Growth factor independence and BCR/ABL transformation: promise and pitfalls of murine model systems and assays

[1]  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.

[2]  D. Williams,et al.  Deficiency of the hematopoietic cell-specific Rho family GTPase Rac2 is characterized by abnormalities in neutrophil function and host defense. , 1999, Immunity.

[3]  Stefan N. Constantinescu,et al.  The Erythropoietin Receptor: Structure, Activation and Intracellular Signal Transduction , 1999, Trends in Endocrinology & Metabolism.

[4]  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 .

[5]  X Zhang,et al.  Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: a novel model for chronic myelogenous leukemia. , 1998, Blood.

[6]  G. Daley,et al.  Control of hematopoietic differentiation: lack of specificity in signaling by cytokine receptors. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[7]  M. Bernard,et al.  BCR-ABL and constitutively active erythropoietin receptor (cEpoR) activate distinct mechanisms for growth factor-independence and inhibition of apoptosis in Ba/F3 cell line , 1998, Oncogene.

[8]  B. Calabretta,et al.  The SH3 domain contributes to BCR/ABL-dependent leukemogenesis in vivo: role in adhesion, invasion, and homing. , 1998, Blood.

[9]  R. Forés,et al.  Typical chronic myelogenous leukemia with e19a2 junction BCR/ABL transcript. , 1997, Blood.

[10]  C. Eaves,et al.  Selective expansion of primitive normal hematopoietic cells in cytokine-supplemented cultures of purified cells from patients with chronic myeloid leukemia. , 1997, Blood.

[11]  C. Sawyers.  Signal transduction pathways involved in BCR-ABL transformation. , 1997, Bailliere's clinical haematology.

[12]  P. Leymarie,et al.  A new case of chronic myeloid leukemia with c3/a2 BCR/ABL junction. Is it really a distinct disease? , 1997, Blood.

[13]  C. Verfaillie,et al.  Activation of β1 integrins on CML progenitors reveals cooperation between β1 integrins and CD44 in the regulation of adhesion and proliferation , 1997, Leukemia.

[14]  R. Marasca,et al.  Relationship between BCR/ABL fusion proteins and leukemia phenotype. , 1997, Blood.

[15]  S. Ghaffari,et al.  Diverse effects of anti‐CD44 antibodies on the stromal cell‐mediated support of normal but not leukaemic (CML) haemopoiesis in vitro , 1997, British journal of haematology.

[16]  H. Lodish,et al.  Identification of a novel pathway important for proliferation and differentiation of primary erythroid progenitors. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[17]  H. Lodish,et al.  Functional interaction of erythropoietin and stem cell factor receptors is essential for erythroid colony formation. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[18]  R. Salgia,et al.  Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABL. , 1997, Cytokine & growth factor reviews.

[19]  C. Der,et al.  Dbl family proteins. , 1997, Biochimica et biophysica acta.

[20]  G. Meloni,et al.  Neutrophilic-chronic myeloid leukemia: a distinct disease with a specific molecular marker (BCR/ABL with C3/A2 junction) , 1996, Blood.

[21]  U Klingmüller,et al.  Multiple tyrosine residues in the cytosolic domain of the erythropoietin receptor promote activation of STAT5. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[22]  C. Verfaillie,et al.  Interferon-alpha restores normal beta 1 integrin-mediated inhibition of hematopoietic progenitor proliferation by the marrow microenvironment in chronic myelogenous leukemia. , 1996, Blood.

[23]  M. Shibuya,et al.  Deletion of the ABL SH3 domain reactivates de‐oligomerized BCR‐ABL for growth factor independence , 1996, FEBS letters.

[24]  R. V. van Etten,et al.  The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells. , 1995, Blood.

[25]  J. Krosl,et al.  Tyrosine 343 in the erythropoietin receptor positively regulates erythropoietin‐induced cell proliferation and Stat5 activation. , 1995, The EMBO journal.

[26]  G M Bokoch,et al.  Abr and Bcr are multifunctional regulators of the Rho GTP-binding protein family. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[27]  D. Cortez,et al.  Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis , 1995, Molecular and cellular biology.

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

[29]  V. Kaartinen,et al.  Increased neutrophil respiratory burst in bcr-null mutants , 1995, Cell.

[30]  J. Wang,et al.  The human leukemia oncogene bcr-abl abrogates the anchorage requirement but not the growth factor requirement for proliferation , 1995, Molecular and cellular biology.

