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Age-related features of lung cancer treatment using reprogrammed CD8 positive T cells in mice subjected to injection of Lewis lung carcinoma cells

Skurikhin, E., Zhukova, M., Ermakova, N., Pan, E., Widera, D. ORCID: https://orcid.org/0000-0003-1686-130X, Sandrikina, L., Kogai, L., Kushlinskii, N., Kubatiev, A., Morozov, S. and Dygai, A. (2024) Age-related features of lung cancer treatment using reprogrammed CD8 positive T cells in mice subjected to injection of Lewis lung carcinoma cells. Thoracic Cancer. ISSN 1759-7714

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To link to this item DOI: 10.1111/1759-7714.15426

Abstract/Summary

Background: Awareness of age‐related features of carcinogenesis and the importance of cellular immunity is crucial for developing effective antitumor therapies for specific patient groups. Methods: In this study, we examined different populations of cancer stem cells (CSCs) and circulating tumor cells (CTCs) in "young" (8‐10 weeks) and "aged" (80‐82 weeks) C57BL/6 male mice. We used an orthotopic model of Lewis lung carcinoma (LLC) to evaluate the effectiveness of cell therapy targeting lung cancer through reprogrammed CD8‐positive T cells (rCD8+ T cells) in mice from two different ages. Results: The findings revealed that tumor progression with age is primarily caused by impaired recruitment of T cells to the lungs. Additionally, a lower number of CTCs and CSCs were observed in younger mice compared to the older mice. The antitumor effect of rCD8+ T cells in aged mice was found to be inferior to that in young mice, which can be attributed to the reduced impact of therapy on specific CSCs populations. Conclusions: These results offer new insights into the treatment of lung cancer using rCD8+ T cells. Considering the age‐related characteristics influencing disease progression, this therapy has the potential to significantly enhance the effectiveness of treatment methods.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy > Division of Pharmacology
ID Code:117850
Publisher:Wiley

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