Martin Sattler

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells
    M Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 275:24273-8. 2000
  2. ncbi request reprint 2-methoxyestradiol alters cell motility, migration, and adhesion
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Blood 102:289-96. 2003
  3. ncbi request reprint Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cells
    Martin Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
    Oncogene 21:1423-33. 2002
  4. pmc BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis
    M Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 19:7473-80. 1999
  5. ncbi request reprint Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABL
    M Sattler
    Division of Hematologic Malignancies, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cytokine Growth Factor Rev 8:63-79. 1997
  6. ncbi request reprint c-MET mutational analysis in small cell lung cancer: novel juxtamembrane domain mutations regulating cytoskeletal functions
    Patrick C Ma
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 63:6272-81. 2003
  7. ncbi request reprint Critical role for hematopoietic cell kinase (Hck)-mediated phosphorylation of Gab1 and Gab2 docking proteins in interleukin 6-induced proliferation and survival of multiple myeloma cells
    Klaus Podar
    Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    J Biol Chem 279:21658-65. 2004
  8. ncbi request reprint Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen species
    Jeong H Kim
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
    Blood 105:1717-23. 2005
  9. ncbi request reprint Regulation of cellular proliferation, cytoskeletal function, and signal transduction through CXCR4 and c-Kit in small cell lung cancer cells
    Takashi Kijima
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 62:6304-11. 2002
  10. pmc The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes
    Gerlinde Wernig
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Blood 111:3751-9. 2008

Detail Information

Publications55

  1. ncbi request reprint The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells
    M Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 275:24273-8. 2000
    ..Further, treatment of MO7e cells with H(2)O(2) or pervanadate increased the tyrosine kinase activity of c-ABL. Drugs that alter ROS metabolism or reactivate PTPases may antagonize BCR/ABL transformation...
  2. ncbi request reprint 2-methoxyestradiol alters cell motility, migration, and adhesion
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Blood 102:289-96. 2003
    ..Combination of 2ME2 with other anticancer drugs may be beneficial to treatment of drug-resistant cancers...
  3. ncbi request reprint Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cells
    Martin Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
    Oncogene 21:1423-33. 2002
    ..These results demonstrate that BCR/ABL signals differentially through CBL and CBL-B, with downregulation of the CBL-B protein potentially contributing to BCR/ABL-mediated transformation...
  4. pmc BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis
    M Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 19:7473-80. 1999
    ..Reexpression of SHIP in BCR/ABL-transformed Ba/F3 cells altered the biological behavior of cells in culture. The reduction of SHIP due to BCR/ABL is likely to directly contribute to the pathogenesis of CML...
  5. ncbi request reprint Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABL
    M Sattler
    Division of Hematologic Malignancies, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cytokine Growth Factor Rev 8:63-79. 1997
    ..In this review, we will describe the molecular and biological abnormalities in CML and several signal transduction mechanisms utilized by BCR/ABL as compared to hematopoietic growth factors...
  6. ncbi request reprint c-MET mutational analysis in small cell lung cancer: novel juxtamembrane domain mutations regulating cytoskeletal functions
    Patrick C Ma
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 63:6272-81. 2003
    ..It would now be useful to study the inhibition of c-MET as a therapeutic target against SCLC...
  7. ncbi request reprint Critical role for hematopoietic cell kinase (Hck)-mediated phosphorylation of Gab1 and Gab2 docking proteins in interleukin 6-induced proliferation and survival of multiple myeloma cells
    Klaus Podar
    Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    J Biol Chem 279:21658-65. 2004
    ....
  8. ncbi request reprint Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen species
    Jeong H Kim
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
    Blood 105:1717-23. 2005
    ..Finally, these results hint at novel targets for drug development that may aid traditional therapy...
  9. ncbi request reprint Regulation of cellular proliferation, cytoskeletal function, and signal transduction through CXCR4 and c-Kit in small cell lung cancer cells
    Takashi Kijima
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 62:6304-11. 2002
    ..Inhibition of both the CXCR4 and the c-Kit downstream events could be a promising therapeutic approach in SCLC...
  10. pmc The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes
    Gerlinde Wernig
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Blood 111:3751-9. 2008
    ..Overall, our results suggest that constitutive activation of Jak2 requires an intact FERM domain for a transforming phenotype, and is necessary for activation of the major target of Jak2, STAT5...
