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It remains to be seen whether this result can be translated to patients with tumours that possess p mutations.In contrast to chemotherapy, which is administered at the maximum tolerated dose, Prucalopride antiangiogenic therapy dosing might be optimized by titrating against the total angiogenic output of a tumour.This is analogous to the titration of insulin against blood sugar or coumadin against prothrombin levels.At present, however, there is no quantitative method for determining the total angiogenic output of a patients tumour burden, so surrogate markers, such as circulating progenitor endothelial cells, are being studied.In fact, the most slowly growing tumours arevir tually unresponsive to chemotherapy.It has been assumed by some oncologists that slowly growing tumours would be as unresponsive to antiangiogenic therapy as they are to chemotherapy.However, when two types of human bladder cancers a rapidly growing highly vascularized tumour and a slowly growing poorly vascularized tumour were implanted into immunodeficient mice, growth of both tumour types was inhibited by angiogenesis inhibitors.For a given dose of angiogenesis inhibitor, the slower the tumour was growing, the more effective the inhibitor.Fur thermore, in carcinogentreated mice, breast cancers that arose spontaneously and grew very slowly were inhibited andor regressed by treatment with mouse endostatin.Finally, spontaneously arising carcinomas of the pancreatic cells in transgenic mice grew very slowly, but retained a high degree of sensitivity to angiogenesis inhibitors.Some cancer patients who have failed conventional therapy lament that their physician told them they were not candidates for antiangiogenic therapy because their tumour was not vascularized.A distinguished surgeon stated at an international meeting that pancreatic cancer will not respond to antiangiogenic therapy because it is a white avascular tumour.On the basis of these assumptions, some angiogenesis inhibitor clinical trials require a pretreatment biopsy for microvessel density to exclude patients whose tumour microvessel density is too low.Second, intensity of neovascularization cannot be determined by gross inspection of a tumour.A white neurofibrosarcoma of one or more cubic centimetres might have a microvessel density by Vilazodone microscopy that is similar to the microvessel density of a reddish hepatic carcinoma of similar size, except that in the whitish tumour the vessels are more compressed.Third, the lower the vascularity of a tumour, the more susceptible it seems to be to antiangiogenic therapy.Highly vascularized tumours might require higher doses of an angiogenesis inhibitor or combinations of angiogenesis inhibitors to achieve a tumour response.This phenomenon, called mixed response has not been adequately explained.In mice bearing two or more tumours, one tumour might suppress the growth of the other a phenomenon known as concomitant resistance. Furthermore, removal of a tumour by surgery or irradiation often results in the vascularization and growth of dormant metastases.The phenomenon of concomitant resistance can now be explained by the ability of one tumour to inhibit angiogenesis in the other. Certain tumours produce enzymes that activate angiogenesis inhibitors such as angiostatin, endostatin or antiangiogenic antithrombin III, which in turn prevent the growth of remote tumours. Administration of recombinant angiostatin to mice prevents growth of metastases that occurs after surgical removal of a primary tumour or after reduction of the primary tumour by ionizing radiation.

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