Benjamin H Lee

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. pmc JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model
    Thomas Mercher
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Blood 108:2770-9. 2006
  2. pmc Excessive centrosome abnormalities without ongoing numerical chromosome instability in a Burkitt's lymphoma
    Stefan Duensing
    Department of Pathology, Harvard Medical School, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
    Mol Cancer 2:30. 2003
  3. pmc FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemia
    Benjamin 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
  4. pmc MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia
    Yana Pikman
    Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS Med 3:e270. 2006
  5. ncbi Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera
    Gerlinde Wernig
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 13:311-20. 2008
  6. ncbi FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress
    Zuzana Tothova
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Cell 128:325-39. 2007
  7. ncbi FGFR3 as a therapeutic target of the small molecule inhibitor PKC412 in hematopoietic malignancies
    Jing Chen
    Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 24:8259-67. 2005
  8. ncbi Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles
    Stefan Fröhling
    Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 12:501-13. 2007
  9. pmc Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells
    Winnie F Tam
    Hematology Division, Brigham and Women s Hospital, Boston, MA 02115, USA
    Blood 112:1981-92. 2008
  10. pmc Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent
    Elizabeth H Stover
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 103:8078-83. 2006

Research Grants

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Detail Information

Publications27

  1. pmc JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model
    Thomas Mercher
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Blood 108:2770-9. 2006
    ..These findings provide new insights into pathways and therapeutic targets that contribute to the pathogenesis of AMKL...
  2. pmc Excessive centrosome abnormalities without ongoing numerical chromosome instability in a Burkitt's lymphoma
    Stefan Duensing
    Department of Pathology, Harvard Medical School, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
    Mol Cancer 2:30. 2003
    ..Moreover, our results suggest a model in which additional cellular alterations may be required to promote centrosome-related mitotic defects in tumor cells...
  3. pmc FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemia
    Benjamin 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...
  4. pmc MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia
    Yana Pikman
    Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS Med 3:e270. 2006
    ....
  5. ncbi Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera
    Gerlinde Wernig
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 13:311-20. 2008
    ....
  6. ncbi FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress
    Zuzana Tothova
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Cell 128:325-39. 2007
    ..Thus, FoxO proteins play essential roles in the response to physiologic oxidative stress and thereby mediate quiescence and enhanced survival in the HSC compartment, a function that is required for its long-term regenerative potential...
  7. ncbi FGFR3 as a therapeutic target of the small molecule inhibitor PKC412 in hematopoietic malignancies
    Jing 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...
  8. ncbi Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles
    Stefan Fröhling
    Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 12:501-13. 2007
    ....
  9. pmc Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells
    Winnie F Tam
    Hematology Division, Brigham and Women s Hospital, Boston, MA 02115, USA
    Blood 112:1981-92. 2008
    ..These findings indicate that Id1 is an important target of constitutively activated tyrosine kinases and may be a therapeutic target for leukemias associated with oncogenic tyrosine kinases...
  10. pmc Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent
    Elizabeth H Stover
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 103:8078-83. 2006
    ..These results suggest that disruption of the autoinhibitory JM domain is an alternative, dimerization-independent mechanism by which chimeric tyrosine kinases are constitutively activated and induce leukemogenesis...
  11. ncbi FLT3 internal tandem duplication mutations induce myeloproliferative or lymphoid disease in a transgenic mouse model
    Benjamin H Lee
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
    Oncogene 24:7882-92. 2005
    ....
  12. pmc The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model
    Thomas Mercher
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 119:852-64. 2009
    ....
  13. pmc Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model
    Gerlinde Wernig
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Blood 107:4274-81. 2006
    ....
  14. pmc Constitutively activated FGFR3 mutants signal through PLCgamma-dependent and -independent pathways for hematopoietic transformation
    Jing 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...
  15. pmc Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype
    Joseph D Growney
    Division of Hematology and Department of Pathology, Brigham and Women s Hospital, 1 Blackfan Circle, Boston, MA 02115, USA
    Blood 106:494-504. 2005
    ....
  16. pmc The homeobox gene CDX2 is aberrantly expressed in most cases of acute myeloid leukemia and promotes leukemogenesis
    Claudia Scholl
    Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 117:1037-48. 2007
    ....
  17. pmc K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors
    Thomas Kindler
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA, USA
    Blood 112:3373-82. 2008
    ..These data indicate that patients with T-cell leukemia with K-Ras mutations may benefit from therapies that target the NOTCH pathway alone or in combination with inhibition of the PI3K/AKT/MTOR and RAS/MAPK pathways...
  18. pmc Constitutive JAK3 activation induces lymphoproliferative syndromes in murine bone marrow transplantation models
    Melanie G Cornejo
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Blood 113:2746-54. 2009
    ..These data demonstrate that constitutive JAK3 activation disrupts T-cell homeostasis and induces lymphoproliferative diseases in mice...
  19. pmc STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2
    Winnie F Tam
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA, USA
    Cancer Res 73:373-84. 2013
    ..Therefore, targeting aberrantly activated STAT5 or rewired downstream signaling pathways may be a promising therapeutic option...
  20. pmc Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITD
    Jennifer L Rocnik
    Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Blood 108:1339-45. 2006
    ....
  21. pmc Hedgehog signaling is dispensable for adult murine hematopoietic stem cell function and hematopoiesis
    Inga Hofmann
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Cell Stem Cell 4:559-67. 2009
    ..Furthermore, the Hh pathway may not be a compelling target in certain hematopoietic malignancies...
  22. pmc The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRbeta and FIP1L1-PDGFRalpha in vitro and in vivo
    Elizabeth H Stover
    Division of Hematology, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    Blood 106:3206-13. 2005
    ..In summary, AMN107 can inhibit myeloid proliferation driven by TEL-PDGFRbeta and FIP1L1-PDGFRalpha and may be a useful drug for treatment of patients with myeloproliferative disease who harbor these kinase fusions...
  23. ncbi MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors
    Brian 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...
  24. pmc Cdx4 dysregulates Hox gene expression and generates acute myeloid leukemia alone and in cooperation with Meis1a in a murine model
    Dimple 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...
  25. pmc PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder
    Jing Chen
    Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:14479-84. 2004
    ..Therefore, PKC412 may be a useful therapy for treatment of human stem cell leukemia-lymphoma syndrome...
  26. ncbi PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease
    Jan Cools
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 3:459-69. 2003
    ..Our data establish PKC412 as molecularly targeted therapy for HES and other diseases expressing activated PDGFRalpha and demonstrate the potential of alternative kinase inhibitors to overcome resistance in target tyrosine kinases...
  27. ncbi The value of Wilms tumor susceptibility gene 1 in cytologic preparations as a marker for malignant mesothelioma
    Jonathan L Hecht
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Cancer 96:105-9. 2002
    ..This immunohistochemical study evaluates the effectiveness of WT1 as a marker for malignant mesothelioma in paraffin sections of cell block preparations derived from effusion specimens...

Research Grants1