代谢紊乱的子宫内膜癌患者细胞程序性死亡受体的表达。

Q3 Medicine

Experimental oncology Pub Date : 2023-06-26 DOI:10.15407/exp-oncology.2023.01.044

O V Kuzmenko, P P Sorochan, I S Gromakova, V G Shevtsov, M O Ivanenko, M V Polozova

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引用次数: 1

摘要

目的:研究细胞程序性死亡受体(PD-1)及其配体(PD-L1)在子宫内膜癌伴代谢紊乱患者免疫活性细胞中的表达。材料和方法:流式细胞术分析淋巴细胞群和亚群。利用CD279抗体检测CD4+和CD8+ T细胞上的PD-1。使用CD14和CD274抗体检测单核细胞上的PD-L1。结果:重度代谢性疾病患者治疗前后CD8+、CD4+淋巴细胞上PD-1的表达及CD14+细胞上相应PD-L1的表达均高于对照组。结论:免疫活性细胞PD-1和PD-L1受体表达升高可作为子宫内膜癌合并病态肥胖患者预后的新指标。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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EXPRESSION OF PROGRAMMED CELL DEATH RECEPTOR IN ENDOMETRIAL CANCER PATIENTS WITH METABOLIC DISORDERS.

Aim: To study the expression of the programmed cell death receptor (PD-1) and its ligand (PD-L1) by immunocompetent cells in endometrial cancer patients with metabolic disorders.

Materials and methods: Populations and subpopulations of lymphocytes were analyzed by flow cytometry. Antibodies against CD279 were used to detect PD-1 on the CD4+ and CD8+ T cells. Antibodies against CD14 and CD274 were used to detect PD-L1 on monocytes.

Results: In patients with severe metabolic disorders, the expression of PD-1 on CD8+ and CD4+ lymphocytes and the expression of the corresponding PD-L1 on CD14+ cells before treatment and after radiation therapy were higher than in the control group.

Conclusion: Theincreased expression of PD-1 and PD-L1 receptors by immunocompetent cells can be considered a new prognostic marker in endometrial cancer patients with morbid obesity.

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来源期刊

Experimental oncology Medicine-Oncology

CiteScore

1.40

自引率

0.00%

发文量

期刊介绍： The Experimental Oncology is an English-language journal that publishes review articles, original contributions, short communications, case reports and technical advances presenting new data in the field of experimental and fundamental oncology. Manuscripts should be written in English, contain original work, which has not been published or submitted for publication elsewhere. It also implies the transfer of the Copyright from the author to “Experimental Oncology”. No part of journal publications may be reproduced, stored in a retrieval system or transmitted in any form or by any means without the prior permission of the publisher.