Chronic Myeloid Leukemia , Version 1 . 2019 Clinical Practice Guidelines in Oncology
暂无分享,去创建一个
J. Radich | H. Kantarjian | K. Gregory | Hema M Sundar | M. Deininger | D. DeAngelo | B. Smith | M. Talpaz | C. Abboud | J. Altman | G. Hobbs | M. Patnaik | P. Curtin | J. Gotlib | E. Purev | Joseph O. Moore | N. Shah | R. Bhatia | B. Bhatnagar | E. Berman | M. Jagasia | L. Maness | L. Metheny | A. Pallera | P. Pancari | M. Rose | D. Snyder | K. Sweet | James E. Thompson | David T Yang | J. Moore | Philip A. Pancari
[1] Martin C. Müller,et al. Ponatinib efficacy and safety in Philadelphia chromosome-positive leukemia: final 5-year results of the phase 2 PACE trial. , 2018, Blood.
[2] Z. Estrov,et al. Early results of lower dose dasatinib (50 mg daily) as frontline therapy for newly diagnosed chronic‐phase chronic myeloid leukemia , 2018, Cancer.
[3] Martin C. Müller,et al. Discontinuation of tyrosine kinase inhibitor therapy in chronic myeloid leukaemia (EURO-SKI): a prespecified interim analysis of a prospective, multicentre, non-randomised, trial. , 2018, The Lancet. Oncology.
[4] J. Sakamoto,et al. Final 3‐year Results of the Dasatinib Discontinuation Trial in Patients With Chronic Myeloid Leukemia Who Received Dasatinib as a Second‐line Treatment , 2018, Clinical lymphoma, myeloma & leukemia.
[5] J. Radich,et al. Durable treatment-free remission in patients with chronic myeloid leukemia in chronic phase following frontline nilotinib: 96-week update of the ENESTfreedom study , 2018, Journal of Cancer Research and Clinical Oncology.
[6] J. Lipton,et al. Treatment-Free Remission After Second-Line Nilotinib Treatment in Patients With Chronic Myeloid Leukemia in Chronic Phase , 2018, Annals of Internal Medicine.
[7] H. Kantarjian,et al. Prognostic significance of additional chromosomal abnormalities at the time of diagnosis in patients with chronic myeloid leukemia treated with frontline tyrosine kinase inhibitors , 2018, American journal of hematology.
[8] T. Brümmendorf,et al. Bosutinib Versus Imatinib for Newly Diagnosed Chronic Myeloid Leukemia: Results From the Randomized BFORE Trial , 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[9] P. Rousselot,et al. Second tyrosine kinase inhibitor discontinuation attempt in patients with chronic myeloid leukemia , 2017, Cancer.
[10] H. Kantarjian,et al. Clonal chromosomal abnormalities appearing in Philadelphia chromosome-negative metaphases during CML treatment. , 2017, Blood.
[11] T. Brümmendorf,et al. Assessment of imatinib as first-line treatment of chronic myeloid leukemia: 10-year survival results of the randomized CML study IV and impact of non-CML determinants , 2017, Leukemia.
[12] J. Byrne,et al. De-escalation of tyrosine kinase inhibitor dose in patients with chronic myeloid leukaemia with stable major molecular response (DESTINY): an interim analysis of a non-randomised, phase 2 trial. , 2017, The Lancet. Haematology.
[13] Francisco Cervantes,et al. Long‐Term Outcomes of Imatinib Treatment for Chronic Myeloid Leukemia , 2017, The New England journal of medicine.
[14] M. Tulliez,et al. Discontinuation of dasatinib or nilotinib in chronic myeloid leukemia: interim analysis of the STOP 2G-TKI study. , 2017, Blood.
[15] M. Tulliez,et al. Long-Term Follow-Up of the French Stop Imatinib (STIM1) Study in Patients With Chronic Myeloid Leukemia. , 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[16] U. Olsson‐Strömberg,et al. Increased proportion of mature NK cells is associated with successful imatinib discontinuation in chronic myeloid leukemia , 2016, Leukemia.
