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REFERENCES

  • 1
    O'Brien SG, Guilhot F, Larson RA, et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med. 2003; 348: 994-1004.
  • 2
    Hochhaus A, O'Brien SG, Guilhot F, et al. Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia. 2009; 23: 1054-1061.
  • 3
    Baccarani M, Cortes J, Pane F, et al. Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet. J Clin Oncol. 2009; 27: 6041-6051.
  • 4
    National Comprehensive Cancer Network. NCCN: Clinical Practice Guidelines in Oncology. Chronic Myelogenous Leukemia. Version 2. Jenkintown, PA: NCCN; 2010.
  • 5
    Shah NP. Medical management of CML. Hematology Am Soc Hematol Educ Program. 2007: 371-375.
  • 6
    Deininger MW. Optimizing therapy of chronic myeloid leukemia. Exp Hematol. 2007; 35: 144-154.
  • 7
    Zhang WW, Cortes JE, Yao H, et al. Predictors of primary imatinib resistance in chronic myelogenous leukemia are distinct from those in secondary imatinib resistance. J Clin Oncol. 2009; 27: 3642-3649.
  • 8
    Mahon FX, Belloc F, Lagarde V, et al. MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood. 2003; 101: 2368-2373.
  • 9
    Mukai M, Che XF, Furukawa T, et al. Reversal of the resistance to STI571 in human chronic myelogenous leukemia K562 cells. Cancer Sci. 2003; 94: 557-563.
  • 10
    Galimberti S, Cervetti G, Guerrini F, et al. Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during imatinib treatment. Cancer Genet Cytogenet. 2005; 162: 57-62.
  • 11
    Dohse M, Scharenberg C, Shukla S, et al. Comparison of ATP-binding cassette transporter interactions with the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib. Drug Metab Dispos. 2010; 38: 1371-1380.
  • 12
    Burger H, van Tol H, Boersma AW, et al. Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump. Blood. 2004; 104: 2940-2942.
  • 13
    White DL, Dang P, Engler J, et al. Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. J Clin Oncol. 2010; 28: 2761-2767.
  • 14
    White DL, Saunders VA, Dang P, et al. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood. 2007; 110: 4064-4072.
  • 15
    Crossman LC, Druker BJ, Deininger MW, Pirmohamed M, Wang L, Clark RE. hOCT-1 and resistance to imatinib. Blood. 2005; 106: 1133-1134; author reply 1134.
  • 16
    Davies A, Jordanides NE, Giannoudis A, 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. Leukemia. 2009; 23: 1999-2006.
  • 17
    Hegedus C, Ozvegy-Laczka C, Apati A, et al. Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti-cancer effects and pharmacological properties. Br J Pharmacol. 2009; 158: 1153-1164.
  • 18
    Hiwase DK, Saunders V, Hewett D, et al. Dasatinib cellular uptake and efflux in chronic myeloid leukemia cells: therapeutic implications. Clin Cancer Res. 2008; 14: 3881-3888.
  • 19
    Soverini S, Colarossi S, Gnani A, 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. Clin Cancer Res. 2006; 12: 7374-7379.
  • 20
    Nicolini FE, Corm S, Le QH, 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(phi)-LMC Group). Leukemia. 2006; 20: 1061-1066.
  • 21
    Kantarjian HM, Larson RA, Guilhot F, et al. Efficacy of imatinib dose escalation in patients with chronic myeloid leukemia in chronic phase. Cancer. 2009; 115: 551-560.
  • 22
    Jabbour E, Kantarjian HM, Jones D, 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: 2154-2160.
  • 23
    Tasigna (Nilotinib) [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2010.
  • 24
    Sprycel (Dasatinib) [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2009.
  • 25
    Apperley JF. Part II: management of resistance to imatinib in chronic myeloid leukemia. Lancet Oncol. 2007; 8: 1116-1128.
  • 26
    Hochhaus A, Baccarani M, Deininger M, et al. Dasatinib induces durable cytogenetic responses in patients with chronic myelogenous leukemia in chronic phase with resistance or intolerance to imatinib. Leukemia. 2008; 22: 1200-1206.
  • 27
    Shah NP, Kim DW, Kantarjian H, et al. Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib. Hematologica. 2010; 95: 232-240.
