Research Topics
Genomes and Genes | Brian J P HuntlySummaryAffiliation: Brigham and Women's Hospital Country: USA Publications
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Publications
The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemiaJan Cools
Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
Blood 103:2802-5. 2004....- Leukaemia stem cells and the evolution of cancer-stem-cell researchBrian J P Huntly
Brian J P Huntly is at the Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Nat Rev Cancer 5:311-21. 2005.... 
FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemiaBenjamin H Lee
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 12:367-80. 2007..This model provides insights into the consequences of constitutive signaling by an oncogenic tyrosine kinase on hematopoietic progenitor quiescence, function, and cell fate...- FLT3 internal tandem duplication mutations induce myeloproliferative or lymphoid disease in a transgenic mouse modelBenjamin H Lee
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Oncogene 24:7882-92. 2005.... - FGFR3 as a therapeutic target of the small molecule inhibitor PKC412 in hematopoietic malignanciesJing Chen
Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
Oncogene 24:8259-67. 2005..These data indicate that PKC412 may be a useful molecularly targeted therapy for MM associated with overexpression of FGFR3, and perhaps other diseases associated with dysregulation of FGFR3 or related mutants... - The homeobox gene CDX2 is aberrantly expressed in most cases of acute myeloid leukemia and promotes leukemogenesisClaudia Scholl
Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
J Clin Invest 117:1037-48. 2007.... - HOX gene regulation in acute myeloid leukemia: CDX marks the spot?Stefan Fröhling
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, Massachusetts, USA
Cell Cycle 6:2241-5. 2007..Taken together, these studies implicate CDX proteins as master regulators of HOX gene regulation in AML... - The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemiaRoss L Levine
Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Blood 106:3377-9. 2005..These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies... - Constitutively activated FGFR3 mutants signal through PLCgamma-dependent and -independent pathways for hematopoietic transformationJing Chen
Howard Hughes Medical Institute, Harvard Medical Scgool, Boston, MA, USA
Blood 106:328-37. 2005..These data indicate that engagement of multiple signaling pathways, including PLCgamma-dependent and PLCgamma-independent pathways, is required for full hematopoietic transformation by constitutively activated FGFR3 mutants... - Blasts from the past: new lessons in stem cell biology from chronic myelogenous leukemiaBrian J P Huntly
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Cancer Cell 6:199-201. 2004.... - Cdx4 dysregulates Hox gene expression and generates acute myeloid leukemia alone and in cooperation with Meis1a in a murine modelDimple Bansal
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 103:16924-9. 2006..Inasmuch as many human leukemias show dysregulated expression of a spectrum of HOX family members, these collective findings also suggest a central role for CDX4 expression in the genesis of acute leukemia... - MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitorsBrian J P Huntly
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Cancer Cell 6:587-96. 2004..These data demonstrate that some, but not all, leukemia oncogenes can confer properties of leukemic stem cells to hematopoietic progenitors destined to undergo apoptotic cell death... - Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosisRoss L Levine
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 7:387-97. 2005..In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase... - Targeting cancer stem cellsBrynn T Kvinlaug
University of Cambridge, Department of Haematology, Cambridge Institute for Medical Research, Cambridge, CB2 2XY, UK
Expert Opin Ther Targets 11:915-27. 2007..Finally, the authors give their opinion of the direction in which one must travel to successfully target the CSC and improve treatment outcomes in malignant disease... - Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformationPeter J Campbell
Department of Haematology, University of Cambridge, Cambridge, United Kingdom
Blood 108:3548-55. 2006..In 3 patients the leukemic cells were V617F(-), suggesting that in these patients the leukemia arose in a V617F(-) cell... 
Leukemia stem cells in acute myeloid leukemiaWai In Chan
Department of Haematology, University of Cambridge, Cambridge Institute for Medical Research, Cambridge, UK
Semin Oncol 35:326-35. 2008....