[17] M. Baccarani,et al. Prognostic Discrimination in "GoodRisk" Chronic Granulocytic Leukemia , 2017 .
[18] J. Cortes,et al. Switching to nilotinib versus imatinib dose escalation in patients with chronic myeloid leukaemia in chronic phase with suboptimal response to imatinib (LASOR): a randomised, open-label trial. , 2016, The Lancet. Haematology.
[19] T. Brümmendorf,et al. Long‐term bosutinib for chronic phase chronic myeloid leukemia after failure of imatinib plus dasatinib and/or nilotinib , 2016, American journal of hematology.
[20] H. Kantarjian,et al. Dasatinib in imatinib‐resistant or ‐intolerant chronic‐phase, chronic myeloid leukemia patients: 7‐year follow‐up of study CA180‐034 , 2016, American journal of hematology.
[21] H. Kantarjian,et al. Risk stratification of chromosomal abnormalities in chronic myelogenous leukemia in the era of tyrosine kinase inhibitor therapy. , 2016, Blood.
[22] Sukjoong Oh,et al. Imatinib withdrawal syndrome and longer duration of imatinib have a close association with a lower molecular relapse after treatment discontinuation: the KID study , 2016, Haematologica.
[23] J. Cortes,et al. Evaluating the Impact of a Switch to Nilotinib on Imatinib-Related Chronic Low-Grade Adverse Events in Patients With CML-CP: The ENRICH Study. , 2016, Clinical lymphoma, myeloma & leukemia.
[24] M. Baccarani,et al. Final 5-Year Study Results of DASISION: The Dasatinib Versus Imatinib Study in Treatment-Naïve Chronic Myeloid Leukemia Patients Trial. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[25] Martin C. Müller,et al. Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients. , 2016, Blood.
[26] I. Flinn,et al. Long-term benefits and risks of frontline nilotinib vs imatinib for chronic myeloid leukemia in chronic phase: 5-year update of the randomized ENESTnd trial , 2016, Leukemia.
[27] T. McDonnell,et al. Clinical and prognostic significance of 3q26.2 and other chromosome 3 abnormalities in CML in the era of tyrosine kinase inhibitors. , 2015, Blood.
[28] S. Redaelli,et al. Age and dPCR can predict relapse in CML patients who discontinued imatinib: The ISAV study , 2015, American journal of hematology.
[29] Martin C. Müller,et al. Impact of unbalanced minor route versus major route karyotypes at diagnosis on prognosis of CML , 2015, Annals of Hematology.
[30] J. Cortes,et al. Chromosomal rearrangement involving 11q23 locus in chronic myelogenous leukemia: a rare phenomenon frequently associated with disease progression and poor prognosis , 2015, Journal of Hematology & Oncology.
[31] J. Sakamoto,et al. Shorter halving time of BCR‐ABL1 transcripts is a novel predictor for achievement of molecular responses in newly diagnosed chronic‐phase chronic myeloid leukemia treated with dasatinib: Results of the D‐first study of Kanto CML study group , 2015, American journal of hematology.
[32] C. Tam,et al. TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets. , 2015, Blood.
[33] J. Seymour,et al. The Adverse Effect of High Sokal Risk for First Line Imatinib Treated Patients Is Overcome By a Rapid Rate of BCR-ABL Decline Measured As Early As 1 Month of Treatment , 2014 .
[34] M. Baccarani,et al. Impact of Dose Intensity of Ponatinib on Selected Adverse Events: Multivariate Analyses from a Pooled Population of Clinical Trial Patients , 2014 .
[35] H. Einsele,et al. Velocity of early BCR-ABL transcript elimination as an optimized predictor of outcome in chronic myeloid leukemia (CML) patients in chronic phase on treatment with imatinib , 2014, Leukemia.
