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[“Inhibitor Jelentése

For example, retinoblastomas in the posterior eye Naftifine hydrochloride induce iris neovascularization in the anterior chamber.Cer tain brain tumors induce angiogenesis in remote areas of the brain.Bone pain in metastatic prostate cancer may be related in part to neovascularization.A problem in the diagnosis of a primary bone tumor is that if the biopsy specimen contains only the neovascular response at the periphery of the tumor, it may be mistaken forgranulation tissue or inflammation.A variety of cancer syndromes, such as inappropriate hormonal activity, hypercoagulation, and cachexia, are secondary to the presence of biologically active peptides released into the circulation from vascularized tumors.Therefore, it might be predicted that an early therapeutic effect of antiangiogenic therapy would be increased appetite, weight gain, and disappearance of cer tain cancer syndromes.This early therapeutic effect would be most apparent with those angiogenesis inhibitors that had the least side effects.However, two recent reports validate the eff icacy of antiangiogenic therapy for recur rent tumors when conventional therapy has failed.Kaban and colleagues report complete and durable regression of recurrent high grade giant cell tumors of the maxilla and mandible in adults and children by lowdose daily interferon for eight months, initiated hours after simple enucleation surgery.Albamycinsodium Aiello and colleagues report thefirst case of treatment of an ocular hemangioblastoma with an angiogenesis inhibitor that blocks the receptor for VEGF.In this patient there was rapid and durable return of vision.The rapidity of return of eyesight was at the outset due to inhibition of increased permeability of the tumor by the antiVEGF regimen.There is a need for surrogate markers of antiangiogenic eff icacy.Maximum tolerated dose is not a useful indicator for antiangiogenic therapy.Administration of antiangiogenic therapy may be more analogous to insulin therapy than to chemotherapy.However, there is as yet no way to titrate dosing of angiogenesis inhibitors to the output of proangiogenic activity of the patients tumor burden.Microvessel density, although useful as a prognostic indicator, is not as useful to determine eff icacy of therapy.Quantif ication of proangiogenic factors such as VEGF, although correlative with prognosis in a few reports, may not measure all of the positive and negative regulators of angiogenesis generated in a tumor bed.Preliminary data indicates that quantif ication of circulating endothelial cells may become a promising sur rogate marker of eff icacy of antiangiogenic therapy, but much work remains to be done.Detection of novel circulating molecular markers of ongoing angiogenesis is a wide open opportunity for molecular biologists.For example, it will be important to know whether bisphosphonates are synergistic with certain natural angiogenesis inhibitors such as angiostatin, endostatin, thrombospondin, or tumstatin.Because antiangiogenic therapy is generally less toxic and less susceptible to induction of acquired drug resistance, it is possible that angiogenesis inhibitors could be used as prophylactic therapy in patients who have a high risk for cancer or for recurrence of cancer.An experimental study of spontaneous carcinogeninduced breast cancer in rats revealed that endostatin prevented the onset of breast cancer and also prolonged survival, compared with untreated controls.Another example of preventive antiangiogenic therapy would be therapy guided by a molecular marker even before a tumor is visible.

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