Monitoring treatment of chronic myeloid leukemia

Monitoring treatment of chronic myeloid leukemia is not only important for ensuring that a patient is receiving the best treatment, but is also convenient from a pharmacoeconomic point of view. See related papers on pages 178 and 186.

[1]  Martin C. Müller,et al.  Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib , 2008, Haematologica.

[2]  S. Mustjoki,et al.  Comparison of bone marrow high mitotic index metaphase fluorescence in situ hybridization to peripheral blood and bone marrow real time quantitative polymerase chain reaction on the International Scale for detecting residual disease in chronic myeloid leukemia , 2008, Haematologica.

[3]  G. Church,et al.  Quantitative monitoring by polymerase colony assay of known mutations resistant to ABL kinase inhibitors , 2008, Oncogene.

[4]  J. Goldman.  How I treat chronic myeloid leukemia in the imatinib era. , 2007, Blood.

[5]  M. Baccarani,et al.  The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome‐negative cells , 2007, Cancer.

[6]  M. Deininger,et al.  Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. , 2007, Blood.

[7]  D. Colomer,et al.  Monosomy 7 with severe myelodysplasia developing during imatinib treatment of Philadelphia‐positive chronic myeloid leukemia: Two cases with a different outcome , 2007, American journal of hematology.

[8]  Andreas Hochhaus,et al.  Chronic myeloid leukaemia , 2007, The Lancet.

[9]  Martin C. Müller,et al.  An international study to standardize the detection and quantitation of BCR-ABL transcripts from stabilized peripheral blood preparations by quantitative RT-PCR. , 2007, Haematologica.

[10]  G. Mann,et al.  Imatinib Disposition and ABCB1 (MDR1, P‐Glycoprotein) Genotype , 2007, Clinical pharmacology and therapeutics.

[11]  J. Cayuela,et al.  Characterization of a reference material for BCR-ABL (M-BCR) mRNA quantitation by real-time amplification assays: towards new standards for gene expression measurements , 2007, Leukemia.

[12]  A. Mauriello,et al.  Characterization of Ph‐negative abnormal clones emerging during imatinib therapy , 2007, Cancer.

[13]  Junia V. Melo,et al.  Chronic myeloid leukaemia as a model of disease evolution in human cancer , 2007, Nature Reviews Cancer.

[14]  H. Kantarjian,et al.  Current and emerging treatment options in chronic myeloid leukemia , 2007, Cancer.

[15]  J. Melo,et al.  Resistance to imatinib mesylate in chronic myeloid leukaemia. , 2007, Cancer letters.

[16]  C. Eaves,et al.  Instability of BCR-ABL gene in primary and cultured chronic myeloid leukemia stem cells. , 2007, Journal of the National Cancer Institute.

[17]  B. Johansson,et al.  Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes , 2007, Genes, chromosomes & cancer.

[18]  Nicholas Moore,et al.  Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia. , 2007, Blood.

[19]  J. Eshleman,et al.  Evaluation of the Cepheid GeneXpert BCR-ABL assay. , 2007, The Journal of molecular diagnostics : JMD.

[20]  M. Baccarani,et al.  Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL. , 2007, The Lancet. Oncology.

[21]  B. Druker,et al.  Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib , 2007, Leukemia.

[22]  N. Shaw,et al.  Piloting the new specialist training year 1 (ST1) interview process – using the OSCE , 2007, Medical teacher.

[23]  M. Baccarani,et al.  Contribution of ABL Kinase Domain Mutations to Imatinib Resistance in Different Subsets of Philadelphia-Positive Patients: By the GIMEMA Working Party on Chronic Myeloid Leukemia , 2006, Clinical Cancer Research.

[24]  Francisco Cervantes,et al.  Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. , 2006, The New England journal of medicine.

[25]  M. Baccarani,et al.  Monitoring minimal residual disease and controlling drug resistance in chronic myeloid leukaemia patients in treatment with imatinib as a guide to clinical management , 2006, Hematological oncology.

[26]  M. Baccarani,et al.  Presence or the emergence of a F317L BCR-ABL mutation may be associated with resistance to dasatinib in Philadelphia chromosome-positive leukemia. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[27]  B. Druker,et al.  Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen: high efficacy of drug combinations. , 2006, Blood.