[36] J. Radich,et al. Correlations between cytogenetic and molecular monitoring among patients with newly diagnosed chronic myeloid leukemia in chronic phase: post hoc analyses of the Rationale and Insight for Gleevec High-Dose Therapy study. , 2014, Archives of pathology & laboratory medicine.
[37] Nicola D. Roberts,et al. Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline. , 2014, Blood.
[38] Susan Branford,et al. Long-term response to imatinib is not affected by the initial dose in patients with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: final update from the Tyrosine Kinase Inhibitor Optimization and Selectivity (TOPS) study , 2014, International Journal of Hematology.
[39] S. Goldberg,et al. Association between regular molecular monitoring and tyrosine kinase inhibitor therapy adherence in chronic myelogenous leukemia in the chronic phase , 2014, Current medical research and opinion.
[40] J. Cayuela,et al. Loss of major molecular response as a trigger for restarting tyrosine kinase inhibitor therapy in patients with chronic-phase chronic myelogenous leukemia who have stopped imatinib after durable undetectable disease. , 2014, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[41] M. Baccarani,et al. Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION). , 2014, Blood.
[42] J. Radich,et al. Imatinib 800 mg daily induces deeper molecular responses than imatinib 400 mg daily: results of SWOG S0325, an intergroup randomized PHASE II trial in newly diagnosed chronic phase chronic myeloid leukaemia , 2014, British journal of haematology.
[43] Y. Ishigatsubo,et al. European Treatment and Outcome Study score does not predict imatinib treatment response and outcome in chronic myeloid leukemia patients , 2014, Cancer science.
[44] Martin C. Müller,et al. Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia. , 2014, Leukemia research.
[45] N. Moore,et al. Therapeutic drug monitoring of imatinib in chronic myeloid leukemia: experience from 1216 patients at a centralized laboratory , 2013, Fundamental & clinical pharmacology.
[46] H. Kantarjian,et al. Assessment at 6 months may be warranted for patients with chronic myeloid leukemia with no major cytogenetic response at 3 months , 2013, Haematologica.
[47] M. Baccarani,et al. Subcutaneous omacetaxine mepesuccinate in patients with chronic-phase chronic myeloid leukemia previously treated with 2 or more tyrosine kinase inhibitors including imatinib. , 2013, Clinical lymphoma, myeloma & leukemia.
[48] W. M. Smit,et al. Imatinib discontinuation in chronic phase myeloid leukaemia patients in sustained complete molecular response: a randomised trial of the Dutch-Belgian Cooperative Trial for Haemato-Oncology (HOVON). , 2013, European journal of cancer.
[49] J. Melo,et al. Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study. , 2013, Blood.
[50] R. Maki,et al. Effect of long term imatinib on bone in adults with chronic myelogenous leukemia and gastrointestinal stromal tumors. , 2013, Leukemia research.
[51] F. Giles,et al. Rates of peripheral arterial occlusive disease in patients with chronic myeloid leukemia in the chronic phase treated with imatinib, nilotinib, or non-tyrosine kinase therapy: a retrospective cohort analysis , 2013, Leukemia.
[52] H. Kantarjian,et al. Phase 2 study of subcutaneous omacetaxine mepesuccinate for chronic‐phase chronic myeloid leukemia patients resistant to or intolerant of tyrosine kinase inhibitors , 2013, American journal of hematology.
[53] K. Rezvani,et al. Combining BCR-ABL1 transcript levels at 3 and 6 months in chronic myeloid leukemia: implications for early intervention strategies. , 2013, Blood.
[54] G. Specchia,et al. Chronic fatigue is the most important factor limiting health-related quality of life of chronic myeloid leukemia patients treated with imatinib , 2013, Leukemia.
[55] J. Radich,et al. Nilotinib in imatinib-resistant or imatinib-intolerant patients with chronic myeloid leukemia in chronic phase: 48-month follow-up results of a phase II study , 2013, Leukemia.
