期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 121, 期 5, 页码 1969-1973出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI44562
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资金
- Cancer Research UK
- European Research Council
- Associazione Italiana per la Ricerca sul Cancro
- Cancer Research UK [9993, 13028] Funding Source: researchfish
- Fondazione Telethon Funding Source: Custom
Vascular-disrupting agents (VDAs) such as combretastatin A4 phosphate (CA4P) selectively disrupt blood vessels in tumors and induce tumor necrosis. However, tumors rapidly repopulate after treatment with such compounds. Here, we show that CA4P-induced vessel narrowing, hypoxia, and hemorrhagic necrosis in murine mammary tumors were accompanied by elevated tumor levels of the chemokine CXCL12 and infiltration by proangiogenic TIE2-expressing macrophages (TEMs). Inhibiting TEM recruitment to CA4P-treated tumors either by interfering pharmacologically with the CXCL12/CXCR4 axis or by genetically depleting TEMs in tumor-bearing mice markedly increased the efficacy of CA4P treatment. These data suggest that TEMs limit VDA-induced tumor injury and represent a potential target for improving the clinical efficacy of VDA-based therapies.
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