[28]  Francisco Cervantes,et al.  Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet. , 2006, Blood.

[29]  J. Goldman,et al.  Rationale for the recommendations for harmonizing current methodology for detecting BCR-ABL transcripts in patients with chronic myeloid leukaemia , 2006, Leukemia.

[30]  P. Manley,et al.  OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. , 2006, Blood.

[31]  Simona Soverini,et al.  Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. , 2006, Blood.

[32]  M. Wittekind,et al.  The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. , 2006, Cancer research.

[33]  J. Melo,et al.  The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib , 2006, Leukemia.

[34]  T. Hughes,et al.  Limited clinical value of regular bone marrow cytogenetic analysis in imatinib-treated chronic phase CML patients monitored by RQ-PCR for BCR-ABL , 2006, Leukemia.

[35]  T. Lamark,et al.  Selecting and deselecting imatinib-resistant clones: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL , 2005, Leukemia.

[36]  H. Kantarjian,et al.  Chromosomal abnormalities in Philadelphia chromosome negative metaphases appearing during imatinib mesylate therapy in patients with newly diagnosed chronic myeloid leukemia in chronic phase. , 2005, Blood.

[37]  J. Mestan,et al.  Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study. , 2005, Blood.

[38]  J. Mestan,et al.  Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107). , 2005, Blood.

[39]  S. McWeeney,et al.  High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy. , 2005, Blood.

[40]  N. Sorel,et al.  Double-gradient-denaturing-gradient gel electrophoresis for mutation screening of the BCR-ABL tyrosine kinase domain in chronic myeloid leukemia patients. , 2005, Clinical chemistry.

[41]  J. Mestan,et al.  In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. , 2005, Cancer research.

[42]  C. Sawyers,et al.  Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[43]  C. Sawyers,et al.  Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment. , 2005, Blood.

[44]  M. Baccarani,et al.  Imatinib and pegylated human recombinant interferon-alpha2b in early chronic-phase chronic myeloid leukemia. , 2004, Blood.

[45]  Munir Pirmohamed,et al.  Active transport of imatinib into and out of cells: implications for drug resistance. , 2004, Blood.

[46]  R. Herrmann,et al.  Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations. , 2004, Blood.

[47]  Mariël Brok,et al.  Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump. , 2004, Blood.

[48]  A. Nagler,et al.  Assessment of the response to imatinib in chronic myeloid leukemia patients – comparison between the FISH, multiplex and RT‐PCR methods , 2004, European journal of haematology.

[49]  Ping Chen,et al.  Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor , 2004, Science.

[50]  M. Baccarani,et al.  Denaturing-HPLC-based assay for detection of ABL mutations in chronic myeloid leukemia patients resistant to Imatinib. , 2004, Clinical chemistry.

[51]  A. Hall,et al.  Use of denaturing HPLC for detection of mutations in the BCR-ABL kinase domain in patients resistant to Imatinib. , 2004, Clinical chemistry.

[52]  H. Kantarjian,et al.  High-dose imatinib mesylate therapy in newly diagnosed Philadelphia chromosome-positive chronic phase chronic myeloid leukemia. , 2004, Blood.

[53]  B. Druker,et al.  Detection of ABL kinase domain mutations with denaturing high-performance liquid chromatography , 2004, Leukemia.

[54]  Yi-Ching Hsieh,et al.  Clonal evolution and lack of cytogenetic response are adverse prognostic factors for hematologic relapse of chronic phase CML patients treated with imatinib mesylate. , 2004, Blood.

[55]  F. Watzinger,et al.  Evaluation of candidate control genes for diagnosis and residual disease detection in leukemic patients using ‘real-time’ quantitative reverse-transcriptase polymerase chain reaction (RQ-PCR) – a Europe against cancer program , 2003, Leukemia.

[56]  H. Cavé,et al.  Standardization and quality control studies of ‘real-time’ quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia – A Europe Against Cancer Program , 2003, Leukemia.

[57]  Susan Branford,et al.  Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. , 2003, The New England journal of medicine.