[56] H. Kantarjian,et al. Phase 2 study of subcutaneous omacetaxine mepesuccinate after TKI failure in patients with chronic-phase CML with T315I mutation. , 2012, Blood.
[57] H. Einsele,et al. Early molecular and cytogenetic response is predictive for long-term progression-free and overall survival in chronic myeloid leukemia (CML) , 2012, Leukemia.
[58] J. Radich,et al. Chronic phase chronic myeloid leukemia patients with low OCT-1 activity randomized to high-dose imatinib achieve better responses and have lower failure rates than those randomized to standard-dose imatinib , 2012, Haematologica.
[59] H. Kantarjian,et al. EUTOS score is not predictive for survival and outcome in patients with early chronic phase chronic myeloid leukemia treated with tyrosine kinase inhibitors: a single institution experience. , 2012, Blood.
[60] M. Humbert,et al. Résultats tardifs de la commissurotomie mitrale percutanée à 20 ans Création et validation d ’ un score de risque prédisant les résultats fonctionnels à long terme à partir d ’ une série de 912 patients , 2012 .
[61] Katayoun Rezvani,et al. Assessment of BCR-ABL1 transcript levels at 3 months is the only requirement for predicting outcome for patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[62] S. Oliveria,et al. Adherence to treatment with second-line therapies, dasatinib and nilotinib, in patients with chronic myeloid leukemia , 2012, Current medical research and opinion.
[63] M. Bissell. Peripheral Blood Monitoring of Chronic Myeloid Leukemia During Treatment With Imatinib, Second-Line Agents, and Beyond , 2012 .
[64] E. Jabbour,et al. Managing side effects of tyrosine kinase inhibitor therapy to optimize adherence in patients with chronic myeloid leukemia: the role of the midlevel practitioner. , 2012, The journal of supportive oncology.
[65] S. Ghio,et al. Reversible pulmonary arterial hypertension likely related to long-term, low-dose dasatinib treatment for chronic myeloid leukaemia. , 2012, Leukemia research.
[66] Martin C. Müller,et al. Impact of additional cytogenetic aberrations at diagnosis on prognosis of CML: long-term observation of 1151 patients from the randomized CML Study IV. , 2011, Blood.
[67] H. Kantarjian,et al. Front-line therapy with second-generation tyrosine kinase inhibitors in patients with early chronic phase chronic myeloid leukemia: what is the optimal response? , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[68] D. Marin,et al. European Treatment and Outcome Study (EUTOS) score for chronic myeloid leukemia still requires more confirmation. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[69] J. Hasford,et al. Predicting complete cytogenetic response and subsequent progression-free survival in 2060 patients with CML on imatinib treatment: the EUTOS score. , 2011, Blood.
[70] P. Valent,et al. Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML , 2011, American journal of hematology.
[71] C. Baldwin,et al. Comparison of autologous stem cell transplantation versus consolidation chemotherapy for patients with cytogenetically normal acute myeloid leukemia (CN‐AML) and FLT3ITD , 2011, American journal of hematology.
[72] H. Kantarjian,et al. Considerations in the management of patients with Philadelphia chromosome-positive chronic myeloid leukemia receiving tyrosine kinase inhibitor therapy. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[73] Stefan W Krause,et al. Tolerability-adapted imatinib 800 mg/d versus 400 mg/d versus 400 mg/d plus interferon-α in newly diagnosed chronic myeloid leukemia. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[74] H. Kantarjian,et al. Long‐term prognostic impact of the use of erythropoietic‐stimulating agents in patients with chronic myeloid leukemia in chronic phase treated with imatinib , 2011, Cancer.
[75] T. Buclin,et al. Drug interactions with the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib. , 2011, Blood.
[76] Y. Aizawa,et al. Myelodysplastic syndrome with Ph negative monosomy 7 chromosome following transient bone marrow dysplasia during imatinib treatment for chronic myeloid leukemia. , 2011, Internal medicine.
[77] K. Rezvani,et al. Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy. , 2010, Blood.
