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		<property:Processing_error_message rdf:datatype="http://www.w3.org/2001/XMLSchema#string">[2,"smw-datavalue-wikipage-property-invalid-title","Has original text","Celebrex (and other NSAIDs)\n\nCarcinogenesis of several types involves an inflammatory process. When anti-\ninflammatory drugs such as aspirin or ibuprofen are taken on a regular basis the\nincidence of colon cancer is reduced as much as 50%. This substantial effectiveness has\nmotivated investigation of the mechanisms of these benefits. One component of the\ninflammatory process is angiogenesis, which is now believed to be a critical component of\ncancer growth. COX-2 enzymes play an important role in inflammation, so that COX-2\ninhibitors should reduce angiogenesis and inhibit tumor growth. Many nonsteroidal anti-\ninflammatory drugs (NSAIDs) are known to be COX-2 inhibitors, but most (e.g.,\nibuprofen) also inhibit COX-1 enzymes, which are necessary for healthy maintenance of\nthe stomach lining, which is why many users of NSAIDs eventually develop intolerance\nto them. Thus, much recent attention has been given to the new COX-2 inhibitors such as\nCelebrex that were developed to avoid COX-1 inhibition for the purposes of arthritis\ntreatment. Because inhibition of angiogenesis is one of the major new approaches to the\ntreatment of cancer, some oncologists have begun adding Celebrex to their regular\ntreatment protocols, based on laboratory findings that COX-2 inhibitors inhibit tumor\ngrowth. In recent meetings of American Society for Clinical Oncology (ASCO), there\n\nhave been various clinical trials reported that combined one or another COX-2 inhibitor\nwith conventional radiation, chemotherapy, and new targeted treatments. The great\nmajority of these were phase 2 clinical trials which had only historical controls with the\nconventional treatment alone to assess the value of the added COX-2 inhibitors, but most\nconcluded there appeared to be a significant benefit, Some larger randomized clinical\ntrials (115, 116) have shown substantial outcome improvements when celebrex has been\nadded to standard chemotherapy protocols, but others have failed to find a benefit.\n\nTwo clinical trials have been reported that have used celebrex in the treatment of gliomas\nIn a clinical trial conducted jointly by several hospitals in New York, Temodar was\ncombined with celebrex (117). For the 46 patients in the study (37 with GBM), the PFS-6\nwas 35%. However, an unusual schedule of Temodar was also used, so whether the results\nwere due to the new schedule or the celebrex is uncertain. Celebrex has also been\ncombined with CPT-11 (118), a chemotherapy agent used widely for colon cancer, with\n\ufffdpatients with recurrent tumors, and produced a PFS-6 value of 25%.\n\nBecause of the mild toxicity of NSAIDS, considerable recent research has investigated\nthe mechanisms of their clinical benefit. Whereas initial research focused on the anti-\nangiogenic properties of this class of drugs, several other mechanisms have been\nidentified, including the enhancement of various aspects of the immune system, and\ninhibition of the genes that prevent damaged cells from undergoing apoptosis (119). It is\ncritical to note that many of the mechanisms by which NSAIDS work are strongly\ninvolved in the growth of high-grade gliomas, and that the expression of the\ncyclooxygenase enzyme that is the target of COX-2 inhibitors correlates strongly with the\nproliferation rate of glioblastoma tumors and correlates inversely with survival time (120,\n121)."]</property:Processing_error_message>
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