ArticlePloS one2013
Beneficial impact of CCL2 and CCL12 neutralization on experimental malignant pleural effusion.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Pathobiology and clinical significance of malignant pleural effusions.EMBO molecular medicine · 2026Review
- Assessment of Angiogenic Properties of Malignant Pleural Effusion (MPE) Fluid.Methods in molecular biology (Clifton, N.J.) · 2025Article
- A potential target for the future treatment of malignant pleural effusion: Monocyte chemoattractant protein-1 (MCP-1).Cancer biomarkers : section A of Disease markers · 2025Article
- CCL11/CCR3-dependent eosinophilia alleviates malignant pleural effusions and improves prognosis.NPJ precision oncology · 2024Article
- Monocytes subtypes from pleural effusion reveal biomarker candidates for the diagnosis of tuberculosis and malignancy.Journal of clinical laboratory analysis · 2022Article
- Review
- CSF1/CSF1R signaling mediates malignant pleural effusion formation.JCI insight · 2022Article
- An In Vivo Inflammatory Loop Potentiates KRAS Blockade.Biomedicines · 2022Article
- The role of angiogenesis in malignant pleural effusion: from basic research to clinical application.American journal of cancer research · 2022Review
- Article
- Host Wnt5a Potentiates Microenvironmental Regulation of Ovarian Cancer Metastasis.Cancer research · 2020Article
- Immuno-PET identifies the myeloid compartment as a key contributor to the outcome of the antitumor response under PD-1 blockade.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Migrated T lymphocytes into malignant pleural effusions: an indicator of good prognosis in lung adenocarcinoma patients.Scientific reports · 2019Article
- Prolonged retention of liposomes in the pleural cavity of normal mice and high tumor distribution in mice with malignant pleural effusion, after intrapleural injection.International journal of nanomedicine · 2019Article
- RANK-c attenuates aggressive properties of ER-negative breast cancer by inhibiting NF-κB activation and EGFR signaling.Oncogene · 2018Article
- Myeloid-derived interleukin-1β drives oncogenic KRAS-NF-κΒ addiction in malignant pleural effusion.Nature communications · 2018Article
- Mutant KRAS promotes malignant pleural effusion formation.Nature communications · 2017Article
- Article
- The Role of Chemokines in Promoting Colorectal Cancer Invasion/Metastasis.International journal of molecular sciences · 2016Review
- EGFR-L858R mutant enhances lung adenocarcinoma cell invasive ability and promotes malignant pleural effusion formation through activation of the CXCL12-CXCR4 pathway.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using genetic interventions, we previously determined that C-C motif chemokine ligand 2 (CCL2) promotes malignant pleural effusion (MPE) formation in mice. Here we conducted preclinical studies aimed at assessing the specific therapeutic potential of antibody-mediated CCL2 blockade against MPE. For this, murine MPEs or skin tumors were generated in C57BL/6 mice by intrapleural or subcutaneous delivery of lung (LLC) or colon (MC38) adenocarcinoma cells. Human lung adenocarcinoma cells (A549) were used to induce MPEs in severe combined immunodeficient mice. Intraperitoneal antibodies neutralizing mouse CCL2 and/or CCL12, a murine CCL2 ortholog, were administered at 10 or 50 mg/kg every three days. We found that high doses of CCL2/12 neutralizing antibody treatment (50 mg/kg) were required to limit MPE formation by LLC cells. CCL2 and CCL12 blockade were equally potent inhibitors of MPE development by LLC cells. Combined CCL2 and CCL12 neutralization was also effective against MC38-induced MPE and prolonged the survival of mice in both syngeneic models. Mouse-specific CCL2-blockade limited A549-caused xenogeneic MPE, indicating that host-derived CCL2 also contributes to MPE precipitation in mice. The impact of CCL2/12 antagonism was associated with inhibition of immune and vascular MPE-related phenomena, such as inflammation, new blood vessel assembly and plasma extravasation into the pleural space. We conclude that CCL2 and CCL12 blockade are effective against experimental MPE induced by murine and human adenocarcinoma in mice. These results suggest that CCL2-targeted therapies may hold promise for future use against human MPE.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.