[78] H. Kantarjian,et al. The achievement of an early complete cytogenetic response is a major determinant for outcome in patients with early chronic phase chronic myeloid leukemia treated with tyrosine kinase inhibitors. , 2010, Blood.
[79] B. Druker,et al. patients treated with imatinib mesylate prognostic factors for hematologic relapse of chronic phase CML Clonal evolution and lack of cytogenetic response are adverse , 2011 .
[80] Claude Preudhomme,et al. Imatinib plus peginterferon alfa-2a in chronic myeloid leukemia. , 2010, The New England journal of medicine.
[81] J. Griffin,et al. Retrospective real-world comparison of medical visits, costs, and adherence between nilotinib and dasatinib in chronic myeloid leukemia , 2010, Current medical research and opinion.
[82] Martin C. Müller,et al. Long-term prognostic significance of early molecular response to imatinib in newly diagnosed chronic myeloid leukemia: an analysis from the International Randomized Study of Interferon and STI571 (IRIS). , 2010, Blood.
[83] Philippe Rousselot,et al. Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial. , 2010, The Lancet. Oncology.
[84] D. Colomer,et al. Early intervention during imatinib therapy in patients with newly diagnosed chronic-phase chronic myeloid leukemia: a study of the Spanish PETHEMA group , 2010, Haematologica.
[85] Z. Estrov,et al. Survival outcomes for clonal evolution in chronic myeloid leukemia patients on second generation tyrosine kinase inhibitor therapy , 2010, Cancer.
[86] D. Marin,et al. Adherence is the critical factor for achieving molecular responses in patients with chronic myeloid leukemia who achieve complete cytogenetic responses on imatinib. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[87] J. Cortes,et al. Dasatinib 100 mg once daily minimizes the occurrence of pleural effusion in patients with chronic myeloid leukemia in chronic phase and efficacy is unaffected in patients who develop pleural effusion , 2010, Cancer.
[88] S. Sanabani,et al. Efficacy and Tolerability after Unusually Low Doses of Dasatinib in Chronic Myeloid Leukemia Patients Intolerant to Standard-Dose Dasatinib Therapy , 2010, Clinical Medicine Insights. Oncology.
[89] J. Radich,et al. Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia , 2010, Leukemia.
[90] R. A. Larson,et al. Clinical Trials and Observations , 2022 .
[91] C. Carcassi,et al. Chronic myeloid leukemia: a prospective comparison of interphase fluorescence in situ hybridization and chromosome banding analysis for the definition of complete cytogenetic response: a study of the GIMEMA CML WP. , 2009, Blood.
[92] Martin C. Müller,et al. Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. , 2009, Blood.
[93] Z. Estrov,et al. The use of nilotinib or dasatinib after failure to 2 prior tyrosine kinase inhibitors: long-term follow-up. , 2009, Blood.
[94] M. Pirmohamed,et al. Nilotinib concentration in cell lines and primary CD34+ chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters , 2009, Leukemia.
[95] Susan O'Brien,et al. NCCN clinical practice guidelines in oncology: chronic myelogenous leukemia. , 2009, Journal of the National Comprehensive Cancer Network : JNCCN.
[96] G. Szakács,et al. Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti‐cancer effects and pharmacological properties , 2009, British journal of pharmacology.
[97] M. Deininger,et al. Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib. , 2009, Blood.
[98] H. Kantarjian,et al. Chronic myeloid leukemia (CML) with P190 BCR-ABL: analysis of characteristics, outcomes, and prognostic significance. , 2009, Blood.
[99] M. Baccarani,et al. Philadelphia-positive patients who already harbor imatinib-resistant Bcr-Abl kinase domain mutations have a higher likelihood of developing additional mutations associated with resistance to second- or third-line tyrosine kinase inhibitors. , 2009, Blood.
[100] Martin C. Müller,et al. Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[101] N. Cross. Standardisation of molecular monitoring for chronic myeloid leukaemia. , 2009, Best practice & research. Clinical haematology.
