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Cell therapy with human reprogrammed CD8+ T-cells has antimetastatic effects on Lewis lung carcinoma in C57BL/6 mice E. G. Skurikhin, O. Pershina, N. N. Ermakova [et al.]

Contributor(s): Skurikhin, Evgenii G | Pershina, Olga | Ermakova, Natalia N | Pakhomova, Angelina | Zhukova, Mariia | Pan, Edgar S | Sandrikina, Lyubov A | Widera, Darius | Kogai, Lena | Kushlinskii, Nikolai | Kubatiev, Aslan A | Morozov, Sergey G | Dygai, Alexander MMaterial type: ArticleArticleContent type: Текст Media type: электронный Subject(s): Льюиса карцинома легких | ксенотрансплантация | мыши | антиметастатическая активность | CD8+Т-клетки | перепрограммированиеGenre/Form: статьи в журналах Online resources: Click here to access online In: International journal of molecular sciences Vol. 23, № 24. P. 15780 (1-16)Abstract: Using a model of Lewis lung carcinoma (LLC) in vitro and in vivo, we previously demonstrated increased antitumor activity in CD8+ T-cells reprogrammed with an MEK inhibitor and PD-1 blocker. In this follow-up study, we carried out the reprogramming of human CD8+ T-cells (hrT-cell) using the MEK inhibitor and PD-1 blocker and targeted LLC cells. The effects of hrT-cell therapy were studied in a mouse model of spontaneous metastasis of a solid LLC tumor. We found antimetastatic activity of hrT-cells, a decrease in the number of cancer cells and cancer stem cells in the lungs, and an increase in the number of T-cells in the blood (including effector T-cells). Thus, reprogramming of human CD8+ T-cells with an MEK inhibitor and PD-1 blocker with targeted training by tumor target cells is a potential platform for developing a new approach to targeted lung cancer therapy.
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Using a model of Lewis lung carcinoma (LLC) in vitro and in vivo, we previously demonstrated increased antitumor activity in CD8+ T-cells reprogrammed with an MEK inhibitor and PD-1 blocker. In this follow-up study, we carried out the reprogramming of human CD8+ T-cells (hrT-cell) using the MEK inhibitor and PD-1 blocker and targeted LLC cells. The effects of hrT-cell therapy were studied in a mouse model of spontaneous metastasis of a solid LLC tumor. We found antimetastatic activity of hrT-cells, a decrease in the number of cancer cells and cancer stem cells in the lungs, and an increase in the number of T-cells in the blood (including effector T-cells). Thus, reprogramming of human CD8+ T-cells with an MEK inhibitor and PD-1 blocker with targeted training by tumor target cells is a potential platform for developing a new approach to targeted lung cancer therapy.

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