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Tumor-associated macrophages affect the treatment of lung cancer.
Yu, Zhuchen; Zou, Juntao; Xu, Fei.
Afiliação
  • Yu Z; Clinical Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China.
  • Zou J; Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China.
  • Xu F; Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China.
Heliyon ; 10(7): e29332, 2024 Apr 15.
Article em En | MEDLINE | ID: mdl-38623256
ABSTRACT
As one of the most common malignant tumors in the world, lung cancer has limited benefits for patients despite its diverse treatment methods due to factors such as personalized medicine targeting histological type, immune checkpoint expression, and driver gene mutations. The high mortality rate of lung cancer is partly due to the immune-suppressive which limits the effectiveness of anti-cancer drugs and induces tumor cell resistance. The currently widely recognized TAM phenotypes include the anti-tumor M1 and pro-tumor M2 phenotypes. M2 macrophages promote the formation of an immune-suppressive microenvironment and hinder immune cell infiltration, thereby inhibiting activation of the anti-tumor immune system and aiding tumor cells in resisting treatment. Analyzing the relationship between different treatment methods and macrophages in the TME can help us better understand the impact of TAMs on lung cancer and confirm the feasibility of targeted TAM therapy. Targeting TAMs to reduce the M2/M1 ratio and reverse the immune-suppressive microenvironment can improve the clinical efficacy of conventional treatment methods and potentially open up more efficient combination treatment strategies, maximizing the benefit for lung cancer patients.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article