[102] H. Kantarjian,et al. Dynamics and management of cytopenias associated with dasatinib therapy in patients with chronic myeloid leukemia in chronic phase after imatinib failure , 2009, Cancer.
[103] H. Kantarjian,et al. Significance of increasing levels of minimal residual disease in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in complete cytogenetic response. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[104] H. Kantarjian,et al. Tyrosine kinase inhibitor-induced platelet dysfunction in patients with chronic myeloid leukemia. , 2009, Blood.
[105] L. Staudt,et al. Clinical Trials and Observations , 2007 .
[106] K. Rezvani,et al. Does a rise in the BCR‐ABL1 transcript level identify chronic phase CML patients responding to imatinib who have a high risk of cytogenetic relapse? , 2009, British journal of haematology.
[107] A. Aleem. Hypopigmentation of the skin due to imatinib mesylate in patients with chronic myeloid leukemia. , 2009, Hematology/oncology and stem cell therapy.
[108] H. Kantarjian,et al. Imatinib mesylate dose escalation is associated with durable responses in patients with chronic myeloid leukemia after cytogenetic failure on standard-dose imatinib therapy. , 2009 .
[109] R. Larson,et al. Efficacy of imatinib dose escalation in patients with chronic myeloid leukemia in chronic phase , 2009, Cancer.
[110] H. Kantarjian,et al. Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors. , 2008, Blood.
[111] B. Turcq,et al. Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression. , 2008, Cancer research.
[112] K. Rezvani,et al. European LeukemiaNet criteria for failure or suboptimal response reliably identify patients with CML in early chronic phase treated with imatinib whose eventual outcome is poor. , 2008, Blood.
[113] M. Pirmohamed,et al. Effective dasatinib uptake may occur without human organic cation transporter 1 (hOCT1): implications for the treatment of imatinib-resistant chronic myeloid leukemia. , 2008, Blood.
[114] Martin C. Müller,et al. Desirable performance characteristics for BCR-ABL measurement on an international reporting scale to allow consistent interpretation of individual patient response and comparison of response rates between clinical trials. , 2008, Blood.
[115] D. Marin,et al. Finding of kinase domain mutations in patients with chronic phase chronic myeloid leukemia responding to imatinib may identify those at high risk of disease progression. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[116] Jaspal Kaeda,et al. Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[117] J. Melo,et al. Dasatinib Cellular Uptake and Efflux in Chronic Myeloid Leukemia Cells: Therapeutic Implications , 2008, Clinical Cancer Research.
[118] Tillmann Krahnke,et al. Imatinib pharmacokinetics and its correlation with response and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study. , 2008, Blood.
[119] H. Kantarjian,et al. Practical management of toxicities associated with tyrosine kinase inhibitors in chronic myeloid leukemia. , 2008, Clinical lymphoma & myeloma.
[120] H. Kantarjian,et al. Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. , 2007, Blood.
[121] V. Meignin,et al. Lung abnormalities after dasatinib treatment for chronic myeloid leukemia: a case series. , 2007, American journal of respiratory and critical care medicine.
[122] B. Druker,et al. A Half-Log Increase in BCR-ABL RNA Predicts a Higher Risk of Relapse in Patients with Chronic Myeloid Leukemia with an Imatinib-Induced Complete Cytogenetic Response , 2007, Clinical Cancer Research.
[123] M. Baccarani,et al. The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome‐negative cells , 2007, Cancer.
[124] 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.
[125] C. Preudhomme,et al. Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation , 2007, Haematologica.
[126] 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.
[127] M. Baccarani,et al. Resistance to dasatinib in Philadelphia-positive leukemia patients and the presence or the selection of mutations at residues 315 and 317 in the BCR-ABL kinase domain. , 2007, Haematologica.
[128] 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.
[129] P. Loehrer. Altered Bone and Mineral Metabolism in Patients Receiving Imatinib Mesylate , 2007 .
[130] 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.
