University of Wisconsin Hematology

Chronic myelogenous leukemia

General

  1. Cortes et al. Chronic myeloid leukaemia. Lancet 2021;398:1914
  2. Quintás-Cardama and Cortes. Molecular biology of bcr-abl1–positive chronic myeloid leukemia. Blood 2009;113:1619
  3. Schemionek et al. BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells. Blood 2010; 115:3185
  4. Kim et al. Spectrum of somatic mutation dynamics in chronic myeloid leukemia following tyrosine kinase inhibitor therapy. Blood 2017;129:38(With editorial)
  5. Verma et al. Chronic myeloid leukemia (CML) with P190BCR-ABL: analysis of characteristics, outcomes, and prognostic significance. Blood 2009;114:2232
  6. Holyoake and Vetrie. The chronic myeloid leukemia stem cell: stemming the tide of persistence. Blood 2017;129:1595
  7. Radivoyevitch et al. Quantitative modeling of chronic myeloid leukemia: insights from radiobiology. Blood 2012;119:4363
  8. Hochhaus A. Managing chronic myeloid leukemia as a chronic disease. Hematology 2011:128
  9. Melo and Ross. Minimal Residual Disease and Discontinuation of Therapy in Chronic Myeloid Leukemia: Can We Aim at a Cure? Hematology 2011:136
  10. Shanmuganathan and Hughes. Molecular monitoring in CML: how deep? How often? How should it influence therapy? Blood 2018;132:2125
  11. Radich et al. New approaches to molecular monitoring in CML (and other diseases). Blood 2019;134:1578
  12. Kantarjian et al. Significance of Increasing Levels of Minimal Residual Disease in Patients With Philadelphia Chromosome–Positive Chronic Myelogenous Leukemia in Complete Cytogenetic Response. J Clin Oncol 2009;27:3659
  13. Kreutzman et al. Mono/oligoclonal T and NK cells are common in chronic myeloid leukemia patients at diagnosis and expand during dasatinib therapy. Blood 2010;116:772
  14. Fabarius 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. Blood 2011;118:6760(Add’nl Ph chromosome, trisomy 8, isochromosome 17q and trisomy 19 associated with worse prognosis and progression to blast crisis)
  15. Wang et al. Risk stratification of chromosomal abnormalities in chronic myelogenous leukemia in the era of tyrosine kinase inhibitor therapy. Blood 2016;127:2742
  16. Saußele et al. Impact of comorbidities on overall survival in patients with chronic myeloid leukemia: results of the randomized CML Study IV. Blood 2015;126:42
  17. Prost et al. Erosion of the chronic myeloid leukaemia stem cell pool by PPARγ agonists. Nature 2015;525:380(Pioglitazone treatment resulted in sustained molecular remission in 3 patients with residual disease despite nilotinib treatment. See also NEJM summaryof this research)
  18. Kuntz et al. Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells. Nat Med 2017;23:1234
  19. Giustacchini et al. Single-cell transcriptomics uncovers distinct molecular signatures of stem cells in chronic myeloid leukemia. Nat Med 2017;23:692(Identifies a population of leukemic stem cells that may give rise to therapy-resistant relapse; with editorial)
  20. Kesarwani et al. Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia. Nat Med 2017;23:472
  21. Zhang et al. Bone marrow niche trafficking of miR-126 controls the self-renewal of leukemia stem cells in chronic myelogenous leukemia. Nat Med 2018;24:450

