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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/10111


    Title: Endothelial cell colony forming units derived from malignant breast diseases are resistant to tumor necrosis factor-alpha-induced apoptosis
    Other Titles: Endothelial cell colony forming units derived from malignant breast diseases are resistant to tumor necrosis factor-α-induced apoptosis
    Authors: Chou, CP;Jiang, SS;Pan, HB;Yen, YC;Tseng, HH;Hung, YT;Wang, SH;Chen, YL;Chen, YW
    Contributors: National Institute of Cancer Research
    Abstract: Mobilisation of endothelial progenitor cells (EPCs) from the bone marrow is a crucial step in the formation of de novo blood vessels, and levels of peripheral blood EPCs have been shown to be elevated in certain malignant states. Using flow cytometry and a Hill-based colony forming unit (CFU) assay, the present study indicated that higher levels of CD34 and vascular endothelial growth factor receptor 2 (VEGFR2) double-positive EPCs, as well as increased formation of endothelial cell colony-forming units (EC-CFUs) are associated with benign and malignant breast diseases, providing possible indicators for breast disease detection. Gene expression profiles revealed a genetic difference between CD34+ VEGFR2+ EPCs and EC-CFUs. Decreased expression of tumour necrosis factor receptor 2 (TNFR2) signalling-related genes and inhibition of tumour necrosis factor (TNF)-induced signalling were demonstrated in EC-CFUs derived from patients with malignant breast disease in comparison with those from healthy controls. Interestingly, our data provided the first evidence that EC-CFUs derived from patients with malignant breast disease were resistant to TNF-alpha-induced apoptosis, indicating a plausible target for future therapeutic interventions.
    Date: 2016-11-24
    Relation: Scientific Reports. 2016 Nov 24;6:Article number 37450.
    Link to: http://dx.doi.org/10.1038/srep37450
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2045-2322&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000388797400001
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84997294958
    Appears in Collections:[陳雅雯] 期刊論文
    [江士昇] 期刊論文

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