Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia

[1]  R. Yacobi,et al.  Autoinhibition of Bcr-Abl through Its SH3 Domain , 2003, Molecular Cell.

[2]  J. Griffin,et al.  Molecular mechanisms of transformation by the BCR-ABL oncogene. , 2003, Seminars in hematology.

[3]  M. Warmuth,et al.  The interaction of the Bcr-Abl tyrosine kinase with the Src kinase Hck is mediated by multiple binding domains , 2003, Leukemia.

[4]  N. Donato,et al.  BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. , 2003, Blood.

[5]  D. Fabbro,et al.  Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases. , 2003, Blood.

[6]  B. Druker,et al.  Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571). , 2002, Cancer research.

[7]  R. A. Etten.  Studying the pathogenesis of BCR–ABL+ leukemia in mice , 2002, Oncogene.

[8]  Matthew B. Wilson,et al.  Selective pyrrolo-pyrimidine inhibitors reveal a necessary role for Src family kinases in Bcr–Abl signal transduction and oncogenesis , 2002, Oncogene.

[9]  Matthew B. Wilson,et al.  The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells , 2002, The EMBO journal.

[10]  T. Skorski,et al.  Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571 , 2002, Oncogene.

[11]  J. Kuriyan,et al.  Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. , 2002, Cancer cell.

[12]  G. Daley,et al.  Overcoming STI571 resistance with the farnesyl transferase inhibitor SCH66336. , 2002, Blood.

[13]  C. Sawyers,et al.  Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[14]  D. Housman,et al.  A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9 , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[15]  R. Herrmann,et al.  High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. , 2002, Blood.

[16]  W. Pear,et al.  The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl. , 2002, Blood.

[17]  M. Baccarani,et al.  Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. , 2002, The New England journal of medicine.

[18]  R. Ren,et al.  Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia , 2001, Oncogene.

[19]  R. V. van Etten,et al.  Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling , 2001, The EMBO journal.

[20]  R. Ilaria,et al.  Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571. , 2001, Blood.

[21]  P. N. Rao,et al.  Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification , 2001, Science.

[22]  C. Sawyers,et al.  Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. , 2001, The New England journal of medicine.

[23]  M. Tomasson,et al.  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. , 2001, Blood.

[24]  M. Roussel,et al.  Stat5a/b contribute to interleukin 7-induced B-cell precursor expansion, but abl- and bcr/abl-induced transformation are independent of stat5. , 2000, Blood.

[25]  R. V. van Etten,et al.  The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase. , 2000, Blood.

[26]  Matthew B. Wilson,et al.  Transformation of Myeloid Leukemia Cells to Cytokine Independence by Bcr-Abl Is Suppressed by Kinase-defective Hck* , 2000, The Journal of Biological Chemistry.

[27]  George Q. Daley,et al.  The P190, P210, and P230 Forms of the BCR/ABL Oncogene Induce a Similar Chronic Myeloid Leukemia–like Syndrome in Mice but Have Different Lymphoid Leukemogenic Activity , 1999, The Journal of experimental medicine.

[28]  Jon C. Aster,et al.  Efficient and Rapid Induction of a Chronic Myelogenous Leukemia-Like Myeloproliferative Disease in Mice Receiving P210 bcr/abl-Transduced Bone Marrow , 1998 .

[29]  T. Yi,et al.  SHP-1 deficiency in B-lineage cells is associated with heightened lyn protein expression and increased lyn kinase activity. , 1998, Experimental hematology.

[30]  M. Warmuth,et al.  The Src Family Kinase Hck Interacts with Bcr-Abl by a Kinase-independent Mechanism and Phosphorylates the Grb2-binding Site of Bcr* , 1997, The Journal of Biological Chemistry.

[31]  Philippe Soriano,et al.  Characterization of the B lymphocyte populations in Lyn-deficient mice and the role of Lyn in signal initiation and down-regulation. , 1997, Immunity.

[32]  F. Meng,et al.  Lipopolysaccharide (LPS)-induced Macrophage Activation and Signal Transduction in the Absence of Src-Family Kinases Hck, Fgr, and Lyn , 1997, The Journal of experimental medicine.

[33]  M. Warmuth,et al.  Activation of Src kinases p53/56lyn and p59hck by p210bcr/abl in myeloid cells. , 1996, Cancer research.

[34]  O. Witte,et al.  Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene , 1995, Cell.

[35]  T. Pawson,et al.  SH2-containing phosphotyrosine phosphatase Syp is a target of p210bcr-abl tyrosine kinase. , 1994, The Journal of biological chemistry.

[36]  R. Gale,et al.  Chronic myeloid leukemia. , 1992, The American journal of medicine.

[37]  O. Witte,et al.  In vitro transformation of immature hematopoietic cells by the P210 BCR/ABL oncogene product of the Philadelphia chromosome. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[38]  G. Daley,et al.  Overcoming STI 571 resistance with the farnesyl transferase inhibitor SCH 66336 , 2002 .

[39]  D. Green,et al.  Death receptors bind SHP-1 and block cytokine-induced anti-apoptotic signaling in neutrophils , 2002, Nature Medicine.

[40]  R. V. van Etten,et al.  The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase. , 2001, Blood.

[41]  M. Roussel,et al.  Stat 5 a / b contribute to interleukin 7 – induced B-cell precursor expansion , but abl-and bcr / abl-induced transformation are independent of Stat 5 , 2000 .

[42]  J. Aster,et al.  Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. , 1998, Blood.

[43]  T. Dull,et al.  kat: a high-efficiency retroviral transduction system for primary human T lymphocytes. , 1994, Blood.