Research Topics
Genomes and Genes
| Richard A Van EttenSummaryAffiliation: Tufts-New England Medical Center Country: USA Publications
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Detail Information
Publications
Aberrant cytokine signaling in leukemiaR 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...
Oncogenic signaling: new insights and controversies from chronic myeloid leukemiaRichard 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...- Focus on myeloproliferative diseases and myelodysplastic syndromesRichard A Van Etten
Molecular Oncology Research Institute, Tufts-New England Medical Center, Boston, MA 02111, USA
Cancer Cell 6:547-52. 2004 
A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinaseRyan 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...- Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in miceChristoph 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... 
Murine retroviral bone marrow transplantation models for the study of human myeloproliferative disordersL 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...- Requirement for CD44 in homing and engraftment of BCR-ABL-expressing leukemic stem cellsDaniela 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... - Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loopSergei 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... - Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617FVirginia 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... - Autoinhibition of Bcr-Abl through its SH3 domainKristen 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... - Adoptive immunotherapy of BCR-ABL-induced chronic myeloid leukemia-like myeloproliferative disease in a murine modelDaniela 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... - Tyrosine kinases as targets for cancer therapyDaniela 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 - The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in miceRyan 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... - Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocationsSergei 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... - Critical role for Gab2 in transformation by BCR/ABLMartin 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... - Distinct graft-versus-leukemic stem cell effects of early or delayed donor leukocyte infusions in a mouse chronic myeloid leukemia modelYi 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... - Right on target: eradicating leukemic stem cellsDaniela 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... - GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38Jian 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... - Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib eraRichard 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... - Ubiquitous and uniform in vivo fluorescence in ROSA26-EGFP BAC transgenic miceMaryann 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... - The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issuesRichard 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... - Navigating the road toward optimal initial therapy for chronic myeloid leukemiaRoss 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... - CDK6 kinase activity is required for thymocyte developmentMiaofen 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... - Peroxiredoxin1 prevents excessive endothelial activation and early atherosclerosisJanka 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... - Studying the pathogenesis of BCR-ABL+ leukemia in miceRichard 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... - A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9Ajeeta 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... - Targeting CXCR4 with cell-penetrating pepducins in lymphoma and lymphocytic leukemiaKatie 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... - Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3M 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.... - The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene productsS 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... - Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABLS 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... - Activation of c-Abl kinase activity and transformation by a chemical inducer of dimerizationK M Smith
Center for Blood Research, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115-5717, USA
J Biol Chem 276:24372-9. 2001.... - Bedside to bench: interfering with leukemic stem cellsDaniela S Krause
Nat Med 14:494-5. 2008 - Cardiotoxicity of the cancer therapeutic agent imatinib mesylateRisto 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... - Suppression of E-protein activity interferes with the development of BCR-ABL-mediated myeloproliferative diseaseJinkyung 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... - JAKing up hematopoietic proliferationKevin 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... - Imatinib mesylate radiosensitizes human glioblastoma cells through inhibition of platelet-derived growth factor receptorMatthias Holdhoff
, Campus Virchow, Charit, , 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... - Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemiaYiguo 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...