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Cocktail and Poster Display session

34P - Cocktail peptide vaccines targeting cancer stem cells for enhanced therapeutic efficacy in oral cancers

Date

26 Feb 2024

Session

Cocktail and Poster Display session

Topics

Immunotherapy

Tumour Site

Presenters

Sho Miyamoto

Citation

Annals of Oncology (2024) 9 (suppl_1): 1-7. 10.1016/esmoop/esmoop102270

Authors

S. Miyamoto1, Y. Hirohashi2, T. Torigoe2, A. Miyazaki1

Author affiliations

  • 1 Oral Surgery, Sapporo Medical University School of Medicine, 060-8543 - Sapporo/JP
  • 2 Department Of Pathology, Sapporo Medical University School of Medicine, 060-8543 - Sapporo/JP

Resources

This content is available to ESMO members and event participants.

Abstract 34P

Background

Cancer stem cells (CSCs) account for the resistance to chemo/radiotherapies and the cancer-initiating abilities of low numbers of cells in vivo. CSCs significantly contribute to cancer recurrence and metastasis, presenting a formidable challenge to oral cancer prognosis. While targeting CSCs with a peptide vaccine has demonstrated greater efficacy, the use of a singular peptide vaccine may pose a risk of immune evasion. Our objective was to develop an innovative cocktail peptide vaccine by combining multiple peptides to effectively target CSCs.

Methods

The well-established CSC marker CD44 facilitated the isolation of oral CSCs. CD44-positive cell groups exhibited elevated CSC markers, enhanced sphere-forming ability, and heightened resistance to chemotherapy and radiation therapy, confirming CSC properties. We searched for genes enriched in oral CSCs and investigated whether cytotoxic T lymphocytes (CTLs) induced by peptides from these genes demonstrated effective cytotoxicity.

Results

Comparative gene expression showed elevated levels of oral CSCs compared to non-CSCs for OR7C1, an olfactory receptor involved in odorant detection, and a colorectal CSC gene, CLSPN, a key regulator in the DNA replication checkpoint pathway for precise cell cycle progression. Stimulation of donor PBMCs with an HLA-A24-restricted OR7C1 peptide induced OR7C1-specific CTLs, targeting and damaging cancer cells expressing HLA-A24 and OR7C1. Similarly, an HLA-A2-restricted CLSPN peptide induced CLSPN-specific CTLs, targeting and damaging cancer cells expressing HLA-A2 and CLSPN. The Survivin 2B peptide, already applied clinically, induced specific CTLs and damaged cancer cells expressing HLA-A24 and Survivin 2B. Survivin 2B gene expression was comparable in both CSC and non-CSC populations.

Conclusions

OR7C1 and CLSPN peptides induced CSC-specific CTLs. Survivin 2B peptide exhibited reactivity against both CSC and non-CSC populations. A more effective therapeutic outcome is proposed with personalized, HLA-tailored cocktail vaccines, promising advancements in oral cancer treatment strategies.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Japan Society for the Promotion of Science.

Disclosure

All authors have declared no conflicts of interest.

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