ArticleBlood advances2024
Increased CCL2/CCR2 axis promotes tumor progression by increasing M2 macrophages in MYC/BCL2 double-expressor DLBCL.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Tumor-derived HMGB2 induces M2-like macrophage polarization via TRIM65-mediated NLRP3 degradation to promote DLBCL progression.Journal for immunotherapy of cancer · 2026Article
- Prognostic model for diffuse large B-cell lymphoma based on an HBV-associated gene signature and immune microenvironment insights.Annals of hematology · 2026Article
- CCL chemokines as prognostic and immunotherapeutic markers in prostate cancer: a comprehensive analysis.World journal of surgical oncology · 2026Article
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- Macrophage polarization in hematologic cancers: mechanisms and therapeutic strategies.Blood research · 2026Review
- Review
- Convergent Multistage Evidence Implicates the CCR2-Artemin Immune-Inflammation Axis in Acute Myeloid Leukemia.Mediators of inflammation · 2026Article
- Cancer Manipulates Adjacent Adipose Tissue to Exploit Fatty Acids via HIF-1α/CCL2/PPARα Axis: A Metabolic Circuit to Support Tumor Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrated single-cell and bulk transcriptomic analyses reveal cDC1-centered ubiquitination dysregulation and identify UBE2F as a critical regulator in sepsis.Frontiers in immunology · 2026Article
- Exhausted CD4Frontiers in immunology · 2026Article
- Leveraging immunologically based therapies to treat diffuse large B-cell lymphoma.Trends in cancer · 2025Review
- Pancreatic Tissue Remodeling and Fibrosis After Irreversible Electroporation: A Histopathological and Thermal Perspective.Biomedicines · 2025Article
- Osteosarcoma cell-derived CCL2 facilitates lung metastasis via accumulation of tumor-associated macrophages.Cancer immunology, immunotherapy : CII · 2025Article
- Tumor-Associated Macrophages as Key Modulators of Disease Progression in Diffuse Large B-Cell Lymphoma.Biomedicines · 2025Review
- Baseline PET/CT metabolic parameters in the double-expressor subtype of diffuse large B-cell lymphoma: development of a clinical-radiologic-pathologic predictive model.Frontiers in oncology · 2025Article
- eNAMPT/Ac-STAT3/DIRAS2 Axis Promotes Development and Cancer Stemness in Triple-Negative Breast Cancer by Enhancing Cytokine Crosstalk Between Tumor-Associated Macrophages and Cancer Cells.International journal of biological sciences · 2025Article
- ENO1-related gene signature predicts prognosis and therapeutic response in diffuse large B-cell lymphoma.Frontiers in immunology · 2025Article
- Macrophage Polarization in the Tumor Microenvironment of Hepatocellular Carcinoma: From Mechanistic Insights to Translational Therapies.Cancer control : journal of the Moffitt Cancer CenterReview
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10 authors.
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Abstract
abstractThe pathogenesis of myelocytomatosis oncogene (MYC) and B-cell lymphoma 2 (BCL2) double-expressor diffuse large B-cell lymphoma (DE-DLBCL) remains unclear. To investigate how MYC and BCL2 contribute to tumor aggressiveness, we analyzed tumors from 14 patients each with DE-DLBCL and non-DE-DLBCL using whole transcriptome sequencing. Validation was performed using publicly available data sets, tumor tissues from 126 patients, DLBCL cell lines, and a syngeneic mouse lymphoma model. Our transcriptome analysis revealed significantly elevated messenger RNA levels of C-C motif chemokine ligand 2 (CCL2) and C-C chemokine receptor type 2 (CCR2) in DE-DLBCLs when compared with non-DE-DLBCLs (adjusted P value < .05). Transcriptomic analysis of public data sets and immunohistochemistry corroborated these findings, indicating increased levels of M2 macrophages but a reduction in T-cell infiltration in DE-DLBCLs when compared with non-DE-DLBCLs (all P < .05). CCR2 expression was observed mainly in tumor-infiltrating macrophages and not in DLBCL cells. Increased expression of CCL2 and CCR2 was significantly associated with a poor prognosis in patients with DLBCL. In the in vitro analyses, MYChigh/BCL2high DLBCL cells showed higher CCL2 expression and secretion than MYClow/BCL2low cells. MYC and BCL2 increased CCL2 expression and secretion by upregulation of nuclear factor κB p65 in DLBCL cells, and CCL2 promoted M2 polarization of macrophages. In a mouse lymphoma model, CCL2 contributed to the immunosuppressive microenvironment and tumor growth of MYChigh/BCL2high tumors. We demonstrated that the increased CCL2/CCR2 axis confers aggressiveness to DE-DLBCL by increasing M2 polarization and can be a potential therapeutic target.
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