammation.
  • Further investigation into these cellular differences may reveal phenotypes linked to patient outcomes.
  • These findings underscore the distinct nature of EBVaGCs and their TME.