Patients with chronic myeloid leukemia who maintain a complete molecular response after stopping imatinib treatment have evidence of persistent leukemia by DNA PCR

[1]  J. Melo,et al.  In search of the original leukemic clone in chronic myeloid leukemia patients in complete molecular remission after stem cell transplantation or imatinib. , 2010, Blood.

[2]  J. Reiffers,et al.  Persistence of complete molecular remission in chronic myeloid leukemia after imatinib discontinuation: Interim analysis of the STIM trial. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  J. Reynolds,et al.  The Majority of Chronic Myeloid Leukaemia Patients Who Cease Imatinib after Achieving a Sustained Complete Molecular Response (CMR) Remain in CMR, and Any Relapses Occur Early. , 2008 .

[4]  J. Bussel,et al.  Long-Term Treatment with Romiplostim in Patients with Chronic Immune Thrombocytopenic Purpura (ITP): 3-Year Update from An Open-Label Extension Study , 2008 .

[5]  T. Hughes,et al.  Reverse transcription with random pentadecamer primers improves the detection limit of a quantitative PCR assay for BCR-ABL transcripts in chronic myeloid leukemia: implications for defining sensitivity in minimal residual disease. , 2008, Clinical chemistry.

[6]  A. Venco,et al.  Microhomologies and interspersed repeat elements at genomic breakpoints in chronic myeloid leukemia , 2008, Genes, chromosomes & cancer.

[7]  Holden T Maecker,et al.  Development and dynamics of robust T-cell responses to CML under imatinib treatment. , 2008, Blood.

[8]  Z. Rudzki,et al.  BCR-ABL Messenger RNA Levels Continue to Decline in Patients with Chronic Phase Chronic Myeloid Leukemia Treated with Imatinib for More Than 5 Years and Approximately Half of All First-Line Treated Patients Have Stable Undetectable BCR-ABL Using Strict Sensitivity Criteria , 2007, Clinical Cancer Research.

[9]  M. Calasanz,et al.  Analysis of T(9;22) breakpoints indicates that P210 and P190 BCR-ABL are formed by distinct mechanisms , 2007 .

[10]  J. Cayuela,et al.  Analysis of minimal residual disease by Ig/TCR gene rearrangements: guidelines for interpretation of real-time quantitative PCR data , 2007, Leukemia.

[11]  Ingo Roeder,et al.  Dynamic modeling of imatinib-treated chronic myeloid leukemia: functional insights and clinical implications , 2006, Nature Medicine.

[12]  D. Marin,et al.  Serial measurement of BCR-ABL transcripts in the peripheral blood after allogeneic stem cell transplantation for chronic myeloid leukemia: an attempt to define patients who may not require further therapy. , 2006, Blood.

[13]  J. Goldman,et al.  Why do chronic myelogenous leukemia stem cells survive allogeneic stem cell transplantation or imatinib: does it really matter? , 2006, Leukemia & lymphoma.

[14]  M. Deininger,et al.  Durability of molecular remission in chronic myeloid leukemia patients treated with imatinib vs allogeneic stem cell transplantation , 2005, Leukemia.

[15]  Martin A. Nowak,et al.  Dynamics of chronic myeloid leukaemia , 2005, Nature.

[16]  P. Paschka,et al.  Dynamics of BCR-ABL mRNA expression in first-line therapy of chronic myelogenous leukemia patients with imatinib or interferon α/ara-C , 2003, Leukemia.

[17]  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.

[18]  Mark M. Davis,et al.  Evidence that specific T lymphocytes may participate in the elimination of chronic myelogenous leukemia , 2000, Nature Medicine.

[19]  C. Waller,et al.  Long-template DNA polymerase chain reaction for the detection of the bcr/abl translocation in patients with chronic myelogenous leukemia. , 1999, Clinical cancer research : an official journal of the American Association for Cancer Research.

[20]  J. Melo,et al.  The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: biologic significance and implications for the assessment of minimal residual disease. , 1998, Blood.

[21]  G. Huez,et al.  Detection of major bcr-abl gene expression at a very low level in blood cells of some healthy individuals. , 1995, Blood.

[22]  J. Goldman,et al.  Characterization of genomic BCR‐ABL breakpoints in chronic myeloid leukaemia by PCR , 1995, British journal of haematology.

[23]  P. Martiat,et al.  Minimal residual disease after allogeneic bone marrow transplantation for chronic myeloid leukaemia in first chronic phase: correlations with acute graft‐versus‐host disease and relapse , 1993, British journal of haematology.

[24]  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.

[25]  T. Hughes,et al.  Diagnosis and monitoring of chronic myeloid leukemia by qualitative and quantitative RT-PCR. , 2006, Methods in molecular medicine.

[26]  Martin C. Müller,et al.  Interferon-alpha, but not the ABL-kinase inhibitor imatinib (STI571), induces expression of myeloblastin and a specific T-cell response in chronic myeloid leukemia. , 2003, Blood.

[27]  Martin C. Müller,et al.  Interferon-α, but not the ABL-kinase inhibitor imatinib (STI571), induces expression of myeloblastin and a specific T-cell response in chronic myeloid leukemia , 2003 .