  • 28
    Kantarjian H, Cortes J, Kim DW, et al. Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up. Blood. 2009; 113: 6322-6329.
  • 29
    Kantarjian H, Shah NP, Hochhaus A, et al. Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med. 2010; 362: 2260-2270.
  • 30
    Cortes J, Borthakur G, O'Brien S, et al. Efficacy of dasatinib in patients (pts) with previously untreated chronic myelogenous leukemia (CML) in early chronic phase (CML-CP) [abstract]. Blood (ASH Annual Meeting Abstracts). 2009; 114: 143. Abstract 338.
  • 31
    Kantarjian HM, Giles FJ, Bhalla KN, et al. Update on imatinib-resistant chronic myeloid leukemia patients in chronic phase (CML-CP) on nilotinib therapy at 24 months: clinical response, safety, and long-term outcomes [abstract]. Blood (ASH Annual Meeting Abstracts). 2009;114:464. Abstract 1129.
  • 32
    le Coutre P, Hochhaus A, Apperley J, et al. Nilotinib in imatinib-resistant or -intolerant patients with chronic myelogenous leukemia in accelerated phase (CML-AP): update of a phase 2 study [abstract]. Hematologica. 2008; 93: 47. Abstract 0118.
  • 33
    Nicolini F, Alimena G, Al-Ali HK, et al. Final safety analysis of 1793 CML patients the from ENACT (Expanding Nilotinib Access in Clinical Trials) study in adult patients with imatinib-resistant or -intolerant chronic myeloid leukemia (CML) [abstract]. Hematologica. 2009; 94: 255. 256. Abstract 0630.
  • 34
    le Coutre PD, Ceglarek B, Turkina A, et al. Patterns and management of selected adverse events of adult patients with imatinib-resistant or -intolerant chronic myeloid leukemia (CML) from the ENACT (Expanding Nilotinib Access in Clinical Trials) study [abstract]. Blood (ASH Annual Meeting Abstracts). 2009 ; 114: 457-458. Abstract 0115.
  • 35
    Jabbour E, Kantarjian HM, Baccarani M, et al. Minimal cross-intolerance between nilotinib and imatinib in patients with imatinib-intolerant chronic myeloid leukemia in chronic phase (CML-CP) or accelerated phase (CML-AP) [abstract]. Blood (ASH Annual Meeting Abstracts). 2008; 112: 1103. Abstract 3215.
  • 36
    Saglio G, Kim DW, Issaragrisil S, et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med. 2010; 362: 2251-2259.
  • 37
    Rosti G, Palandri F, Castagnetti F, et al. Nilotinib for the frontline treatment of Ph(+) chronic myeloid leukemia. Blood. 2009; 114: 4933-4938.
  • 38
    Cortes JE, Jones D, O'Brien S, et al. Nilotinib as front-line treatment for patients with chronic myeloid leukemia in early chronic phase. J Clin Oncol. 2010; 28: 392-397.
  • 39
    O'Dwyer M, Swords R, Giles F, et al. Nilotinib 300 mg twice daily is effective and well tolerated as first line treatment of Ph-positive chronic myeloid leukemia in chronic phase: updated results of the ICORG 0802 phase 2 study [abstract]. Hematologica. 2010; 95: 340. Abstract 0812.
  • 40
    Larson RA, le Coutre PD, Reiffers J, et al. Comparison of nilotinib and imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd beyond one year [abstract]. J Clin Oncol. 2010; 28( 15S): 487s. Abstract 6501.
  • 41
    Hochhaus A, Lobo C, Pasquini R, et al. Continued superiority of nilotinib vs imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd beyond 1 year [abstract]. Hematologica. 2010; 95: 459. Abstract 1113.
  • 42
    Shah NP, Nicoll JM, Nagar B, 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. Cancer Cell. 2002; 2: 117-125.
  • 43
    Ernst T, Erben P, Muller MC, et al. Dynamics of BCR-ABL mutated clones before hematologic or cytogenetic resistance to imatinib. Hematologica. 2008; 93: 186-192.
  • 44
    Azam M, Latek RR, Daley GQ. Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. Cell. 2003; 112: 831-843.
