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. 2022 Apr 11;24:e17. doi: 10.1017/erm.2022.8

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© The Author(s) 2022

This is an Open Access article, distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike licence (http://creativecommons.org/licenses/by-nc-sa/4.0), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the same Creative Commons licence is used to distribute the re-used or adapted article and the original article is properly cited. The written permission of Cambridge University Press must be obtained prior to any commercial use.

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Fig. 3. — Macrophages are involved in chemotherapy resistance (blue box), radiotherapy resistance (green box) and immunotherapy resistance (pink box). ①: Chemotherapy (neoadjuvant) induced mammary epithelial cells to produce macrophage recruitment factors, including colony-stimulating factor 1 (CSF1) and interleukin-34, and a higher percentage of CD45⁺CD11b⁺CD14⁺ macrophages infiltrated in breast cancer biopsy samples. ②: (MRC1⁺ TIE2^Hi CXCR4^Hi) macrophages promoted tumour revascularisation and relapse after chemotherapy (Doxorubicin) via VEGF-A release. ③: CD11b⁺ Ly6C⁺ macrophages abundantly expressed TIE2 and prevented macrophages from apoptosis via the AKT-dependent signalling pathway. ④: Radiotherapy increased the expression of macrophage recruitment factors, including colony-stimulating factor 1 (CSF1), CCL2 and interleukin-34, promoting M2 macrophages polarisation. ⑤: M2 macrophages elevated the level of PRKCZ in the tumour and leading to radiation resistance in the end. ⑥: SEPT9 increases irradiation resistance by interacting with the HMGB1-RB axis. ⑦: CSF-1R inhibitors elevated the IGF1 protein level in macrophages via the IL4-NFAT pathway, then IGF-1 secreted into the extracellular environment and resulted in activation of IGF-1R and PI3K signalling in tumour cells. ⑧: VEGFR inhibitors elevated TIE2 protein level in macrophages via ANG2, upregulating angiogenic pathways. ⑨: CD40 inhibitors increased PD-L1 expression in macrophages.