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No human HB EGF mRNA expression was detected in mouse TECs, demonstrating that these TECs were not contaminated with human tumour cells.
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We isolated tumour endothelial cells (TECs), demonstrated their abnormalities, compared gene expression profiles of TECs and normal endothelial cells (NECs) by microarray analysis and identified several genes upregulated in TECs.
These results suggested that biglycan is specifically expressed in mouse TECs in vitro and in vivo.
These results suggested that biglycan is specifically expressed in human and mouse TECs.
Furthermore, immunostaining revealed strong biglycan expression in vivo in human tumour vessels, as in mouse TECs.
This suggests the presence of a functional autocrine pathway related to VEGF-A or COX-2 in mouse TECs.
Mouse TECs were defined as CD45neg EpCAMpos, and were further subdivided into Ly-51pos cTECs and Ly-51neg mTECs.
In our isolated mouse TECs, several genes, such as VEGFR-2, CD13 (Pasqualini et al, 2000), and Dkk-3 (Untergasser et al, 2008; Fong et al, 2009), which are reported to be the upregulated genes in TECs, were indeed upregulated.
The trough structure in GPS-TEC demonstrates a smooth shape.
However, in recurrent or more advanced cases, TC and TEC demonstrated similar effects on survival (p = 0.55 for progression-free survival and p = 0.63 for overall survival).
We identified miRNAs with TEC-specific expression in mouse and human TECs and demonstrated that there is a larger overlap in miRNA expression between immature and mature mTECs than between either of these and cTECs.
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