期刊
TUMOR BIOLOGY
卷 36, 期 9, 页码 6603-6614出版社
SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-015-3823-2
关键词
Endothelial progenitor cells; Tumour vascularisation; Renal cellular carcinoma; Vascular endothelial growth factor; Anti-angiogenic therapy; Patient refractoriness; Ca2+ signalling
类别
资金
- Cariplo Foundation [2010-0807]
- Associazione Italiana per la Ricerca sul Cancro (AIRC
- Milan, Italy)
- Special Program Molecular Clinical Oncology 5x1000 to AIRC-Gruppo Italiano Malattie Mieloproliferative (AGIMM) [1005]
Endothelial progenitor cells (EPCs) have recently been shown to promote the angiogenic switch in solid neoplasms, thereby promoting tumour growth and metastatisation. The genetic suppression of EPC mobilization from bone marrow prevents tumour development and colonization of remote organs. Therefore, it has been assumed that anti-angiogenic treatments, which target vascular endothelial growth factor (VEGF) signalling in both normal endothelial cells and EPCs, could interfere with EPC activation in cancer patients. Our recent data, however, show that VEGF fails to stimulate tumour endothelial colony-forming cells (ECFCs), i.e. the only EPC subtype truly belonging to the endothelial lineage. The present article will survey current evidence about EPC involvement in the angiogenic switch: we will focus on the controversy about EPC definition and on the debate around their actual incorporation into tumour neovessels. We will then discuss how ECFC insensitivity to VEGF stimulation in cancer patients could underpin their well-known resistance to anti-VEGF therapies.
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