Tyrosine kinase inhibitors in CML – general

  1. Guilhot and Hellmann. Long-term outcomes of tyrosine kinase inhibitors in chronic myeloid leukemia. Blood 2025;145:910
  2. Berman E. How I treat chronic-phase chronic myelogenous leukemia. Blood 2022;139:3138
  3. Hughes and Ross. Moving treatment-free remission into mainstream clinical practice in CML. Blood 2016;128:17(About half of patients with stable deep molecular response can maintain remission off TKI therapy)
  4. Larson RA. Is there a best TKI for chronic phase CML? Blood 2015;126:2370
  5. Cortes J. How to manage CML patients with comorbidities. Blood 2020;136:2507
  6. Smith and Shah. Tyrosine Kinase Inhibitor Therapy for Chronic Myeloid Leukemia: Approach to Patients with Treatment-Naive or Refractory Chronic-Phase Disease. Hematology 2011:121
  7. Soverini et al. Prospective assessment of NGS-detectable mutations in CML patients with nonoptimal response: the NEXT-in-CML study. Blood 2020;135:534(Improved dectection of low-level TKI mutations that can cause treatment failure)
  8. Jabbour 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. Blood 2011;118:4541
  9. Branford et al. Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML. Blood 2013;121:3818
  10. Jain et al. Early responses predict better outcomes in patients with newly diagnosed chronic myeloid leukemia: results with four tyrosine kinase inhibitor modalities. Blood 2013;121:4867
  11. Branford et al. Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline. Blood 2014;124:511
  12. Sobrinho-Simões et al. In search of the original leukemic clone in chronic myeloid leukemia patients in complete molecular remission after stem cell transplantation or imatinib. Blood 2010;116:1329(Absence of detectable BCR-ABL transcripts does not imply the absence of the leukemic clone)
  13. Iacobucci et al. Comparison Between Patients With Philadelphia-Positive Chronic Phase Chronic Myeloid Leukemia Who Obtained a Complete Cytogenetic Response Within 1 Year of Imatinib Therapy and Those Who Achieved Such a Response After 12 Months of Treatment. J Clin Oncol 2006;24:454(DFS at 4 years similar in early and late responders)
  14. Ibrahim et al. Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy. Blood 2011;117:3733
  15. Russo et al. Effects and outcome of a policy of intermittent imatinib treatment in elderly patients with chronic myeloid leukemia. Blood 2013;121:5138(Some patients had molecular or cytogenetic progress, none had blast crisis or new cytogenetic abnormality; all responded to imatinib when re-treated)
  16. Branford et al. Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter? Blood 2009;114:5426
  17. Kantarjian et al. New Insights into the Pathophysiology of Chronic Myeloid Leukemia and Imatinib Resistance. Ann Intern Med 2006;145:913
  18. O’Hare et al.Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood 2007;110:2242
  19. Soverini et al. BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet. Blood 2011;118:1208
  20. Parker et al. Poor response to second-line kinase inhibitors in chronic myeloid leukemia patients with multiple low-level mutations, irrespective of their resistance profile. Blood 2012;199:2234
  21. Jain et al. Impact of BCR-ABL transcript type on outcome in patients with chronic-phase CML treated with tyrosine kinase inhibitors. Blood 2016;127:1269
  22. Jabbour et al. Predictive factors for outcome and response in patients treated with second-generation tyrosine kinase inhibitors for chronic myeloid leukemia in chronic phase after imatinib failure. Blood 2011;117:1822(Poor performance status, no cytogenetic response to imatinib associated with low response rate)
  23. Milojkovic et al. Responses to second-line tyrosine kinase inhibitors are durable: an intention-to-treat analysis in chronic myeloid leukemia patients. Blood 2012;119:1838
  24. Tam et al. Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia. Blood 2008;112:516
  25. Garg et al. The use of nilotinib or dasatinib after failure to 2 prior tyrosine kinase inhibitors: long-term follow-up. Blood 2009;114:4361(Third-line TKI therapy typically does not give durable response)
  26. Dahlén et al. Cardiovascular Events Associated With Use of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Population-Based Cohort Study. Ann Intern Med 2016;165:161(1.5-fold higher risk of arterial events, 2-fold higher VTE risk in TKI-treated patients)
  27. Moslehi et al. Tyrosine Kinase Inhibitor–Associated Cardiovascular Toxicity in Chronic Myeloid Leukemia. J Clin Oncol 2015;33:4210
  28. Quintás-Cardama et al. Tyrosine kinase inhibitor–induced platelet dysfunction in patients with chronic myeloid leukemia. Blood 2009; 114:261(Dasatinib treatment causes impaired platelet aggregation)
  29. Haouala et al. Drug interactions with the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib. Blood 2011;117:e75
  30. Verma et al. Malignancies occurring during therapy with tyrosine kinase inhibitors (TKIs) for chronic myeloid leukemia (CML) and other hematologic malignancies. Blood 2011;118:4353(No evidence that TKIs increase risk of 2nd malignancies)
  31. Efficace et al. Health-related quality of life in chronic myeloid leukemia patients receiving long-term therapy with imatinib compared with the general population. Blood 2011;118:4554(Fatigue most common problem, especially in younger patients)
  32. Hughes et al. The evolution of treatment-free remission. Blood 2025;145:921
  33. Rousselot 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. J Clin Oncol 2014;32:424
  34. Rea et al. Discontinuation of dasatinib or nilotinib in chronic myeloid leukemia: interim analysis of the STOP 2G-TKI study. Blood 2017;129:846(43% had molecular relapse at median of 4 mo, all patients responded to retreatment)
  35. Clark 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. Lancet Haematol 2017;4:e310(Cutting TKI dose in half safe for most patients in MMR)
  36. Etienne et al. Long-Term Follow-Up of the French Stop Imatinib (STIM1) Study in Patients With Chronic Myeloid Leukemia. J Clin Oncol 2017;35:298(38% remained in molecular remission at 5 yrs; almost all patients who progressed responded to restarting treatment)
  37. Kimura et al. Treatment-free remission after first-line dasatinib discontinuation in patients with chronic myeloid leukaemia (first-line DADI trial): a single-arm, multicentre, phase 2 trial. Lancet Haematol 2020;7:e218(55% of patients with deep molecular response after 3 years of treatment remained in remission 6 mo after stopping therapy)
  38. Hughes et al. Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure. NEJM 2019;381:2315
  39. Yeung et al. Asciminib: a new therapeutic option in chronic-phase CML with treatment failure. Blood 2022;139:3474
  40. Hochhaus et al. Asciminib in Newly Diagnosed Chronic Myeloid Leukemia. NEJM 2024 ;391:885
  41. Berman et al. Chronic Myelogenous Leukemia: Pregnancy in the Era of Stopping Tyrosine Kinase Inhibitor Therapy. J Clin Oncol 2018;36:1250

