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<https://discovery.ucl.ac.uk/id/eprint/10097692> <http://purl.org/dc/terms/title> "Targeting the Src Pathway Enhances the Efficacy of Selective FGFR Inhibitors in Urothelial Cancers with FGFR3 Alterations"^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/10097692> <http://purl.org/ontology/bibo/abstract> "Selective FGFR inhibitors such as infigratinib (BGJ398) and erdafitinib (JNJ-42756493) have\r\nbeen evaluated in clinical trials for cancers with FGFR3 molecular alterations, particularly in urothelial\r\ncarcinoma patients. However, a substantial proportion of these patients (up to 50%) display intrinsic\r\nresistance to these drugs and receive minimal clinical benefit. There is thus an unmet need for\r\nalternative therapeutic strategies to overcome primary resistance to selective FGFR inhibitors. In this\r\nstudy, we demonstrate that cells expressing cancer-associated activating FGFR3 mutants and the\r\nFGFR3-TACC3 fusion showed primary resistance to infigratinib in long-term colony formation assays\r\nin both NIH-3T3 and urothelial carcinoma models. We find that expression of these FGFR3 molecular\r\nalterations resulted in elevated constitutive Src activation compared to wildtype FGFR3 and that\r\ncells co-opted this pathway as a means to achieve intrinsic resistance to infigratinib. Targeting the\r\nSrc pathway with low doses of the kinase inhibitor dasatinib synergistically sensitized multiple\r\nurothelial carcinoma lines harbouring endogenous FGFR3 alterations to infigratinib. Our data provide\r\npreclinical rationale that supports the use of dasatinib in combination with selective FGFR inhibitors\r\nas a means to overcome intrinsic drug resistance in the salvage therapy setting in urothelial cancer\r\npatients with FGFR3 molecular alterations"^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/10097692> <http://purl.org/dc/terms/date> "2020-05-01" .
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