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Poster session 14

758P - A comprehensive analysis of tumor-infiltrating immune cells in HPV-associated cancers

Date

10 Sep 2022

Session

Poster session 14

Topics

Tumour Immunology

Tumour Site

Cervical Cancer;  Head and Neck Cancers

Presenters

Hong Yang

Citation

Annals of Oncology (2022) 33 (suppl_7): S331-S355. 10.1016/annonc/annonc1058

Authors

H. Yang1, A. Lin1, K. Wei1, J. Zhang1, P. Luo2

Author affiliations

  • 1 Department Of Oncology, Zhujiang Hospital of Southern Medical University, 501280 - Guangzhou/CN
  • 2 Department Of Oncology, Zhujiang Hospital of Southern Medical University, 510282 - Guangzhou/CN
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Abstract 758P

Background

With 690,000 (31%) of the 2.2 million new infection-attributable cases of cancer diagnosed in 2018, human papillomavirus (HPV) is the second most important infectious cause of cancer worldwide. The specific tumor microenvironment (TME) after HPV infection could shape tumor progression and influence therapeutic response, yet underlying mechanisms are not fully understood.

Methods

We acquired transcriptomic profiles of cervical, bladder, and head-and-neck cancers from gene expression omnibus (GEO) and The Cancer Genome Atlas (TCGA) database, and estimated immune cell composition by CIBERSORT, xCell, and MCPcounter algorithms. After identifying differentially expressed genes, Gene Set Enrichment Analysis (GSEA) and Single-Sample Gene Set Enrichment Analysis (ssGSEA) were performed with collections from the Molecular Signatures Database (MSigDB) to evaluate pathway enrichment between HPV (+) and HPV (-) groups.

Results

Among all 7 datasets, we observed higher levels of gamma-delta T (γδ T) cells in HPV (+) groups via the xCell algorithm, five of which showed statistical significance (p < 0.05). HPV (+) groups also presented the higher infiltration of B cells and lower infiltration of monocytes. GSEA revealed that HPV infection activated the T-cell receptor (TCR) signaling pathway (TCGA-CESC: NES = 1.76, adj.p = 0.02; TCGA-HNSC: NES = 1.76, adj.p = 0.01; GSE6791: NES = 2.29, adj.p < 0.01; GSE65858: NES = 1.97, adj.p < 0.01), while suppressed pathways promoting immune cells development, growth, and differentiation, such as the Wnt signaling pathway (TCGA-CESC: NES = -1.67, adj.p = 0.01; TCGA-HNSC: NES = -1.94, adj.p < 0.01; GSE65858: NES = -1.65, adj.p = 0.02; GSE181805: NES = -1.48, adj.p = 0.01) and Hedgehog signaling pathway (TCGA-CESC: NES = -1.63, adj.p = 0.03; TCGA-HNSC: NES = -1.55, adj.p = 0.02). Of note, ssGSEA results also proved that the enrichment scores for the TCR signaling pathway were significantly higher while Wnt and Hedgehog signaling pathways showed lower scores in HPV (+) groups (p < 0.05).

Conclusions

In HPV-associated cancers, HPV infection may stimulate the eventual growth and differentiation of tumor-infiltrating γδ T cells via upregulating the TCR signaling pathway and downregulating Wnt and Hedgehog signaling pathways.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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