Imatinib

  1. Druker et al. Efficacy and safety of a specific inhibitor of the bcr-abl tyrosine kinase in chronic myeloid leukemia. NEJM 2001;344:1031
  2. Druker 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. NEJM 2001;344:1038
  3. Picard et al. Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia. Blood 2007;109:3469
  4. Larson et al. Imatinib pharmacokinetics and its correlation with response and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study. Blood 2008;111:4022(Adequate plasma concentration predicts better clinical response)
  5. Kantarjian et al. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. NEJM 2002;346:645
  6. Gugliotta et al. Frontline imatinib treatment of chronic myeloid leukemia: no impact of age on outcome, a survey by the GIMEMA CML Working Party. Blood 2011;117:5591
  7. Hehlmann et al. Deep Molecular Response Is Reached by the Majority of Patients Treated With Imatinib, Predicts Survival, and Is Achieved More Quickly by Optimized High-Dose Imatinib: Results From the Randomized CML-Study IV. J Clin Oncol 2014;32:416(>4.5 log reduction of BCR-ABL)
  8. Kantarjian et al.  High-dose imatinib mesylate therapy in newly diagnosed Philadelphia chromosome–positive chronic phase chronic myeloid leukemia.  Blood 2004;103:2873
  9. Hughes et al. Impact of early dose intensity on cytogenetic and molecular responses in chronic- phase CML patients receiving 600 mg/day of imatinib as initial therapy. Blood 2008;112:3965(escalation to 800 mg in patients with suboptimal response at 6 mo appeared beneficial)
  10. Baccarani et al. Comparison of imatinib 400 mg and 800 mg daily in the front-line treatment of high-risk, Philadelphia-positive chronic myeloid leukemia: a European LeukemiaNet Study. Blood 2009;113:4497(No significant difference in response rate)
  11. Preudhomme et al. Imatinib plus Peginterferon Alfa-2a in Chronic Myeloid Leukemia. NEJM 2010;363:2511(Addition of peginterferon doubled rate of molecular response at 12 months, but caused more toxicity)
  12. Simonsson et al. Combination of pegylated IFN-α2b with imatinib increases molecular response rates in patients with low- or intermediate-risk chronic myeloid leukemia. Blood 2011;118:3228
  13. Druker et al. Five-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid Leukemia. NEJM 2006;355:2408(89% 5-year overall survival, 83% event-free survival)
  14. Hochhaus et al. Favorable long-term follow-up results over 6 years for response, survival, and safety with imatinib mesylate therapy in chronic-phase chronic myeloid leukemia after failure of interferon- treatment. Blood 2008;111:1039
  15. Hochhaus et al. Long-Term Outcomes of Imatinib Treatment for Chronic Myeloid Leukemia. NEJM 2017;376:917(Efficacy maintained over 11 year followup without major toxicity; with editorial)
  16. Rousselot et al. Imatinib mesylate discontinuation in patients with chronic myelogenous leukemia in complete molecular remission for more than 2 years. Blood 2007;109:58 (6 of 12 patients remained in molecular remission during median followup of 18 mo)
  17. Ross et al. Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study. Blood 2013;122:515(About half remained in molecular remission after 2 yr; the rest were all successfully re-treated)
  18. Hughes 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). Blood 2010;116:3758(Patients with major molecular response had durable responses/remissions)
  19. Atallah et al. Congestive heart failure is a rare event in patients receiving imatinib therapy. Blood 2007; 110:1233(1.7% incidence, only 0.6% considered due to drug)
  20. Fitter et al. Long-term imatinib therapy promotes bone formation in CML patients. Blood 2008;111:2538
  21. Vandyke et al. Dysregulation of bone remodeling by imatinib mesylate. Blood 2010;115:766
  22. Pye et al. The effects of imatinib on pregnancy outcome. Blood 2008;111:5505
  23. Mauro MJ. Defining and Managing Imatinib Resistance. Hematology 2006;226-39
  24. Jabbour 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. Blood 2009;113:2154
  25. Yeung et al. TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets. Blood 2015;125:915(This strategy considered to produce excellent results, more cost-effective than routine use of newer agents)

