ArticleScandinavian journal of immunology2019
Molecular model linking Th2 polarized M2 tumour-associated macrophages with deaminase-mediated cancer progression mutation signatures.
Article in Scandinavian journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Epigenetic-Genetic Coupling and Understanding the Molecular and Cellular Basis of Lamarckian Inheritance.International journal of molecular sciences · 2026Review
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025Review
- Expression Characteristics and Prognostic Value of KLRG2 in Endometrial Cancer: A Comprehensive Analysis Based on Multi-Omics Data.Biomedicines · 2025Article
- Tumor-associated macrophages remodel the suppressive tumor immune microenvironment and targeted therapy for immunotherapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Deaminase-Driven Reverse Transcription Mutagenesis in Oncogenesis: Critical Analysis of Transcriptional Strand Asymmetries of Single Base Substitution Signatures.International journal of molecular sciences · 2025Review
- Immune Microenvironment and the Effect of Vascular Endothelial Growth Factor Inhibition in Hepatocellular Carcinoma.International journal of molecular sciences · 2024Review
- New insights into T-cell exhaustion in liver cancer: from mechanism to therapy.Journal of cancer research and clinical oncology · 2023Review
- Epigenetic regulation and therapeutic targets in the tumor microenvironment.Molecular biomedicine · 2023Review
- Integrated analyzes identify CCT3 as a modulator to shape immunosuppressive tumor microenvironment in lung adenocarcinoma.BMC cancer · 2023Article
- Unifying Different Cancer Theories in a Unique Tumour Model: Chronic Inflammation and Deaminases as Meeting Points.International journal of molecular sciences · 2022Review
- M2-like tumor-associated macrophages transmit exosomal miR-27b-3p and maintain glioblastoma stem-like cell properties.Cell death discovery · 2022Article
- Immunosuppression in tumor immune microenvironment and its optimization from CAR-T cell therapy.Theranostics · 2022Review
- Comprehensive Molecular Analyses of a Macrophage-Related Gene Signature With Regard to Prognosis, Immune Features, and Biomarkers for Immunotherapy in Hepatocellular Carcinoma Based on WGCNA and the LASSO Algorithm.Frontiers in immunology · 2022Article
- Hepatocellular Carcinoma Tumor Microenvironment and Its Implications in Terms of Anti-tumor Immunity: Future Perspectives for New Therapeutics.Journal of gastrointestinal cancer · 2021Review
- Review
- Identification and validation of ferroptosis-associated gene-based on immune score as prognosis markers for hepatocellular carcinoma patients.Journal of gastrointestinal oncology · 2021Article
- Cancer: a mirrored room between tumor bulk and tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2021Review
- Tumor Immune Microenvironment and Immunosuppressive Therapy in Hepatocellular Carcinoma: A Review.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A new and diverse range of somatic mutation signatures are observed in late-stage cancers, but the underlying reasons are not fully understood. We advance a "combinatorial association model" for deaminase binding domain (DBD) diversification to explain the generation of previously observed cancer-progression associated mutation signatures. We also propose that changes in the polarization of tumour-associated macrophages (TAMs) are accompanied by the expression of deaminases with a new and diverse range of DBDs, and thus accounting for the generation of new somatic mutation signatures. The mechanism proposed is molecularly reminiscent of combinatorial association of heavy (H) and light (L) protein chains following V(D)J recombination of immunoglobulin molecules (and similarly for protein chains in heterodimers α/β and γ/δ of V(D)Js of T Cell Receptors) required for pathogen antigen recognition by B cells and T cells, respectively. We also discuss whether extracellular vesicles (EVs) emanating from tumour enhancing M2-polarized macrophages represent a likely source of the de novo deaminase DBDs. We conclude that M2-polarized macrophages extruding EVs loaded with deaminase proteins or deaminase-specific transcription/translation regulatory factors and like information may directly trigger deaminase diversification within cancer cells, and thus account for the many new somatic mutation signatures that are indicative of cancer progression. This hypothesis now has a plausible evidentiary base, and it is worth direct testing in future investigations. A long-term objective would be to identify molecular biomarkers predicting cancer progression (or metastatic disease) and to support the development of new drug targets before metastatic pathways are activated.
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