Safety and efficacy of STI-571 (imatinib mesylate) in patients with bcr/abl-positive chronic myelogenous leukemia (CML) after autologous peripheral blood stem cell transplantation (PBSCT)

[1]  R. Larson,et al.  Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. , 2002, Blood.

[2]  M. Baccarani,et al.  Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. , 2002, Blood.

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

[4]  T. Fischer,et al.  BCR-ABL as a target for novel therapeutic interventions , 2002, Expert opinion on therapeutic targets.

[5]  B. Druker,et al.  Chronic myeloid leukemia: current treatment options. , 2001, Blood.

[6]  C. Sawyers,et al.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. , 2001, The New England journal of medicine.

[7]  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.

[8]  K. Kolibaba,et al.  Efficacy of STI571, an abl tyrosine kinase inhibitor, in conjunction with other antileukemic agents against bcr-abl-positive cells. , 2000, Blood.

[9]  P. Seeburg,et al.  Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. , 2000, Science.

[10]  C. L. Perkins,et al.  CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs. , 2000, Blood.

[11]  A. Reiter,et al.  Current trends in the management of chronic myelogenous leukemia , 2000, Annals of Hematology.

[12]  C. Huber,et al.  Autologous transplantation of in vivo purged PBSC in CML: comparison of FISH, cytogenetics, and PCR detection of Philadelphia chromosome in leukapheresis products. , 2000, Cancer genetics and cytogenetics.

[13]  J. Goldman,et al.  Molecular heterogeneity in complete cytogenetic responders after interferon-alpha therapy for chronic myelogenous leukemia: low levels of minimal residual disease are associated with continuing remission. German CML Study Group and the UK MRC CML Study Group. , 2000, Blood.

[14]  A. Reiter,et al.  Accurate and rapid analysis of residual disease in patients with CML using specific fluorescent hybridization probes for real time quantitative RT-PCR , 1999, Leukemia.

[15]  S. Woolf,et al.  An evidence-based analysis of the effect of busulfan, hydroxyurea, interferon, and allogeneic bone marrow transplantation in treating the chronic phase of chronic myeloid leukemia: developed for the American Society of Hematology. , 1999, Blood.

[16]  C. Sawyers.  Chronic myeloid leukemia. , 1999, The New England journal of medicine.

[17]  D. Huhn,et al.  Outcome of peripheral blood stem cell mobilization in advanced phases of CML is dependent on the type of chemotherapy applied , 1998, Annals of Hematology.

[18]  D. Huhn,et al.  Chemotherapy-induced mobilization of karyotypically normal PBSC for autografting in CML , 1998, Bone Marrow Transplantation.

[19]  J. Melo,et al.  The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells. , 1997, Blood.

[20]  Jürg Zimmermann,et al.  Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells , 1996, Nature Medicine.

[21]  T. Meyer,et al.  Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. , 1996, Cancer research.

[22]  A. Deisseroth,et al.  Autologous transplants for chronic myelogenous leukaemia: results from eight transplant groups , 1994, The Lancet.

[23]  S. Heimfeld,et al.  Genetic marking shows that Ph+ cells present in autologous transplants of chronic myelogenous leukemia (CML) contribute to relapse after autologous bone marrow in CML. , 1994, Blood.

[24]  Sante Tura,et al.  Interferon alfa-2a as compared with conventional chemotherapy for the treatment of chronic myeloid leukemia. , 1994, The New England journal of medicine.

[25]  K. Friese,et al.  Routine vs selective episiotomy , 1994, The Lancet.

[26]  J. Melo,et al.  An optimized multiplex polymerase chain reaction (PCR) for detection of BCR-ABL fusion mRNAs in haematological disorders. , 1994, Leukemia.

[27]  N. Rosenberg,et al.  Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[28]  A. Elefanty,et al.  bcr‐abl, the hallmark of chronic myeloid leukaemia in man, induces multiple haemopoietic neoplasms in mice. , 1990, The EMBO journal.

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

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

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

[32]  G. Daley,et al.  The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene. , 1986, Science.

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