ArticleJournal for immunotherapy of cancer2022
Deconvolution of malignant pleural effusions immune landscape unravels a novel macrophage signature associated with worse clinical outcome in lung adenocarcinoma patients.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma.Non-coding RNA research · 2026Article
- Timing of definitive pleural intervention within systemic anticancer therapy in malignant pleural effusion from high-response lung cancers: a retrospective single-center cohort study.Translational lung cancer research · 2026Article
- Pathobiology and clinical significance of malignant pleural effusions.EMBO molecular medicine · 2026Review
- CXCL2/CXCR2 pathway regulates CD169Frontiers in medicine · 2026Article
- Intrapleural dual blockade of IL-6 and PD-L1 reprograms CAF dynamics and the tumor microenvironment in lung cancer-associated malignant pleural effusion.Respiratory research · 2025Article
- Advanced hierarchical computational modeling-based rational development of platinum (II) nanocomplex to improve lung cancer therapy.Advanced functional materials · 2025Article
- Identification of a set of genes potentially responsible for resistance to ferroptosis in lung adenocarcinoma cancer stem cells.Cell death & disease · 2024Article
- Article
- Review
- Complement C1q is a key player in tumor-associated macrophage-mediated CD8International journal of biological sciences · 2024Article
- Upregulated expression of miR-4443 and miR-4488 in drug resistant melanomas promotes migratory and invasive phenotypes through downregulation of intermediate filament nestin.Journal of experimental & clinical cancer research : CR · 2023Article
- Liquid biopsies based on DNA methylation as biomarkers for the detection and prognosis of lung cancer.Clinical epigenetics · 2022Review
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Authors and funding
26 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune checkpoint inhibitors are still unable to provide clinical benefit to the large majority of non-small cell lung cancer (NSCLC) patients. A deeper characterization of the tumor immune microenvironment (TIME) is expected to shed light on the mechanisms of cancer immune evasion and resistance to immunotherapy. Here, we exploited malignant pleural effusions (MPEs) from lung adenocarcinoma (LUAD) patients as a model system to decipher TIME in metastatic NSCLC.
methodsMononuclear cells from MPEs (PEMC) and peripheral blood (PBMC), cell free pleural fluid and/or plasma were collected from a total of 24 LUAD patients and 12 healthy donors. Bulk-RNA sequencing was performed on total RNA extracted from PEMC and matched PBMC. The DEseq2 Bioconductor package was used to perform differential expression analysis and CIBERSORTx for the regression-based immune deconvolution of bulk gene expression data. Cytokinome analysis of cell-free pleural fluid and plasma samples was performed using a 48-Plex Assay panel. THP-1 monocytic cells were used to assess macrophage polarization. Survival analyses on NSCLC patients were performed using KM Plotter (LUAD, N=672; lung squamous cell carcinoma, N=271).
resultsTranscriptomic analysis of immune cells and cytokinome analysis of soluble factors in the pleural fluid depicted MPEs as a metastatic niche in which all the components required for an effective antitumor response are present, but conscripted in a wound-healing, proinflammatory and tumor-supportive mode. The bioinformatic deconvolution analysis revealed an immune landscape dominated by myeloid subsets with the prevalence of monocytes, protumoral macrophages and activated mast cells. Focusing on macrophages we identified an MPEs-distinctive signature associated with worse clinical outcome in LUAD patients.
conclusionsOur study reports for the first time a wide characterization of MPEs LUAD microenvironment, highlighting the importance of specific components of the myeloid compartment and opens new perspectives for the rational design of new therapies for metastatic NSCLC.
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