[58]  B. Druker,et al.  Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. , 2003, Blood.

[59]  C. Preudhomme,et al.  A mutation conferring resistance to imatinib at the time of diagnosis of chronic myelogenous leukemia. , 2003, The New England journal of medicine.

[60]  B. Dörken,et al.  Preexistence and evolution of imatinib mesylate-resistant clones in chronic myelogenous leukemia detected by a PNA-based PCR clamping technique , 2003, Annals of Hematology.

[61]  J. Melo,et al.  MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. , 2003, Blood.

[62]  Francisco Cervantes,et al.  Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. , 2003, The New England journal of medicine.

[63]  R. Silver,et al.  Correlation of three methods of measuring cytogenetic response in chronic myelocytic leukemia. , 2002, Cancer genetics and cytogenetics.

[64]  P. Paschka,et al.  Early reduction of BCR-ABL mRNA transcript levels predicts cytogenetic response in chronic phase CML patients treated with imatinib after failure of interferon α , 2002, Leukemia.

[65]  Claude Preudhomme,et al.  Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment. , 2002, Blood.

[66]  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.

[67]  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.

[68]  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.

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

[70]  R. Bataille,et al.  Fluorescence in situ hybridization on peripheral-blood specimens is a reliable method to evaluate cytogenetic response in chronic myeloid leukemia. , 2000, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[71]  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.

[72]  U. Lass,et al.  LightCycler technology for the quantitation of bcr/abl fusion transcripts. , 1999, Cancer research.

[73]  A. Hagemeijer,et al.  Fluorescence in situ hybridization for the detection and monitoring of the Ph-positive clone in chronic myelogenous leukemia: comparison with metaphase banding analysis , 1998, Leukemia.

[74]  J. Goldman,et al.  The rate and kinetics of molecular response to donor leucocyte transfusions in chronic myeloid leukaemia patients treated for relapse after allogeneic bone marrow transplantation , 1997, British journal of haematology.

[75]  J. Goldman,et al.  Kinetics of increasing BCR-ABL transcript numbers in chronic myeloid leukemia patients who relapse after bone marrow transplantation. , 1996, Blood.

[76]  J. Goldman,et al.  Quantification of residual disease in chronic myelogenous leukemia patients on interferon-alpha therapy by competitive polymerase chain reaction. , 1996, Blood.

[77]  J. Goldman,et al.  Relapse of chronic myeloid leukemia after allogeneic bone marrow transplant: the case for giving donor leukocyte transfusions before the onset of hematologic relapse. , 1994, Blood.

[78]  A. Chase,et al.  Competitive polymerase chain reaction to estimate the number of BCR-ABL transcripts in chronic myeloid leukemia patients after bone marrow transplantation. , 1993, Blood.

[79]  T. Lion,et al.  Early detection of relapse after bone marrow transplantation in patients with chronic myelogenous leukaemia , 1993, The Lancet.

[80]  G. Saglio,et al.  Harmonization of BCR-ABL mRNA quantification using a uniform multifunctional control plasmid in 37 international laboratories , 2008, Leukemia.

[81]  A. Nagler,et al.  High-throughput, sensitive and quantitative assay for the detection of BCR-ABL kinase domain mutations , 2007, Leukemia.

[82]  T. Haferlach,et al.  IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status. , 2010, Blood.

[83]  R. Brand,et al.  Allogeneic hematopoietic stem cell transplantation for chronic myeloid leukemia in Europe 2006: transplant activity, long-term data and current results. An analysis by the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT). , 2006, Haematologica.

[84]  Peter Lloyd,et al.  Clinical Pharmacokinetics of Imatinib , 2005, Clinical pharmacokinetics.

[85]  M. Baccarani,et al.  Interferon-alfa for chronic myeloid leukemia. , 2003, Seminars in hematology.

[86]  W. Hiddemann,et al.  Comparison of chromosome banding analysis, interphase- and hypermetaphase-FISH, qualitative and quantitative PCR for diagnosis and for follow-up in chronic myeloid leukemia: a study on 350 cases , 2002, Leukemia.

[87]  B. Druker,et al.  Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy , 2002, Leukemia.