[31]  K. Arai,et al.  Suppression of apoptotic death in hematopoietic cells by signalling through the IL‐3/GM‐CSF receptors. , 1995, The EMBO journal.

[32]  L. Wiedemann,et al.  A temperature sensitive p210 BCR‐ABL mutant defines the primary consequences of BCR‐ABL tyrosine kinase expression in growth factor dependent cells. , 1994, The EMBO journal.

[33]  W. Vainchenker,et al.  Growth of erythroid colonies in chronic myelogenous leukemia is independent of erythropoietin only in the presence of steel factor. , 1994, Blood.

[34]  J. Wang,et al.  A coiled-coil oligomerization domain of Bcr is essential for the transforming function of Bcr-Abl oncoproteins , 1993, Molecular and cellular biology.

[35]  Nanxin Li,et al.  BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein , 1993, Cell.

[36]  T. Pawson,et al.  Phosphatidylinositol 3-kinase associates, via its Src homology 2 domains, with the activated erythropoietin receptor. , 1993, Blood.

[37]  N. Rosenberg,et al.  En bloc substitution of the Src homology region 2 domain activates the transforming potential of the c-Abl protein tyrosine kinase. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[38]  J. Wang,et al.  An actin‐binding function contributes to transformation by the Bcr‐Abl oncoprotein of Philadelphia chromosome‐positive human leukemias. , 1993, The EMBO journal.

[39]  O. Witte,et al.  SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence , 1993, Molecular and cellular biology.

[40]  T. Pawson,et al.  A limited set of SH2 domains binds BCR through a high-affinity phosphotyrosine-independent interaction , 1992, Molecular and cellular biology.

[41]  O. Witte,et al.  Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro. , 1992, Science.

[42]  H. Lodish,et al.  Mutation in murine erythropoietin receptor induces erythropoietin-independent erythroid proliferation in vitro, polycythemia in vivo. , 1992, Leukemia.

[43]  O. Witte,et al.  The BCR gene encodes a novel serine/threonine kinase activity within a single exon , 1991, Cell.

[44]  O. Witte,et al.  BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner , 1991, Cell.

[45]  C. Hall,et al.  Bcr encodes a GTPase-activating protein for p21rac , 1991, Nature.

[46]  O. Witte,et al.  BCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias , 1991, Molecular and cellular biology.

[47]  J. Wang,et al.  Activation of tyrosinase kinase and microfilament-binding functions of c-abl by bcr sequences in bcr/abl fusion proteins , 1991, Molecular and cellular biology.

[48]  G. Jenster,et al.  Acute leukaemia in bcr/abl transgenic mice , 1990, Nature.

[49]  O. Witte,et al.  Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. , 1990, Science.

[50]  G. Daley,et al.  Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. , 1990, Science.

[51]  G. Daley,et al.  Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[52]  I. Hariharan,et al.  bcr-abl oncogene renders myeloid cell line factor independent: potential autocrine mechanism in chronic myeloid leukemia. , 1988, Oncogene research.

[53]  C. Eaves,et al.  Cell culture studies in CML. , 1987, Bailliere's clinical haematology.

[54]  R. Kurzrock,et al.  Expression of c-abl in Philadelphia-positive acute myelogenous leukemia. , 1987, Blood.

[55]  R. Kurzrock,et al.  A novel c-abl protein product in Philadelphia-positive acute lymphoblastic leukaemia , 1987, Nature.

[56]  T. Lister,et al.  Novel chimaeric protein expressed in Philadelphia positive acute lymphoblastic leukaemia , 1987, Nature.

[57]  Bruce A. Roe,et al.  Alternative splicing of RNAs transcribed from the human abl gene and from the bcr-abl fused gene , 1986, Cell.

[58]  E. Canaani,et al.  Fused transcript of abl and bcr genes in chronic myelogenous leukaemia , 1985, Nature.

[59]  Rosalind C. Lee,et al.  The mouse c-abl locus: Molecular cloning and characterization , 1984, Cell.

[60]  Eaves Ac,et al.  Abnormalities in the erythroid progenitor compartments in patients with chronic myelogenous leukemia (CML). , 1979 .

[61]  J. Rowley.  A New Consistent Chromosomal Abnormality in Chronic Myelogenous Leukaemia identified by Quinacrine Fluorescence and Giemsa Staining , 1973, Nature.