Richard A Van Etten

Summary

Affiliation: Tufts-New England Medical Center
Country: USA

Publications

  1. pmc Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F
    Virginia M Zaleskas
    Molecular Oncology Research Institute, Tufts New England Medical Center, Boston, Massachusetts, United States of America
    PLoS ONE 1:e18. 2006
  2. ncbi request reprint Focus on myeloproliferative diseases and myelodysplastic syndromes
    Richard A Van Etten
    Molecular Oncology Research Institute, Tufts New England Medical Center, Boston, MA 02111, USA
    Cancer Cell 6:547-52. 2004
  3. ncbi request reprint Aberrant cytokine signaling in leukemia
    R A Van Etten
    Molecular Oncology Research Institute and Division of Hematology Oncology, Tufts New England Medical Center, Boston, MA 02111, USA
    Oncogene 26:6738-49. 2007
  4. pmc Oncogenic signaling: new insights and controversies from chronic myeloid leukemia
    Richard A Van Etten
    Molecular Oncology Research Institute and the Division of Hematology Oncology, Tufts New England Medical Center, Boston, MA 02111, USA
    J Exp Med 204:461-5. 2007
  5. pmc A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase
    Ryan P Million
    Molecular Oncology Research Institute, Tufts New England Medical Center, 750 Washington St, Box 5609, Boston, MA 02111, USA
    Mol Cell Biol 24:4685-95. 2004
  6. pmc Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice
    Christoph Walz
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Blood 119:3550-60. 2012
  7. ncbi request reprint Requirement for CD44 in homing and engraftment of BCR-ABL-expressing leukemic stem cells
    Daniela S Krause
    Molecular Oncology Research Institute, Tufts New England Medical Center, 750 Washington Street, Boston, Massachusetts 02111, USA
    Nat Med 12:1175-80. 2006
  8. pmc Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop
    Sergei Roumiantsev
    Center for Blood Research and Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5717, USA
    Proc Natl Acad Sci U S A 99:10700-5. 2002
  9. doi request reprint Murine retroviral bone marrow transplantation models for the study of human myeloproliferative disorders
    L Cristina Gavrilescu
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA
    Curr Protoc Pharmacol . 2008
  10. ncbi request reprint Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations
    Sergei Roumiantsev
    Children s Hospital, 330 Longwood Avenue, Boston, MA 02115, USA
    Cancer Cell 5:287-98. 2004