  11. ncbi request reprint Caveolin-1 is required for vascular endothelial growth factor-triggered multiple myeloma cell migration and is targeted by bortezomib
    Klaus Podar
    Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
    Cancer Res 64:7500-6. 2004
    ....
  12. 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...
  13. doi request reprint Targeting angiogenesis via a c-Myc/hypoxia-inducible factor-1alpha-dependent pathway in multiple myeloma
    Jing Zhang
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Cancer Res 69:5082-90. 2009
    ..Our data, therefore, identify Hif-1alpha as a novel molecular target in MM and add another facet to anti-MM drug activity...
  14. doi request reprint Cell cycle regulation by oncogenic tyrosine kinases in myeloid neoplasias: from molecular redox mechanisms to health implications
    Margret S Rodrigues
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA
    Antioxid Redox Signal 10:1813-48. 2008
    ..The underlying mechanisms leading to elevated oxidative stress are reviewed, and signaling mechanisms that may serve as novel targeted approaches to overcome ROS-dependent cell growth are discussed...
  15. ncbi request reprint Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myeloma
    Klaus Podar
    Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Cancer Res 67:1680-8. 2007
    ..Finally, our data suggest that this mechanism may not only be restricted to MM but may also be important in a broad range of malignancies including erythroleukemia and solid tumors...
  16. doi request reprint The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment: therapeutic implications
    Klaus Podar
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Br J Haematol 155:438-48. 2011
    ..Our data therefore provide the rationale for the clinical evaluation of Natalizumab, preferably in combination with novel agents (e.g. bortezomib) to enhance MM cytotoxicity and improve patient outcome...
  17. pmc Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism
    Margret S Fernandes
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Biol Chem 285:32596-605. 2010
    ..Pathways that are activated by CBL gain-of-function mutations can be efficiently targeted by small molecule drugs...
  18. pmc The small-molecule VEGF receptor inhibitor pazopanib (GW786034B) targets both tumor and endothelial cells in multiple myeloma
    Klaus Podar
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 103:19478-83. 2006
    ....
  19. ncbi request reprint Superoxide-dependent and -independent mitochondrial signaling during apoptosis in multiple myeloma cells
    Dharminder Chauhan
    Department of Medical Oncology, The Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 22:6296-300. 2003
    ....
  20. pmc BCR-ABL promotes the frequency of mutagenic single-strand annealing DNA repair
    Margret S Fernandes
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Blood 114:1813-9. 2009
    ..Therefore, drugs that target growth factor receptor signaling represent potential therapeutic agents to combat tyrosine kinase-induced genomic instability...
  21. pmc Selective Akt inhibitors synergize with tyrosine kinase inhibitors and effectively override stroma-associated cytoprotection of mutant FLT3-positive AML cells
    Ellen Weisberg
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 8:e56473. 2013
    ..As a strategy to improve clinical efficacy, we searched for novel agents capable of potentiating the stroma-diminished effects of TKI treatment of mutant FLT3-expressing cells...
  22. ncbi request reprint A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinase
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 63:5462-9. 2003
    ..The characterization of SU11274 as an effective inhibitor of Met tyrosine kinase activity illustrates the potential of targeting for Met therapeutic use in cancers associated with activated forms of this kinase...
  23. ncbi request reprint Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cells
    Klaus Podar
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 278:5794-801. 2003
    ..Taken together, this study identifies caveolin-1 and other structural membrane components as potential new therapeutic targets in multiple myeloma...
  24. ncbi request reprint p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl
    R Salgia
    Division of Hematologic Malignacies, Dana Farber Cancer Institute, Boston, MA 02115
    Exp Hematol 24:310-3. 1996
    ..The binding of p120c-Cbl to the focal adhesion protein paxillin could contribute to the known adhesive defects of CML cells...
  25. ncbi request reprint Activated Jak2 with the V617F point mutation promotes G1/S phase transition
    Christoph Walz
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    J Biol Chem 281:18177-83. 2006
    ....
  26. ncbi request reprint Mutated tyrosine kinases as therapeutic targets in myeloid leukemias
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Adv Exp Med Biol 532:121-40. 2003
    ..FLT3 tyrosine kinase inhibitors are currently being evaluated in clinical trials and may be very useful therapeutic agents in AML...