Dasatinib

  1. Kantarjian et al. Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. NEJM 2010;362:2260(Dasatinib superior)
  2. Kantarjian et al. Dasatinib or imatinib in newly diagnosed chronic-phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION)(Dasatinib shows “faster and deeper” responses; transformation to accelerated or blast phase occurred in 2.3% vs 5% with imatinib)
  3. Jabbour et al. Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION). Blood 2014;123:494
  4. Radich et al. A randomized trial of dasatinib 100 mg versus imatinib 400 mg in newly diagnosed chronic-phase chronic myeloid leukemia. Blood 2012;120:3898(Dasatanib produced more complete cytogenetic responses, better molecular responses, more toxicity; similar survival in both arms at medial 3 year followup)
  5. Talpaz et al. Dasatinib in Imatinib-Resistant Philadelphia Chromosome�Positive Leukemias. NEJM 2006;354:2531
  6. Hochhaus et al. Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Blood 2007;109:2303
  7. Guilhot et al. Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. Blood 2007;109:4143
  8. Cortes et al. Dasatinib induces complete hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in blast crisis. Blood 2007;109:3207(about a third of patients had good response to dasatinib)
  9. Kantarjian et al. Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib: a randomized phase 2 trial. Blood 2007;109:5143(Dasatinib superior)
  10. Cortes et al. Final 5-Year Study Results of DASISION: The Dasatinib Versus Imatinib Study in Treatment-Naïve Chronic Myeloid Leukemia Patients Trial. J Clin Oncol 2016;34:2333(Modest improvement in outcomes with dasatinib)
  11. Müller et al. Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. Blood 2009; 114:4944
  12. Shah et al. Long-term outcome with dasatinib after imatinib failure in chronic-phase chronic myeloid leukemia: follow-up of a phase 3 study. Blood 2014;123:2317(Long term outcomes good if <10% BCR-ABL transcripts within 3 mo)
  13. Montani et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation 2012;125:2128

