| http://purl.uniprot.org/citations/21263154 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21263154 | http://www.w3.org/2000/01/rdf-schema#comment | "The introduction of cultured p185(BCR-ABL)-expressing (p185+) Arf (-/-) pre-B cells into healthy syngeneic mice induces aggressive acute lymphoblastic leukemia (ALL) that genetically and phenotypically mimics the human disease. We adapted this high-throughput Philadelphia chromosome-positive (Ph(+)) ALL animal model for in vivo luminescent imaging to investigate disease progression, targeted therapeutic response, and ALL relapse in living mice. Mice bearing high leukemic burdens (simulating human Ph(+) ALL at diagnosis) entered remission on maximally intensive, twice-daily dasatinib therapy, but invariably relapsed with disseminated and/or central nervous system disease. Although relapse was frequently accompanied by the eventual appearance of leukemic clones harboring BCR-ABL kinase domain (KD) mutations that confer drug resistance, their clonal emergence required prolonged dasatinib exposure. KD P-loop mutations predominated in mice receiving less intensive therapy, whereas high-dose treatment selected for T315I "gatekeeper" mutations resistant to all 3 Food and Drug Administration-approved BCR-ABL kinase inhibitors. The addition of dexamethasone and/or L-asparaginase to reduced-intensity dasatinib therapy improved long-term survival of the majority of mice that received all 3 drugs. Although non-tumor-cell-autonomous mechanisms can prevent full eradication of dasatinib-refractory ALL in this clinically relevant model, the emergence of resistance to BCR-ABL kinase inhibitors can be effectively circumvented by the addition of "conventional" chemotherapeutic agents with alternate antileukemic mechanisms of action."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2010-08-301267"xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Rehg J.E."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Sherr C.J."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Relling M.V."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Williams R.T."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Mulder H.L."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Boulos N."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Calabrese C.R."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/author | "Morrison J.B."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/pages | "3585-3595"xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/title | "Chemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome-positive acute lymphoblastic leukemia."xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://purl.uniprot.org/core/volume | "117"xsd:string |
| http://purl.uniprot.org/citations/21263154 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21263154 |
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