<rdf:RDF xmlns:community="http://www.bibsonomy.org/ontologies/2008/05/community#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:owl="http://www.w3.org/2002/07/owl#" xmlns:admin="http://webns.net/mvcb/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns:syn="http://purl.org/rss/1.0/modules/syndication/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/" xmlns:cc="http://web.resource.org/cc/" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" xmlns:swrc="http://swrc.ontoware.org/ontology#" xmlns:rdfs="http://www.w3.org/2000/01/rdf-schema#" xmlns="http://purl.org/rss/1.0/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xml:base="http://www.bibsonomy.org/author/Allred"><owl:Ontology rdf:about=""><rdfs:comment>BibSonomy publications for /author/Allred</rdfs:comment><owl:imports rdf:resource="http://swrc.ontoware.org/ontology/portal"/></owl:Ontology><rdf:Description rdf:about="http://www.bibsonomy.org/bibtex/24927b533c5bbdadbcdd4591c087cdbf4/kanefendt"><owl:sameAs rdf:resource="http://www.bibsonomy.org/uri/bibtex/24927b533c5bbdadbcdd4591c087cdbf4/kanefendt"/><rdf:type rdf:resource="http://swrc.ontoware.org/ontology#Article"/><owl:sameAs rdf:resource="/brokenurl#PM:15459012"/><swrc:date>Fri Feb 05 11:28:39 CET 2010</swrc:date><swrc:journal>Blood</swrc:journal><swrc:number>3</swrc:number><swrc:pages>986-993</swrc:pages><swrc:title>A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease</swrc:title><swrc:volume>105</swrc:volume><swrc:year>2005</swrc:year><swrc:keywords>use toxicity therapy therapeutic response protein inhibitors genetics fms-Like drug cells antagonists analysis Vascular Tyrosine Studies SU11248 Research Receptors Receptor Rate Pyrroles Proto-Oncogene Proteins Protein-Tyrosine Platelet-Derived Pharmacokinetics Myeloid Mutation Middle Metabolic Male Lung Leukemia Kinases Kinase Indoles Hypertension Humans Human Growth Genotype Follow-Up Female Factor Endothelial Clearance Aged Acute 3 &amp; </swrc:keywords><swrc:abstract>Fifteen patients with refractory AML were treated in a phase 1 study with SU11248, an oral kinase inhibitor of fms-like tyrosine kinase 3 (Flt3), Kit, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) receptors. Separate cohorts of patients received SU11248 for 4-week cycles followed by either a 2- or a 1-week rest period. At the starting dose level of 50 mg (n = 13), no dose-limiting toxicities were observed. The most frequent grade 2 toxicities were edema, fatigue, and oral ulcerations. Two fatal bleedings possibly related to the disease, one from a concomitant lung cancer and one cerebral bleeding, were observed. At the 75 mg dose level (n = 2), one case each of grade 4 fatigue, hypertension, and cardiac failure was observed, and this dose level was abandoned. All patients with FLT3 mutations (n = 4) had morphologic or partial responses compared with 2 of 10 evaluable patients with wild-type FLT3. Responses, although longer in patients with mutated</swrc:abstract><swrc:author><rdf:Seq><rdf:_1><swrc:Person swrc:name="W. Fiedler"/></rdf:_1><rdf:_2><swrc:Person swrc:name="H. Serve"/></rdf:_2><rdf:_3><swrc:Person swrc:name="H. Dohner"/></rdf:_3><rdf:_4><swrc:Person swrc:name="M. Schwittay"/></rdf:_4><rdf:_5><swrc:Person swrc:name="O. G. Ottmann"/></rdf:_5><rdf:_6><swrc:Person swrc:name="A. M. O&#039;Farrell"/></rdf:_6><rdf:_7><swrc:Person swrc:name="C. L. Bello"/></rdf:_7><rdf:_8><swrc:Person swrc:name="R. Allred"/></rdf:_8><rdf:_9><swrc:Person swrc:name="W. C. Manning"/></rdf:_9><rdf:_10><swrc:Person swrc:name="J. M. Cherrington"/></rdf:_10><rdf:_11><swrc:Person swrc:name="S. G. Louie"/></rdf:_11><rdf:_12><swrc:Person swrc:name="W. Hong"/></rdf:_12><rdf:_13><swrc:Person swrc:name="N. M. Brega"/></rdf:_13><rdf:_14><swrc:Person swrc:name="G. Massimini"/></rdf:_14><rdf:_15><swrc:Person swrc:name="P. Scigalla"/></rdf:_15><rdf:_16><swrc:Person swrc:name="W. E. Berdel"/></rdf:_16><rdf:_17><swrc:Person swrc:name="D. K. Hossfeld"/></rdf:_17></rdf:Seq></swrc:author></rdf:Description><rdf:Description rdf:about="http://www.bibsonomy.org/bibtex/24927b533c5bbdadbcdd4591c087cdbf4/kanefendt"><owl:sameAs rdf:resource="http://www.bibsonomy.org/uri/bibtex/24927b533c5bbdadbcdd4591c087cdbf4/kanefendt"/><rdf:type rdf:resource="http://swrc.ontoware.org/ontology#Article"/><owl:sameAs rdf:resource="/brokenurl#PM:15459012"/><swrc:date>Fri Feb 05 11:28:39 CET 2010</swrc:date><swrc:journal>Blood</swrc:journal><swrc:number>3</swrc:number><swrc:pages>986-993</swrc:pages><swrc:title>A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease</swrc:title><swrc:volume>105</swrc:volume><swrc:year>2005</swrc:year><swrc:keywords>use toxicity therapy therapeutic response protein inhibitors genetics fms-Like drug cells antagonists analysis Vascular Tyrosine Studies SU11248 Research Receptors Receptor Rate Pyrroles Proto-Oncogene Proteins Protein-Tyrosine Platelet-Derived Pharmacokinetics Myeloid Mutation Middle Metabolic Male Lung Leukemia Kinases Kinase Indoles Hypertension Humans Human Growth Genotype Follow-Up Female Factor Endothelial Clearance Aged Acute 3 &amp; </swrc:keywords><swrc:abstract>Fifteen patients with refractory AML were treated in a phase 1 study with SU11248, an oral kinase inhibitor of fms-like tyrosine kinase 3 (Flt3), Kit, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) receptors. Separate cohorts of patients received SU11248 for 4-week cycles followed by either a 2- or a 1-week rest period. At the starting dose level of 50 mg (n = 13), no dose-limiting toxicities were observed. The most frequent grade 2 toxicities were edema, fatigue, and oral ulcerations. Two fatal bleedings possibly related to the disease, one from a concomitant lung cancer and one cerebral bleeding, were observed. At the 75 mg dose level (n = 2), one case each of grade 4 fatigue, hypertension, and cardiac failure was observed, and this dose level was abandoned. All patients with FLT3 mutations (n = 4) had morphologic or partial responses compared with 2 of 10 evaluable patients with wild-type FLT3. Responses, although longer in patients with mutated</swrc:abstract><swrc:author><rdf:Seq><rdf:_1><swrc:Person swrc:name="W. Fiedler"/></rdf:_1><rdf:_2><swrc:Person swrc:name="H. Serve"/></rdf:_2><rdf:_3><swrc:Person swrc:name="H. Dohner"/></rdf:_3><rdf:_4><swrc:Person swrc:name="M. 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