Research Topics
Genomes and Genes
| Martin SattlerSummaryAffiliation: Harvard University Country: USA Publications
| Collaborators
|
Detail Information
Publications
Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cellsMartin 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...- The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cellsM 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... 
BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesisM 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...- Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABLM 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... - 2-methoxyestradiol alters cell motility, migration, and adhesionMartin 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... - c-MET mutational analysis in small cell lung cancer: novel juxtamembrane domain mutations regulating cytoskeletal functionsPatrick 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... - Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen speciesJeong 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... - 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 cellsKlaus 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.... - The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenesGerlinde 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... - Regulation of cellular proliferation, cytoskeletal function, and signal transduction through CXCR4 and c-Kit in small cell lung cancer cellsTakashi 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... - Caveolin-1 is required for vascular endothelial growth factor-triggered multiple myeloma cell migration and is targeted by bortezomibKlaus 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.... - Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myelomaKlaus 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... 
Cell cycle regulation by oncogenic tyrosine kinases in myeloid neoplasias: from molecular redox mechanisms to health implicationsMargret 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...- 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... - Targeting angiogenesis via a c-Myc/hypoxia-inducible factor-1alpha-dependent pathway in multiple myelomaJing 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... - The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment: therapeutic implicationsKlaus 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... - The small-molecule VEGF receptor inhibitor pazopanib (GW786034B) targets both tumor and endothelial cells in multiple myelomaKlaus 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.... - Superoxide-dependent and -independent mitochondrial signaling during apoptosis in multiple myeloma cellsDharminder 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.... - Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolismMargret 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... - BCR-ABL promotes the frequency of mutagenic single-strand annealing DNA repairMargret 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... - A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinaseMartin 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... - Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cellsKlaus 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... - p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-CblR 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... - Activated Jak2 with the V617F point mutation promotes G1/S phase transitionChristoph Walz
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
J Biol Chem 281:18177-83. 2006.... - Mutated tyrosine kinases as therapeutic targets in myeloid leukemiasMartin 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... - 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... - The BCR/ABL oncogene alters interaction of the adapter proteins CRKL and CRK with cellular proteinsN 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... - Mechanisms of transformation by the BCR/ABL oncogeneM 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... - Therapeutic targeting of the receptor tyrosine kinase MetMartin 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 - EGFR-targeted therapeutics: focus on SCCHN and NSCLCMartin 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... - Vascular endothelial growth factor-induced migration of multiple myeloma cells is associated with beta 1 integrin- and phosphatidylinositol 3-kinase-dependent PKC alpha activationKlaus 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... - p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogeneR 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... - Reversible resistance induced by FLT3 inhibition: a novel resistance mechanism in mutant FLT3-expressing cellsEllen 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... - 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... - CRKL links p210BCR/ABL with paxillin in chronic myelogenous leukemia cellsR 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... - 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 cellsS 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... - 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... - 2-Methoxyestradiol overcomes drug resistance in multiple myeloma cellsDharminder 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... - Cell motility, adhesion, homing, and migration assays in the studies of tyrosine kinasesMartin 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 - SHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKLM 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... - BCR/ABL induces multiple abnormalities of cytoskeletal functionR 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... - Drug resistance in mutant FLT3-positive AMLE Weisberg
Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Oncogene 29:5120-34. 2010.... - The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alphaR Salgia
Department of Medical Oncology, Division of Hematologic Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Blood 94:4233-46. 1999.... - JAK2 gets histone H3 rollingMartin 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... - Molecular and cellular biology of small cell lung cancerMartin 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... - Molecular mechanisms of transformation by the BCR-ABL oncogeneMartin 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... - Targeting c-Kit mutations: basic science to novel therapiesMartin 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... - Targeting JAK2 in the therapy of myeloproliferative neoplasmsMamatha M Reddy
Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02215, USA
Expert Opin Ther Targets 16:313-24. 2012..The discovery of JAK2 mutations that cause secondary resistance in vitro would further highlight the need for the development of next-generation JAK2 inhibitors and novel synergistic approaches... - The role of the c-Met pathway in lung cancer and the potential for targeted therapyMartin 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... - Targeting mutated tyrosine kinases in the therapy of myeloid leukaemiasLolita 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... - Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemiaAkinori 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... - Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migrationK 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... - Chronic myelogenous leukemia progenitors display a genetically unstable personalityMargret S Rodrigues
J Natl Cancer Inst 99:662-3. 2007 - A sensitive high-throughput method to detect activating mutations of Jak2 in peripheral-blood samplesMartin Sattler
Blood 107:1237-8. 2006