The DOI matches its Crossref record; 154 of the 154 references it cites were found in a registry or an index.
Anti‐tumour strategies aiming to target tumour‐associated macrophages
Open accessAbstract
Summary: Tumour‐associated macrophages (TAM s) represent a predominant population of inflammatory cells that present in solid tumours. TAM s are mostly characterized as alternatively activated M2‐like macrophages and are known to orchestrate nearly all stages of tumour progression. Experimental investigations indicate that TAM s contribute to drug‐resistance and radio‐protective effects, and clinical evidence shows that an elevated number of TAM s and their M2 profile are correlated with therapy failure and poor prognosis in cancer patients. Recently, many studies on TAM‐targeted strategies have made significant progress and some pilot works have achieved encouraging results. Among these, connections between some anti‐tumour drugs and their influence on TAM s have been suggested. In this review, we will summarize recent advances in TAM‐targeted strategies for tumour therapy. Based on the proposed mechanisms, those strategies are grouped into four categories: (i) inhibiting macrophage recruitment; (ii) suppressing TAM survival; (iii) enhancing M1‐like tumoricidal activity of TAM s; (iv) blocking M2‐like tumour‐promoting activity of TAM s. It is desired that further attention be drawn to this research field and more effort be made to promote TAM‐targeted tumour therapy.
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1 retracted
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Self-citationRetracted
Metadata
- Authors
- Tang, X., Mo, C., Wang, Y., Wei, D., & Xiao, H.
- Venue
- Immunology
- Publisher
- Wiley
- Published
- 2013-01-16
- Volume
- 138
- Issue
- 2
- Pages
- 93-104
- ISSN
- 0019-2805 (ISSN-L)
- 1365-2567
- OpenAlex
- W2019179700
- Cited by
- 278
- References
- 154
- FWCI
- 7.03
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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