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dc.contributor.authorRen, MingQiang
dc.contributor.authorTidwell, Josephine A.
dc.contributor.authorSharma, Suash
dc.contributor.authorCowell, John K.
dc.date.accessioned2012-10-26T20:30:45Z
dc.date.available2012-10-26T20:30:45Z
dc.date.issued2012-06-6en_US
dc.identifier.citationPLoS One. 2012 Jun 6; 7(6):e38265en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22701616en_US
dc.identifier.doi10.1371/journal.pone.0038265en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/796
dc.description.abstractConstitutive activation of FGFR1, through rearrangement with various dimerization domains, leads to atypical myeloproliferative disorders where, although T cell lymphoma are common, the BCR-FGFR1 chimeric kinase results in CML-like leukemia. As with the human disease, mouse bone marrow transduction/transplantation with BCR-FGFR1 leads to CML-like myeloproliferation as well as B-cell leukemia/lymphoma. The murine disease described in this report is virtually identical to the human disease in that both showed bi-lineage involvement of myeloid and B-cells, splenomegaly, leukocytosis and bone marrow hypercellularity. A CD19+ IgMâ CD43+ immunophenotype was seen both in primary tumors and two cell lines derived from these tumors. In all primary tumors, subpopulations of these CD19+ IgMâ CD43+ were also either B220+ or B220â , suggesting a block in differentiation at the pro-B cell stage. The B220â phenotype was retained in one of the cell lines while the other was B220+. When the two cell lines were transplanted into syngeneic mice, all animals developed the same B-lymphoblastic leukemia within 2-weeks. Thus, the murine model described here closely mimics the human disease with bilineage myeloid and B-cell leukemia/lymphoma which provides a representative model to investigate therapeutic intervention and a better understanding of the etiology of the disease.
dc.rightsRen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectGeneticsen_US
dc.subjectCancer Geneticsen_US
dc.subjectCytogeneticsen_US
dc.subjectGenetics of Diseaseen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectMedicineen_US
dc.subjectHematologyen_US
dc.subjectHematologic Cancers and Related Disordersen_US
dc.subjectLeukemiasen_US
dc.subjectMyeloproliferative Disordersen_US
dc.subjectOncologyen_US
dc.subjectCancers and Neoplasmsen_US
dc.titleAcute Progression of BCR-FGFR1 Induced Murine B-Lympho/Myeloproliferative Disorder Suggests Involvement of Lineages at the Pro-B Cell Stageen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3368885en_US
dc.contributor.corporatenameGHSU Cancer Center
dc.contributor.corporatenameDepartment of Pathology
refterms.dateFOA2019-04-10T00:54:57Z
html.description.abstractConstitutive activation of FGFR1, through rearrangement with various dimerization domains, leads to atypical myeloproliferative disorders where, although T cell lymphoma are common, the BCR-FGFR1 chimeric kinase results in CML-like leukemia. As with the human disease, mouse bone marrow transduction/transplantation with BCR-FGFR1 leads to CML-like myeloproliferation as well as B-cell leukemia/lymphoma. The murine disease described in this report is virtually identical to the human disease in that both showed bi-lineage involvement of myeloid and B-cells, splenomegaly, leukocytosis and bone marrow hypercellularity. A CD19+ IgMâ CD43+ immunophenotype was seen both in primary tumors and two cell lines derived from these tumors. In all primary tumors, subpopulations of these CD19+ IgMâ CD43+ were also either B220+ or B220â , suggesting a block in differentiation at the pro-B cell stage. The B220â phenotype was retained in one of the cell lines while the other was B220+. When the two cell lines were transplanted into syngeneic mice, all animals developed the same B-lymphoblastic leukemia within 2-weeks. Thus, the murine model described here closely mimics the human disease with bilineage myeloid and B-cell leukemia/lymphoma which provides a representative model to investigate therapeutic intervention and a better understanding of the etiology of the disease.


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