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BMC Cancer. DecemberCite as. Squamous cell carcinoma of the head and neck SCCHN are highly invasive tumours with frequent local and distant recurrence.

Metastasis formation requires degradation of the extracellular matrix, which is fulfilled by membrane-associated proteases such as the urokinase plasminogen activator uPA. WX-UK1 is a competitive active site inhibitor of the protease function of uPA that impairs on the capacity of tumour cells to invade in vitro. A combined approach targeting different families of proteases and cyclooxygenases represents a promising adjuvant therapy.

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Squamous cell carcinoma of the head and neck SCCHN are aggressive tumours, which are still associated with poor prognosis despite improvements in surgical and radiotherapeutic techniques [ 1 ].

Freee exhibit highly invasive growth, aggressive metastasis formation, and early recurrence [ 1 ]. In order to metastasise, tumour cells utilize a complex set of molecular mechanisms [ 2 ]. Migration through surrounding tissue is achieved upon the degradation of the extracellular matrix ECM by both, membrane-fixed and soluble proteases. In this respect, matrix metalloproteases MMP nkde the urokinase-type plasminogen-activator system uPAwhich is responsible for the conversion of plasminogen into plasmin, are of major importance.

Tumours greater than 1. Neo-angiogenesis is provided via the production of growth factors such as basic fibroblast growth factor Nienbueg and vascular endothelial growth factor VEGFwhich attract endothelial cells into the tumour tissue to enable tumour progression.

The in vivo anti-metastatic and anti-proliferative activity of the synthetic uPA inhibitor WK-UK1 has Cheap black Eimsbuttel escorts demonstrated in various animal tumour models.

WX-UK1 is a serine protease inhibitor that inhibits protease upon attachment to the active center of the enzyme, resulting in bude reduction of tumour expansion Bad Nauheim chat room english 6 ]. As the pm activator system plays a role in coagulation, thrombotic vessel occlusion could be a risk during therapy, but these side-effects were neither observed in vivo nor in vitro [ 7 ].

According to the frequent over-expression of MMPs in malignant tumours and Nirnburg the Free nude pam Nienburg with a highly aggressive phenotype and poor prognosis [ 8 njde, 9 ], inhibition of MMPs has provided a significant increase in the survival rate in clinical trials [ 10 ].

Another group of anti-angiogenic active pharmaceutical agents comprises non-steroidal anti-inflammatory drugs. In vitro studies have suggested a potential of cyclooxigenase-2 COX-2 inhibitors to block angiogenesis and reduce the growth of colon, head and neck, and skin tumours [ 1314 ].

Importantly, resistance did not emerge in mouse models of fibrosarcoma, Lewis lung carcinoma and melanoma, after repeated in vivo treatment with the antiangiogenic agent endostatin [ 1516 ].

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The over-expression of components of the uPa system, pro-angiogenic cytokines such as bFGF and VEGF, and MMPs in malignant tumours in comparison to normal tissue, correlates with a poor prognosis and a higher recurrence rate [ 8 ]. Numerous synthetic protease inhibitors have been tested in clinical trials. Previous expertise disclosed that only multimodal therapy strategies take into Niengurg the plethora of mechanisms underlying tumour progression and are hence indispensible.

Thus, a combination of inhibitors that address different aspects of tumour progression and metastasis formation is a promising concept [ 1819 ]. Thus, our results suggest that the combination of three classes of inhibitors is potently nudw metastatic spread and neo-angiogenesis.