The DOI matches its Crossref record; 151 of the 151 references it cites were found in a registry or an index.
Reprogramming of Tumor-Associated Macrophages with Anticancer Therapies: Radiotherapy versus Chemo- and Immunotherapies
Open accessAbstract
Tumor-associated macrophages (TAMs) play a central role in tumor progression, metastasis, and recurrence after treatment. Macrophage plasticity and diversity allow their classification along a M1-M2 polarization axis. Tumor-associated macrophages usually display a M2-like phenotype, associated with pro-tumoral features whereas M1 macrophages exert antitumor functions. Targeting the reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression. This can be achieved through therapies including chemotherapy, immunotherapy, and radiotherapy (RT). In this review, we first describe how chemo- and immunotherapies can target TAMs and, second, we detail how RT modifies macrophage phenotype and present the molecular pathways that may be involved. The identification of irradiation dose inducing macrophage reprogramming and of the underlying mechanisms could lead to the design of novel therapeutic strategies and improve synergy in combined treatments.
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Cited by
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Tumor-associated macrophages: an effective player of the tumor microenvironment
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Metadata
- Authors
- Genard, G., Lucas, S., & Michiels, C.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2017-07-14
- Volume
- 8
- Pages
- 828-828
- ISSN
- 1664-3224 (ISSN-L)
- OpenAlex
- W2735818385
- Cited by
- 419
- References
- 151
- FWCI
- 15.49
- Type
- journal article
- Language
- en
- Open access
- gold
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- Genard, G., Lucas, S., & Michiels, C. (2017). Reprogramming of Tumor-Associated Macrophages with Anticancer Therapies: Radiotherapy versus Chemo- and Immunotherapies. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2017.00828
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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