Detail Information

Publications45

  1. pmc Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F
    Virginia M Zaleskas
    Molecular Oncology Research Institute, Tufts New England Medical Center, Boston, Massachusetts, United States of America
    PLoS ONE 1:e18. 2006
    ..However, the role of mutant JAK2 in disease pathogenesis is unclear...
  2. ncbi request reprint Focus on myeloproliferative diseases and myelodysplastic syndromes
    Richard A Van Etten
    Molecular Oncology Research Institute, Tufts New England Medical Center, Boston, MA 02111, USA
    Cancer Cell 6:547-52. 2004
  3. ncbi request reprint Aberrant cytokine signaling in leukemia
    R A Van Etten
    Molecular Oncology Research Institute and Division of Hematology Oncology, Tufts New England Medical Center, Boston, MA 02111, USA
    Oncogene 26:6738-49. 2007
    ..A better understanding of aberrant cytokine signaling in leukemia should provide additional targets for the rational therapy of these diseases...
  4. pmc Oncogenic signaling: new insights and controversies from chronic myeloid leukemia
    Richard A Van Etten
    Molecular Oncology Research Institute and the Division of Hematology Oncology, Tufts New England Medical Center, Boston, MA 02111, USA
    J Exp Med 204:461-5. 2007
    ..The development of better therapies will depend on a full understanding of signaling pathways in CML, facilitated by model studies using mutant mice...
  5. pmc A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase
    Ryan P Million
    Molecular Oncology Research Institute, Tufts New England Medical Center, 750 Washington St, Box 5609, Boston, MA 02111, USA
    Mol Cell Biol 24:4685-95. 2004
    ..These results suggest that direct binding of Grb2 is a common mechanism contributing to leukemogenesis by oncogenic Abl fusion proteins...
  6. pmc Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice
    Christoph Walz
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Blood 119:3550-60. 2012
    ..These results demonstrate that STAT5a/b is essential for the induction of CML-like leukemia by BCR-ABL1 and of polycythemia by JAK2(V617F), and validate STAT5a/b and the genes they regulate as targets for therapy in these MPNs...
  7. ncbi request reprint Requirement for CD44 in homing and engraftment of BCR-ABL-expressing leukemic stem cells
    Daniela S Krause
    Molecular Oncology Research Institute, Tufts New England Medical Center, 750 Washington Street, Boston, Massachusetts 02111, USA
    Nat Med 12:1175-80. 2006
    ..These results show that BCR-ABL-expressing leukemic stem cells depend to a greater extent on CD44 for homing and engraftment than do normal HSCs, and argue that CD44 blockade may be beneficial in autologous transplantation in CML...
  8. pmc Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop
    Sergei Roumiantsev
    Center for Blood Research and Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5717, USA
    Proc Natl Acad Sci U S A 99:10700-5. 2002
    ..Because clinical resistance induced by the Y253F mutation might be overcome by dose escalation of STI-571, molecular genotyping of STI-571-resistant patients may provide information useful for rational therapeutic management...
  9. doi request reprint Murine retroviral bone marrow transplantation models for the study of human myeloproliferative disorders
    L Cristina Gavrilescu
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA
    Curr Protoc Pharmacol . 2008
    ..An alternate protocol describes a similar technique that allows specific induction of lymphoproliferative disease by some TKs. Support protocols for generating and titering retroviral stocks are also included...
  10. ncbi request reprint Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations
    Sergei Roumiantsev
    Children s Hospital, 330 Longwood Avenue, Boston, MA 02115, USA
    Cancer Cell 5:287-98. 2004
    ..These results implicate different signaling pathways originating from both kinase and fusion partner in the pathogenesis of CML and EMS...
  11. ncbi request reprint Tyrosine kinases as targets for cancer therapy
    Daniela S Krause
    Molecular Oncology Research Institute, Division of Hematology Oncology, Tufts New England Medical Center, Boston, MA 02111, USA
    N Engl J Med 353:172-87. 2005
  12. doi request reprint Loss of Ikaros DNA-binding function confers integrin-dependent survival on pre-B cells and progression to acute lymphoblastic leukemia
    Ila Joshi
    Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA
    Nat Immunol 15:294-304. 2014
    ....
  13. ncbi request reprint Autoinhibition of Bcr-Abl through its SH3 domain
    Kristen M Smith
    The Center for Blood Research and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 12:27-37. 2003
    ..The sole function of the coiled-coil domain is to disrupt the autoinhibited conformation through oligomerization and intermolecular autophosphorylation...
  14. ncbi request reprint Adoptive immunotherapy of BCR-ABL-induced chronic myeloid leukemia-like myeloproliferative disease in a murine model
    Daniela S Krause
    Center for Blood Research, Institute for Biomedical Research, Harvard Medical School, Boston, MA, USA
    Blood 104:4236-44. 2004
    ..These results suggest that depletion of CD8(+) cells from DLI could impair GvL against CML, while increased MHC disparity between donor and recipient may improve the responsiveness of Philadelphia(+) B-lymphoblastic leukemia to DLI...
  15. doi request reprint Peroxiredoxin1 prevents excessive endothelial activation and early atherosclerosis
    Janka Kisucka
    Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Circ Res 103:598-605. 2008
    ..Thus, Prdx1 protects against excessive endothelial activation and atherosclerosis, and the Prdx1(-/-) mice could serve as an animal model susceptible to chronic inflammation...
  16. ncbi request reprint Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era
    Richard A Van Etten
    Molecular Oncology Research Institute, Tufts New England Medical Center, 750 Washington Street, Boston, MA 02111, USA
    Leuk Res 28:S21-8. 2004
    ..Here, I summarize some recent advances in our understanding of the regulatory and signaling mechanisms of Bcr-Abl, with an emphasis on therapeutic implications...
  17. ncbi request reprint The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in mice
    Ryan P Million
    The Center for Blood Research and Department of Genetics, Brigham and Women s Hospital, Harvard Institutes of Medicine, Boston, MA 02115, USA
    Blood 99:4568-77. 2002
    ..These results show that Tel-Abl has leukemogenic properties from distinct from those of Bcr-Abl and may act in a different bone marrow progenitor...
  18. ncbi request reprint Critical role for Gab2 in transformation by BCR/ABL
    Martin Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Cancer Cell 1:479-92. 2002
    ..Our results identify Gab2 and its associated proteins as key determinants of the lineage and severity of BCR/ABL transformation...
  19. pmc CDK6 kinase activity is required for thymocyte development
    Miaofen G Hu
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA, USA
    Blood 117:6120-31. 2011
    ..This role of CDK6 as a downstream mediator of Notch identifies CDK6 kinase activity as a potential therapeutic target in human lymphoid malignancies...
  20. pmc A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9
    Ajeeta B Dash
    Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:7622-7. 2002
    ..Furthermore, these data indicate that despite acquisition of additional mutations, CML blast crisis cells retain their dependence on BCR/ABL for proliferation and survival...
  21. pmc Navigating the road toward optimal initial therapy for chronic myeloid leukemia
    Ross A Okimoto
    Division of Hematology Oncology, Tufts Medical Center, Boston, Massachusetts 02111, USA
    Curr Opin Hematol 18:89-97. 2011
    ..A fourth drug, bosutinib, may also win FDA approval in 2011. The goal of this review is to summarize the most recent information on initial treatment of CML and to aid clinicians in managing newly diagnosed CML patients...
  22. pmc Distinct graft-versus-leukemic stem cell effects of early or delayed donor leukocyte infusions in a mouse chronic myeloid leukemia model
    Yi Fen Lu
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA, USA
    Blood 119:273-84. 2012
    ..These results define a physiologic model of adoptive immunotherapy of CML that will be useful for investigating the cellular and molecular mechanisms of GVL...
  23. pmc GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38
    Jian Zhong
    The Molecular Cardiology Research Institute, and Department of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 106:4372-7. 2009
    ..Extracellular signal-regulated kinase (ERK) and nuclear factor-kappaB (NF-kappaB) activation are largely unaffected. Thus, GCK is an essential PAMP effector coupling JNK and p38, but not ERK or NF-kappaB to systemic inflammation...
  24. ncbi request reprint Right on target: eradicating leukemic stem cells
    Daniela S Krause
    Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA
    Trends Mol Med 13:470-81. 2007
    ..Here, we review recent advances in LSC research and discuss novel therapeutic strategies to specifically target LSCs...
  25. pmc IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1
    Mo Ying Hsieh
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA
    Blood 123:2401-11. 2014
    ....
  26. pmc Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop
    Richard A Van Etten
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Leuk Lymphoma 54:1151-8. 2013
    ..A report summarizing the pertinent advances in MPN has been published separately...
  27. pmc Signal transduction in the chronic leukemias: implications for targeted therapies
    Wesam Ahmed
    Molecular Oncology Research Institute and Division of Hematology Oncology, Tufts Medical Center, 800 Washington Street, Box 5609, Boston, MA 02111, USA
    Curr Hematol Malig Rep 8:71-80. 2013
    ..We also discuss correlative studies emerging from clinical trials of drugs targeting these pathways...
  28. pmc Autologous stem cell transplant recipients tolerate haploidentical related-donor natural killer cell-enriched infusions
    Hans Klingemann
    Division of Hematology Oncology, Tufts Medical Center, Boston, Massachusetts 02111, USA
    Transfusion 53:412-8; quiz 411. 2013
    ..The graft-versus-tumor effect after autologous stem cell transplantation (ASCT) may result in less disease relapse...
  29. pmc Ubiquitous and uniform in vivo fluorescence in ROSA26-EGFP BAC transgenic mice
    Maryann Giel-Moloney
    Division of Gastroenterology, GRASP Digestive Disease Center, Tufts New England Medical Center, Boston, Massachusetts, USA
    Genesis 45:83-9. 2007
    ..The results suggest that the ROSA26 BAC is an efficient strategy for expressing complex transgene cassettes in vivo...
  30. pmc The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues
    Richard A Van Etten
    Division of Hematology Oncology, Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Haematologica 96:590-601. 2011