[131] Francisco Cervantes,et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. , 2006, The New England journal of medicine.
[132] 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.
[133] 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.
[134] 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.
[135] J. Cayuela,et al. Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(ϕ)-LMC GROUP) , 2006, Leukemia.
[136] Hongyue Dai,et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[137] A. Tefferi,et al. Utility of peripheral blood dual color, double fusion fluorescent in situ hybridization for BCR/ABL fusion to assess cytogenetic remission status in chronic myeloid leukemia , 2006, Leukemia & lymphoma.
[138] R. Clark,et al. The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia. , 2006, Haematologica.
[139] Munir Pirmohamed,et al. Active transport of imatinib into and out of cells: implications for drug resistance. , 2004, Blood.
[140] 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.
[141] Laurie E Ailles,et al. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. , 2004, The New England journal of medicine.
[142] G. Flandrin,et al. Report of 34 patients with clonal chromosomal abnormalities in Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia , 2004, Leukemia.
[143] J. Abgrall,et al. Interphase FISH for follow-up of Philadelphia chromosome-positive chronic myeloid leukemia treatment. , 2004, Anticancer research.
[144] H. Kantarjian,et al. Granulocyte–colony‐stimulating factor (filgrastim) may overcome imatinib‐induced neutropenia in patients with chronic‐phase chronic myelogenous leukemia , 2004, Cancer.
[145] A. Goh,et al. Imatinib mesylate causes hypopigmentation in the skin , 2004, Cancer.
[146] 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.
[147] V. Najfeld,et al. The emergence of Ph-, trisomy -8+ cells in patients with chronic myeloid leukemia treated with imatinib mesylate. , 2003, Experimental hematology.
[148] Susan Branford,et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. , 2003, Blood.
[149] H. Kantarjian,et al. Prognostic significance of cytogenetic clonal evolution in patients with chronic myelogenous leukemia on imatinib mesylate therapy. , 2003, Blood.
[150] K. Krohn,et al. Emergence of clonal cytogenetic abnormalities in Ph- cells in some CML patients in cytogenetic remission to imatinib but restoration of polyclonal hematopoiesis in the majority. , 2003, Blood.
[151] H. Kantarjian,et al. Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia. , 2003, Blood.
[152] H. Kantarjian,et al. Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571; gleevec) in chronic-phase chronic myelogenous leukemia. , 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.
[153] Z. Estrov,et al. The biology of chronic myeloid leukemia. , 1999, The New England journal of medicine.
[154] C. Sawyers. Chronic myeloid leukemia. , 1999, The New England journal of medicine.
[155] 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.
[156] J. Hasford,et al. A new prognostic score for survival of patients with chronic myeloid leukemia treated with interferon alfa. Writing Committee for the Collaborative CML Prognostic Factors Project Group. , 1998, Journal of the National Cancer Institute.
[157] A. Zinsmeister,et al. Highly sensitive fluorescence in situ hybridization method to detect double BCR/ABL fusion and monitor response to therapy in chronic myeloid leukemia. , 1998, Blood.
[158] G. Utermann,et al. Fluorescence in situ hybridization (FISH) on peripheral blood smears for monitoring Philadelphia chromosome‐positive chronic myeloid leukemia (CML) during interferon treatment: A new strategy for remission assessment , 1998, Genes, chromosomes & cancer.
[159] 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.
[160] H. Kantarjian,et al. Hypermetaphase fluorescence in situ hybridization for quantitative monitoring of Philadelphia chromosome-positive cells in patients with chronic myelogenous leukemia during treatment. , 1995, Blood.
[161] F. Mitelman. The cytogenetic scenario of chronic myeloid leukemia. , 1993, Leukemia & lymphoma.
[162] R. Berger. Chromosome abnormalities in chronic myeloid leukemia , 1970 .
[163] K. Krohn. Transient benefit only from increasing the imatinib dose in CML patients who do not achieve complete cytogenetic remissions on conventional doses , 2022 .