Nilotinib

  1. Saglio et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. NEJM 2010;362:2251 (Nilotinib superior)
  2. Cortes et al. Nilotinib as front-line treatment for patients with chronic myeloid leukemia in early chronic phase. J Clin Oncol 2010;28:392
  3. Kantarjian et al. Nilotinib in Imatinib-Resistant CML and Philadelphia Chromosome�Positive ALL. NEJM 2006;354:2542
  4. Katarjian et al. Nilotinib is effective in patients with chronic myeloid leukemia in chronic phase after imatinib resistance or intolerance: 24-month follow-up results. Blood 2011;117:1141
  5. Kantarjian et al. Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome–positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance. Blood 2007;110:3540
  6. le Coutre et al. Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia. Blood 2008;111:1834
  7. Cortes et al. Minimal cross-intolerance with nilotinib in patients with chronic myeloid leukemia in chronic or accelerated phase who are intolerant to imatinib. Blood 2011;117:5600
  8. Rosti et al. Nilotinib for the frontline treatment of Ph+ chronic myeloid leukemia. Blood 2009;114:4933
  9. Wang et al. Phase 3 study of nilotinib vs imatinib in Chinese patients with newly diagnosed chronic myeloid leukemia in chronic phase: ENESTchina. Blood 2015;125:2771(MMR in 28% getting imatinib, 52% getting nilotinib after 1 yr)
  10. Mahon et al. Treatment-Free Remission After Second-Line Nilotinib Treatment in Patients With Chronic Myeloid Leukemia in Chronic Phase: Results From a Single-Group, Phase 2, Open-Label Study. Ann Intern Med 2018;168:461(Over 50% of patients maintained molecular remission after 96 weeks off treatment)

Other TKIs

  1. Cortes et al. Safety and efficacy of bosutinib (SKI-606) in chronic phase Philadelphia chromosome–positive chronic myeloid leukemia patients with resistance or intolerance to imatinib. Blood 2011;118:4567
  2. Khoury et al. Bosutinib is active in chronic phase chronic myeloid leukemia after imatinib and dasatinib and/or nilotinib therapy failure. Blood 2012;119:3403
  3. Cortes et al. Bosutinib Versus Imatinib in Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia: Results From the BELA Trial. J Clin Oncol 2012;30:3486
  4. Kantarjian et al. Bosutinib safety and management of toxicity in leukemia patients with resistance or intolerance to imatinib and other tyrosine kinase inhibitors. Blood 2014;123:1309
  5. Cortes et al. Bosutinib Versus Imatinib for Newly Diagnosed Chronic Myeloid Leukemia: Results From the Randomized BFORE Trial. J Clin Oncol 2018;36:231(12-mo MMR rate 47% with bosutinib, 37% with imatinib)
  6. Cortes et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. NEJM 2012;367:2075
  7. Parker et al. The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib. Blood 2016;127:1870(Ponatinib effective in TKI-resistant disease with multiple mutations in BCR-ABL)
  8. Cortes et al. A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias. NEJM 2013;369:1783 (Ponatinib effective; 9% incidence of serious thrombotic events)
  9. Cortes et al. Ponatinib efficacy and safety in Philadelphia chromosome–positive leukemia: final 5-year results of the phase 2 PACE trial. Blood 2018;132:393
  10. Cortes et al. Ponatinib dose-ranging study in chronic-phase chronic myeloid leukemia: a randomized, open-label phase 2 clinical trial. Blood 2021;138:2042
  11. Yeung et al. Asciminib monotherapy as frontline treatment of chronic-phase chronic myeloid leukemia: results from the ASCEND study. Blood 2024;144:1993 (Very effective and well-tolerated)
  12. Latifi et al. Thrombotic microangiopathy as a cause of cardiovascular toxicity from the BCR-ABL1 tyrosine kinase inhibitor ponatinib. Blood 2019;133:1597

CML: Stem Cell Transplantation

Accelerated phase & blast crisis

  1. Radich J. The biology of CML blast crisis. Hematology 2007:384
  2. Hehlman R. How I treat CML in blast crisis. Blood 2012;120:737
  3. Wadhwa et al. Factors affecting duration of survival after onset of blastic transformation of chronic myeloid leukemia. Blood 2002;99:2304
  4. Apperley et al. Dasatinib in the Treatment of Chronic Myeloid Leukemia in Accelerated Phase After Imatinib Failure: The START A Trial. J Clin Oncol 2009; 27:3472
  5. Jiang et al. Imatinib mesylate versus allogeneic hematopoietic stem cell transplantation for patients with chronic myelogenous leukemia in the accelerated phase. Blood 2011;117:3032(SCT superior in patients with CML > 1yr, Hgb < 10, or periph blasts > 5%)