    ..Finally, the clinical role of the new JAK2- and BCR-ABL1-inhibitors is considered. Much further progress is likely in several of these areas soon...
  31. pmc Targeting CXCR4 with cell-penetrating pepducins in lymphoma and lymphocytic leukemia
    Katie O'Callaghan
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Blood 119:1717-25. 2012
    ..These data demonstrate that CXCL12-CXCR4 signaling can be effectively inhibited by cell-penetrating pepducins, which represents a potential new treatment strategy for lymphoid malignancies...
  32. pmc Differential regulation of myeloid leukemias by the bone marrow microenvironment
    Daniela S Krause
    1 Center for Regenerative Medicine and Cancer Center, Massachusetts General Hospital, Boston, Massachusetts, USA 2 Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts, USA 3 Harvard Stem Cell Institute, Cambridge, Massachusetts, USA 4 Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA
    Nat Med 19:1513-7. 2013
    ..These results demonstrate that LSC niches in CML and AML are distinct and suggest that modulation of the BMM by PTH may be a feasible strategy to reduce LSCs, a prerequisite for the cure of CML. ..
  33. ncbi request reprint Studying the pathogenesis of BCR-ABL+ leukemia in mice
    Richard A Van Etten
    The Center for Blood Research and Department of Genetics, Harvard Medical School, Boston, Massachusetts, MA 02115, USA
    Oncogene 21:8643-51. 2002
    ..Here I review recent studies of leukemias induced in mice by BCR-ABL with an emphasis on the intricate nature of these diseases and the need for careful pathological and molecular analysis...
  34. ncbi request reprint Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression
    Carola A Neumann
    Center for Blood Research and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 424:561-5. 2003
    ..Our results implicate Prdx1 as an important defence against oxidants in ageing mice...
  35. pmc Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036
    Wayne W Chan
    Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA 02111, USA
    Cancer Cell 19:556-68. 2011
    ....
  36. ncbi request reprint Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL
    S Li
    The Center for Blood Research, Dana-Farber Cancer Institute, and Harvard Institutes of Medicine and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA, USA
    Blood 97:1442-50. 2001
    ..These results demonstrate that IL-3 and GM-CSF are not required for BCR/ABL-induced CML-like leukemia in mice and suggest that autocrine production of IL-3 does not play a role in established chronic phase CML in humans...
  37. ncbi request reprint Activation of c-Abl kinase activity and transformation by a chemical inducer of dimerization
    K M Smith
    Center for Blood Research, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115-5717, USA
    J Biol Chem 276:24372-9. 2001
    ....
  38. pmc The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products
    S T Wen
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    EMBO J 15:1583-95. 1996
    ..These results indicate that Abl inhibits cell proliferation by interacting with central elements of the cell cycle control apparatus in the nucleus, and suggest a direct connection between p53 and Rb in this growth-inhibitory pathway...
  39. ncbi request reprint Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3
    M H Tomasson
    Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood 97:1435-41. 2001
    ....
  40. ncbi request reprint Cardiotoxicity of the cancer therapeutic agent imatinib mesylate
    Risto Kerkela
    Center for Translational Medicine, Jefferson Medical College, 1025 Walnut Street, Philadelphia, Pennsylvania 19107, USA
    Nat Med 12:908-16. 2006
    ..Thus, cardiotoxicity is an unanticipated side effect of inhibition of c-Abl by imatinib...
  41. pmc Bedside to bench: interfering with leukemic stem cells
    Daniela S Krause
    Nat Med 14:494-5. 2008
  42. ncbi request reprint JAKing up hematopoietic proliferation
    Kevin Shannon
    Department of Pediatrics and Comprehensive Cancer Center, University of California, San Francisco, California 94143, USA
    Cancer Cell 7:291-3. 2005
    ..These results open new avenues for diagnosing and classifying patients with these disorders, and identify a new molecular target for drug discovery...
  43. ncbi request reprint Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia
    Yiguo Hu
    The Jackson Laboratory, 600 Main St, Bar Harbor, Maine 04609, USA
    Nat Genet 36:453-61. 2004
    ..These results implicate Src family kinases as therapeutic targets in Ph(+) B-ALL and suggest that simultaneous inhibition of Src and Bcr-Abl kinases may benefit individuals with Ph(+) acute leukemia...
  44. ncbi request reprint Imatinib mesylate radiosensitizes human glioblastoma cells through inhibition of platelet-derived growth factor receptor
    Matthias Holdhoff
    Medizinische Klinik für Hämatologie und Onkologie, Campus Virchow, Charite, Humboldt Universitat, Augustenburger Platz 1, 13353 Berlin, Germany
    Blood Cells Mol Dis 34:181-5. 2005
    ..These results suggest that imatinib may have clinical utility as a radiosensitizer in the treatment of human glioblastoma, possibly through disruption of an autocrine PDGF/PDGFR loop...
  45. pmc Suppression of E-protein activity interferes with the development of BCR-ABL-mediated myeloproliferative disease
    Jinkyung Ko
    Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:12967-72. 2008
    ..Collectively, these studies show that suppression of E-protein activity interferes with the development of BCR-ABL-mediated MPD...