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1.
Front Immunol ; 15: 1398166, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-39034998

RESUMEN

Background: Macrophages play a pivotal role in the research landscape of non-small cell lung cancer (NSCLC), contributing significantly to understanding tumor progression, treatment resistance, and immunotherapy efficacy. In this study, we utilized bibliometric techniques to analyze shifts in research hotspots and trends within the field, while also forecasting future research directions. These insights aim to offer guidance for both clinical therapeutic interventions and foundational scientific inquiries. Methods: All publications were released between 1993 and 2023 and focus on research pertaining to macrophages in the field of NSCLC. The articles were identified from the Web of Science Core Collection and analyzed using VOSviewer 1.6.19, CiteSpace 6.2.R2, and Scimago Graphica 1.0.35. Result: A total of 361 articles authored by 3,072 researchers from 48 countries were included in the analysis. TAMs have gained increasing attention for their role in NSCLC development and as potential therapeutic targets. Modulating TAM behavior may offer avenues to suppress tumor growth and drug resistance, improving patient outcomes. International collaboration, particularly between China and the United States, accelerates progress in NSCLC research, benefiting patients worldwide. The research hotspot revolves around understanding the role of macrophages in immunotherapy, focusing on their contribution to tumor progression, therapeutic resistance, and potential as therapeutic targets in NSCLC. Conclusions: The therapeutic significance of macrophages in the field of NSCLC is gaining increasing attention and recognition, highlighting their potential as key players in the development of novel treatment strategies. Future research will focus on understanding TAM molecular mechanisms, interactions with immune cells, and exploring novel therapies, with the aim of improving NSCLC treatment outcomes.


Asunto(s)
Bibliometría , Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Animales , Humanos , Investigación Biomédica/tendencias , Carcinoma de Pulmón de Células no Pequeñas/inmunología , Carcinoma de Pulmón de Células no Pequeñas/terapia , Carcinoma de Pulmón de Células no Pequeñas/patología , Inmunoterapia/métodos , Neoplasias Pulmonares/terapia , Neoplasias Pulmonares/inmunología , Neoplasias Pulmonares/patología , Macrófagos/inmunología , Microambiente Tumoral/inmunología
2.
Zhongguo Fei Ai Za Zhi ; 27(3): 231-240, 2024 Mar 20.
Artículo en Chino | MEDLINE | ID: mdl-38590197

RESUMEN

Tumor-associated macrophage (TAM) play a crucial role in the immune microenvironment of lung cancer. Through changes in their phenotype and phagocytic functions, TAM contribute to the initiation and progression of lung cancer. By promoting the formation of an immune-suppressive microenvironment and accelerating the growth of abnormal tumor vasculature, TAM facilitate the invasion and metastasis of lung cancer. Macrophages can polarize into different subtypes with distinct functions and characteristics in response to various stimuli, categorized as anti-tumor M1 and pro-tumor M2 types. In tumor tissues, TAM typically polarize into the alternatively activated M2 phenotype, exhibiting inhibitory effects on tumor immunity. This article reviews the role of anti-angiogenic drugs in modulating TAM phenotypes, highlighting their potential to reprogram M2-type TAM into an anti-tumor M1 phenotype. Additionally, the functional alterations of TAM play a significant role in anti-angiogenic therapy and immunotherapy strategies. In summary, the regulation of TAM polarization and function opens up new avenues for lung cancer treatment and may serve as a novel target for modulating the immune microenvironment of tumors.
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Asunto(s)
Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/genética , Macrófagos Asociados a Tumores , Microambiente Tumoral , Macrófagos/patología , Inmunoterapia
3.
Thorac Cancer ; 15(7): 559-569, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38294282

RESUMEN

BACKGROUND: Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are closely related to the prognosis of patients with non-small cell lung cancer, but their effect on extensive-stage small cell lung cancer (ES-SCLC) remains uncertain. METHODS: This retrospective study was conducted in ES-SCLC patients treated with first-line atezolizumab or durvalumab and platinum-etoposide. Clinical data from three hospitals were analyzed. Significant risk factors for survival were identified using descriptive statistics and Cox regression. Homogeneity was assessed using t-tests or nonparametric tests. Kaplan-Meier analysis revealed an association between high NLR level and median PFS and OS. RESULTS: A total of 300 ES-SCLC patients were included in the study. Cox regression analysis revealed that an elevated NLR level after the second treatment cycle (defined as NLRT2) was an independent prognostic factor for survival. Stratifying patients based on median NLRT2 showed significant differences in both PFS (HR: 1.863, 95% CI: 1.62-2.12, p < 0.001) and OS (HR: 2.581, 95% CI: 2.19-3.04, p < 0.001) between NLR ≥ 1.75 and NLR < 1.75 groups. mPFS and mOS were 8.2 versus 6.1 months and 13.7 versus 9.5 months, respectively. NLR was also associated with treatment efficacy and occurrence of irAEs. Further stratification based on NLR and irAEs showed that in the NLR < 1.75 group, patients with irAEs had prolonged mPFS and mOS. In the NLR ≥ 1.75 group, only mPFS showed a significant difference between patients with and without irAEs. CONCLUSION: NLRT2 and irAEs can predict the prognosis of ES-SCLC patients with first-line ES-SCLC receiving PD-L1 inhibitors combined with chemotherapy.


Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Carcinoma Pulmonar de Células Pequeñas , Humanos , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Neutrófilos , Pronóstico , Estudios Retrospectivos , Linfocitos
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