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- W2023576344 abstract "<i>Aims</i>—The plasminogen activator system (PAS) consists of the plasminogen activators (urokinase (uPA) and tissue-type (tPA) plasminogen activators), the uPA receptor (uPAR), and the plasminogen activator inhibitors (PAI-1 and PAI-2). Plasminogen activators activate plasminogen to plasmin, which can break down extracellular matrix (ECM) components. Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells and is involved in angiogenesis. VEGF has been shown to upregulate uPA and this may facilitate tumour angiogenesis further. <i>Methods</i>—PAS components and VEGF were determined by enzyme linked immunosorbent assay (ELISA) in paired colorectal tumour and normal tissue (n = 50) and correlated with pathological staging. <i>Results</i>—uPA, uPAR, PAI-1, and VEGF values were significantly higher in tumour tissue (for example, tumour uPA: median, 2.3 (range, 0.1–6.7) ng/mg protein <i>v</i> normal uPA: median, 0.2 (range, 0–2.6) ng/mg protein). tPA was significantly higher in normal mucosa and there was no difference in PAI-2. uPA, uPAR, PAI-1, and VEGF values significantly correlated with each other and with Dukes9s staging (uPA in adenomas: median, 0.42 (range, 0.1–1.2) ng/mg protein; upA in Dukes9s B tumours: median, 2.1 (range, 0.4–4.3) ng/mg protein; and uPA in Dukes9s D tumours: median, 4.0 (range, 3.7–4.2) ng/mg protein) and lymphatic invasion. In addition PAI-1 also correlated with tumour size and differentiation. <i>Conclusion</i>—The involvement of the PAS and VEGF in colorectal cancer appears to be complex. uPA, uPAR, PAI-1, and VEGF were upregulated in tumour tissue and this correlated with Dukes9s staging and lymphatic invasion." @default.
- W2023576344 created "2016-06-24" @default.
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- W2023576344 date "2000-12-01" @default.
- W2023576344 modified "2023-10-18" @default.
- W2023576344 title "Plasminogen activator system, vascular endothelial growth factor, and colorectal cancer progression" @default.
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- W2023576344 doi "https://doi.org/10.1136/mp.53.6.307" @default.
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