The novel tyrosine kinase inhibitor EXEL-0862 induces apoptosis in human FIP1L1-PDGFR-α-expressing cells through caspase-3-mediated cleavage of Mcl-1

[1]  H. Kantarjian,et al.  EXEL-0862, a novel tyrosine kinase inhibitor, induces apoptosis in vitro and ex vivo in human mast cells expressing the KIT D816V mutation. , 2007, Blood.

[2]  H. Kantarjian,et al.  Activity of AMN107, a novel aminopyrimidine tyrosine kinase inhibitor, against human FIP1L1-PDGFR-alpha-expressing cells. , 2006, Leukemia research.

[3]  C. Peschel,et al.  The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). , 2006, Blood.

[4]  P. Marynen,et al.  Sorafenib is a potent inhibitor of FIP1L1-PDGFRα and the imatinib-resistant FIP1L1-PDGFRα T674I mutant , 2006 .

[5]  P. Marynen,et al.  Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. , 2006, Blood.

[6]  Sandra A. Moore,et al.  The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRbeta and FIP1L1-PDGFRalpha in vitro and in vivo. , 2005, Blood.

[7]  M. Konopleva,et al.  Development of a conditional in vivo model to evaluate the efficacy of small molecule inhibitors for the treatment of Raf-transformed hematopoietic cells. , 2005, Cancer research.

[8]  P. Dent,et al.  Apoptosis Induced by the Kinase Inhibitor BAY 43-9006 in Human Leukemia Cells Involves Down-regulation of Mcl-1 through Inhibition of Translation* , 2005, Journal of Biological Chemistry.

[9]  G. Gores,et al.  The role of Mcl-1 downregulation in the proapoptotic activity of the multikinase inhibitor BAY 43-9006 , 2005, Oncogene.

[10]  Daniela S Krause,et al.  Tyrosine kinases as targets for cancer therapy. , 2005, The New England journal of medicine.

[11]  D. Levy,et al.  New and Old Functions of STAT3: A Pivitol Target for Individualized Treatment of Cancer , 2005, Cell cycle.

[12]  Jason Gotlib,et al.  Molecular Classification and Pathogenesis of Eosinophilic Disorders: 2005 Update , 2005, Acta Haematologica.

[13]  Zhi-xiang Xu,et al.  Farnesyltransferase inhibitors induce DNA damage via reactive oxygen species in human cancer cells. , 2005, Cancer research.

[14]  G. Gastl,et al.  Komplette Remission eines idiopathischen hypereosinophilen Syndroms unter imatinib , 2004 .

[15]  R. Craig,et al.  MCL1 is phosphorylated in the PEST region and stabilized upon ERK activation in viable cells, and at additional sites with cytotoxic okadaic acid or taxol , 2004, Oncogene.

[16]  Kam Y. J. Zhang,et al.  Mcl-1 is required for Akata6 B-lymphoma cell survival and is converted to a cell death molecule by efficient caspase-mediated cleavage , 2004, Oncogene.

[17]  J. Clohessy,et al.  Characterisation of Mcl‐1 cleavage during apoptosis of haematopoietic cells , 2004, British journal of haematology.

[18]  P. Marynen,et al.  The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. , 2004, Blood.

[19]  P. Marynen,et al.  FIP1L1-PDGFRalpha in hypereosinophilic syndrome and mastocytosis. , 2004, The hematology journal : the official journal of the European Haematology Association.

[20]  D. Wolf,et al.  [Complete remission of an idiopathic hypereosinophilic syndrome while using imatinib]. , 2004, Deutsche medizinische Wochenschrift.

[21]  B. Druker,et al.  High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib. , 2004, The hematology journal : the official journal of the European Haematology Association.

[22]  J. Sebolt-Leopold,et al.  Central Role of Fas-associated Death Domain Protein in Apoptosis Induction by the Mitogen-activated Protein Kinase Kinase Inhibitor CI-1040 (PD184352) in Acute Lymphocytic Leukemia Cells in Vitro* , 2003, Journal of Biological Chemistry.

[23]  D. Gilliland,et al.  CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy. , 2003, Blood.

[24]  W. Plunkett,et al.  Free radical stress in chronic lymphocytic leukemia cells and its role in cellular sensitivity to ROS-generating anticancer agents. , 2003, Blood.

[25]  D. Fabbro,et al.  PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease. , 2003, Cancer cell.

[26]  Peter Marynen,et al.  A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. , 2003, The New England journal of medicine.

[27]  I. Gojo,et al.  The cyclin-dependent kinase inhibitor flavopiridol induces apoptosis in multiple myeloma cells through transcriptional repression and down-regulation of Mcl-1. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.

[28]  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.

[29]  A. Tefferi,et al.  Treatment of hypereosinophilic syndrome with imatinib mesilate , 2002, The Lancet.

[30]  R. Craig.  MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesis , 2002, Leukemia.

[31]  C. Peschel,et al.  BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study , 2002, The Lancet.

[32]  E. Estey,et al.  Therapeutic targeting of the MEK/MAPK signal transduction module in acute myeloid leukemia. , 2001, The Journal of clinical investigation.

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

[34]  John Calvin Reed,et al.  MEK/ERK signaling pathway regulates the expression of Bcl‐2, Bcl‐XL, and Mcl‐1 and promotes survival of human pancreatic cancer cells , 2000, Journal of cellular biochemistry.

[35]  R. Craig,et al.  Myeloid Cell Leukemia 1 Is Phosphorylated through Two Distinct Pathways, One Associated with Extracellular Signal-regulated Kinase Activation and the Other with G2/M Accumulation or Protein Phosphatase 1/2A Inhibition* , 2000, The Journal of Biological Chemistry.

[36]  W. May,et al.  Survival function of ERK1/2 as IL-3-activated, staurosporine-resistant Bcl2 kinases. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[37]  E. Sausville,et al.  Effects of the bcr/abl kinase inhibitors AG957 and NSC 680410 on chronic myelogenous leukemia cells in vitro. , 2000, Clinical cancer research : an official journal of the American Association for Cancer Research.

[38]  J. Darnell,et al.  Stat3 as an Oncogene , 1999, Cell.

[39]  Z. Estrov,et al.  Selective inhibition of cell proliferation and BCR-ABL phosphorylation in acute lymphoblastic leukemia cells expressing Mr 190,000 BCR-ABL protein by a tyrosine kinase inhibitor (CGP-57148). , 1998, Clinical cancer research : an official journal of the American Association for Cancer Research.

[40]  Y. Lazebnik,et al.  Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE , 1994, Nature.

[41]  R. Treisman,et al.  The SRF accessory protein Elk-1 contains a growth factor-regulated transcriptional activation domain , 1993, Cell.

[42]  James R. Woodgett,et al.  Phosphorylation of c-jun mediated by MAP kinases , 1991, Nature.

[43]  R. Anderson,et al.  The hypereosinophilic syndromes. , 1968, Annals of internal medicine.