  27. ncbi request reprint Steel factor induces tyrosine phosphorylation of CRKL and binding of CRKL to a complex containing c-kit, phosphatidylinositol 3-kinase, and p120(CBL)
    M Sattler
    Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    J Biol Chem 272:10248-53. 1997
    ..Such complexes could be important in propagating signals involving PI3K such as gene expression and adhesion...
  28. ncbi request reprint The BCR/ABL oncogene alters interaction of the adapter proteins CRKL and CRK with cellular proteins
    N Uemura
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Leukemia 11:376-85. 1997
    ..In BCR/ABL-transformed cells, CRKL but not CRK II, appears to form complexes which potentially link BCR/ABL, c-ABL, C3G, and SOS to the protooncoprotein, p120CBL...
  29. ncbi request reprint Mechanisms of transformation by the BCR/ABL oncogene
    M Sattler
    Department of Adult Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Int J Hematol 73:278-91. 2001
    ..This review will describe mechanisms of transformation by the BCR/ABL oncogene and opportunities for clinical intervention with specific signal transduction inhibitors such as STI-571 in CML...
  30. ncbi request reprint 2-Methoxyestradiol overcomes drug resistance in multiple myeloma cells
    Dharminder Chauhan
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02215, USA
    Blood 100:2187-94. 2002
    ..They provide a framework for the use of 2ME2, either alone or in combination with Dex, to overcome drug resistance and to improve outcome in MM...
  31. doi request reprint EGFR-targeted therapeutics: focus on SCCHN and NSCLC
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    ScientificWorldJournal 8:909-19. 2008
    ..This article reviews EGFR-targeted therapies in use and in development, with a focus on the role of EGFR in the pathophysiology of head and neck and lung cancer, and new concepts being investigated to improve outcomes with these agents...
  32. ncbi request reprint Therapeutic targeting of the receptor tyrosine kinase Met
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Cancer Treat Res 119:121-38. 2004
  33. ncbi request reprint Vascular endothelial growth factor-induced migration of multiple myeloma cells is associated with beta 1 integrin- and phosphatidylinositol 3-kinase-dependent PKC alpha activation
    Klaus Podar
    Jerome Lipper Multiple Myeloma Research Center Dana Farber Cancer Institute and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 277:7875-81. 2002
    ..Time-lapse phase contrast video microscopy (TLVM) studies confirm the importance of these signaling components in VEGF-triggered MM cell migration on fibronectin...
  34. ncbi request reprint p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene
    R Salgia
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 271:25198-203. 1996
    ..These alterations in the structure of signaling proteins in focal adhesion like structures could contribute to the known adhesion abnormalities in CML cells...
  35. pmc Reversible resistance induced by FLT3 inhibition: a novel resistance mechanism in mutant FLT3-expressing cells
    Ellen Weisberg
    Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS ONE 6:e25351. 2011
    ..Thus, there is a need for identification of molecular mechanisms of clinical resistance to these drugs. In response, we characterized MOLM13 AML cell lines made resistant to two structurally-independent FLT3 inhibitors...
  36. ncbi request reprint Novel targeted therapies to overcome imatinib mesylate resistance in chronic myeloid leukemia (CML)
    Christoph Walz
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Crit Rev Oncol Hematol 57:145-64. 2006
    ..In this review, we will discuss the underlying mechanisms of resistance to imatinib and novel targeted approaches to overcome imatinib resistance in CML...
  37. ncbi request reprint Involvement of p130(Cas) and p105(HEF1), a novel Cas-like docking protein, in a cytoskeleton-dependent signaling pathway initiated by ligation of integrin or antigen receptor on human B cells
    S N Manie
    Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 272:4230-6. 1997
    ..These associations implicate HEF1 and Cas as important components in a cytoskeleton-linked signaling pathway initiated by ligation of beta1 integrin or BCR on human B cells...
  38. ncbi request reprint Differential signaling after beta1 integrin ligation is mediated through binding of CRKL to p120(CBL) and p110(HEF1)
    M Sattler
    Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    J Biol Chem 272:14320-6. 1997
    ..The shift in association of CRKL and its SH3-associated proteins from p120(CBL) to p110(HEF1) could contribute to different functional outcomes of "outside-in" integrin signaling in different cells...
  39. ncbi request reprint CRKL links p210BCR/ABL with paxillin in chronic myelogenous leukemia cells
    R Salgia
    Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    J Biol Chem 270:29145-50. 1995
    ..These results suggest that the p210BCR/ABL oncogene may be physically linked to the focal adhesion-associated protein paxillin in hematopoietic cells by CRKL. This interaction could contribute to the known adhesive defects of CML cells...
  40. ncbi request reprint Cell motility, adhesion, homing, and migration assays in the studies of tyrosine kinases
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Methods Mol Med 85:87-105. 2003
  41. pmc BCR/ABL induces multiple abnormalities of cytoskeletal function
    R Salgia
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 100:46-57. 1997
    ..The increase in spontaneous motility and other defects of cytoskeletal function described here will be useful biological markers of the functional effects of BCR/ABL in hematopoietic cells...
  42. doi request reprint Drug resistance in mutant FLT3-positive AML
    E Weisberg
    Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Oncogene 29:5120-34. 2010
    ....
  43. ncbi request reprint The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alpha
    R Salgia
    Department of Medical Oncology, Division of Hematologic Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood 94:4233-46. 1999
    ....
  44. ncbi request reprint SHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKL
    M Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 276:2451-8. 2001
    ..Overall, these data suggest that proteins that interact with SHIP1 through Tyr(917) and Tyr(1020), such as DOK1 and SHC, are likely to be involved in the regulation of SHIP1 dependent migration...
  45. ncbi request reprint Molecular and cellular biology of small cell lung cancer
    Martin Sattler
    Department of Medical Oncology, Division of Thoracic Oncology Program, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Semin Oncol 30:57-71. 2003
    ..Some downstream molecules are also activated, such as phosphatidylinositol 3'-kinase, and would serve as good candidates for therapeutic strategies...
  46. ncbi request reprint Targeting c-Kit mutations: basic science to novel therapies
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, Department of Medicine, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    Leuk Res 28:S11-20. 2004
    ..We will also discuss the role and expression of Kit in various malignancies. Ultimately, the understanding of c-Kit biology, biochemistry, and mutational analysis will lead to better therapeutics...
  47. doi request reprint JAK2 gets histone H3 rolling
    Martin Sattler
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 16:365-6. 2009
    ..A paper in the recent issue of Nature demonstrates that phosphorylation of histone H3 by JAK2 releases the transcriptional repressor HP1alpha from chromatin, resulting in gene transcription...
  48. ncbi request reprint Molecular mechanisms of transformation by the BCR-ABL oncogene
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, and Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Semin Hematol 40:4-10. 2003
    ..This review describes molecular mechanisms that are thought to be important for transformation by the BCR-ABL oncoprotein and points at pathways for targeted drug development in the treatment of CML...
  49. doi request reprint Targeting JAK2 in the therapy of myeloproliferative neoplasms
    Mamatha M Reddy
    Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02215, USA
    Expert Opin Ther Targets 16:313-24. 2012
    ..MPNs are frequently associated with activating mutations in JAK2; small-molecule drugs targeting this molecule have entered clinical trials...
  50. pmc The role of the c-Met pathway in lung cancer and the potential for targeted therapy
    Martin Sattler
    Department of Medical Oncology, Dana Farber Cancer Institute, and Brigham and Women s Hospital, Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA
    Ther Adv Med Oncol 3:171-84. 2011
    ..In particular, trials involving MetMAb and ARQ197 (tivantinib) have gained interest. Ultimately, as individualized therapies become a reality for cancers, HGFR will be an important molecular target...
  51. pmc Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia
    Akinori Yoda
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:252-7. 2010
    ..Together, these findings implicate CRLF2 as an important factor in B-ALL with diagnostic, prognostic, and therapeutic implications...
  52. ncbi request reprint Targeting mutated tyrosine kinases in the therapy of myeloid leukaemias
    Lolita Banerji
    Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02115, USA
    Expert Opin Ther Targets 8:221-39. 2004
    ..Here, the authors review the signalling activities, mechanism of transformation and therapeutic targeting of several tyrosine kinase oncogenes important in myeloid leukaemias...
  53. ncbi request reprint Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration
    K Podar
    Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Blood 98:428-35. 2001
    ..These observations provide the framework for novel therapeutic strategies targeting VEGF signaling cascades in MM...
  54. ncbi request reprint Chronic myelogenous leukemia progenitors display a genetically unstable personality
    Margret S Rodrigues
    J Natl Cancer Inst 99:662-3. 2007
  55. pmc A sensitive high-throughput method to detect activating mutations of Jak2 in peripheral-blood samples
    Martin Sattler
    Blood 107:1237-8. 2006