  • 45
    Jabbour E, Kantarjian H, Jones D, et al. Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. Blood. 2008; 112: 53-55.
  • 46
    Mauro MJ. Defining and managing imatinib resistance. Hematology Am Soc Hematol Educ Program. 2006: 219-225.
  • 47
    Deininger M. Resistance to imatinib: mechanisms and management. J Natl Compr Canc Netw. 2005; 3: 757-768.
  • 48
    Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001; 293: 876-880.
  • 49
    Griswold IJ, MacPartlin M, Bumm T, et al. Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib. Mol Cell Biol. 2006; 26: 6082-6093.
  • 50
    Corbin AS, Buchdunger E, Pascal F, Druker BJ. Analysis of the structural basis of specificity of inhibition of the abl kinase by STI571. J Biol Chem. 2002; 277: 32214-32219.
  • 51
    Corbin AS, Louisiana Rosee P, Stoffregen EP, Druker BJ, Deininger MW. Several bcr-abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood. 2003; 101: 4611-4614.
  • 52
    Laneuville P, Di Lea C, Yin O, Woodman R, Mestan J, Manley P. Comparative in vitro cellular data alone are insufficient to predict clinical responses and guide the choice of BCR-ABL inhibitor for treating imatinib-resistant chronic myeloid leukemia [serial online]. J Clin Oncol. 2010; 28: e169-e171.
  • 53
    Branford S, Rudzki Z, Walsh S, 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. Blood. 2003; 102: 276-283.
  • 54
    Soverini S, Martinelli G, Rosti G, et al. ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. J Clin Oncol. 2005; 23: 4100-4109.
  • 55
    Khorashad JS, de Lavallade H, Apperley JF, 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. J Clin Oncol. 2008; 26: 4806-4813.
  • 56
    Jabbour E, Kantarjian H, Jones D, et al. Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate. Leukemia. 2006; 20: 1767-1773.
  • 57
    Willis SG, Lange T, Demehri S, 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. Blood. 2005; 106: 2128-2137.
  • 58
    Khorashad JS, Anand M, Marin D, et al. The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia. 2006; 20: 658-663.
  • 59
    Redaelli S, Piazza R, Rostagno R, et al. Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR-ABL mutants. J Clin Oncol. 2009; 27: 469-471.
  • 60
    Apperley JF. Part I: mechanisms of resistance to imatinib in chronic myeloid leukemia. Lancet Oncol. 2007; 8: 1018-1029.
  • 61
    Muller MC, Cortes JE, Kim DW, et al. Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to pre-existing BCR-ABL mutations. Blood. 2009; 114: 4944-4953.
  • 62
    Jabbour E, Kantarjian HM, Jones D, et al. Characteristics and outcome of patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors. Blood. 2008; 112: 4839-4842.
  • 63
    Hughes T, Saglio G, Branford S, et al. Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. J Clin Oncol. 2009; 27: 4204-4210.
  • 64
    Radich JP, Martinelli G, Hochhaus A, et al. Response and outcomes to nilotinib at 24 months in imatinib-resistant chronic myeloid leukemia patients in chronic phase (CML-CP) and accelerated phase (CML-AP) with and without BCR-ABL mutations [abstract]. Blood (ASH Annual Meeting Abstracts). 2009; 114: 464-465. Abstract 1130.
  • 65
    Soverini S, Gnani A, Colarossi S, 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. Blood. 2009; 114: 2168-2171.
  • 66
    Cortes J, Jabbour E, Kantarjian H, et al. Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors. Blood. 2007; 110: 4005-4011.
  • 67
    Chu S, Xu H, Shah NP, et al. Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment. Blood. 2005; 105: 2093-2098.
  • 68
    Sherbenou DW, Wong MJ, Humayun A, et al. Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib. Leukemia. 2007; 21: 489-493.
  • 69
    Nicolini FE, Hayette S, Corm S, et al. Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation. Hematologica. 2007; 92: 1238-1241.
  • 70
    Cortes JE, Kantarjian H, Brummendorf T, et al. Safety and efficacy of bosutinib (SKI-606) in patients (pts) with chronic phase (CP) chronic myeloid leukemia (CML) following resistance or intolerance to imatinib (IM) [abstract]. J Clin Oncol. 2010;28(15S):487s. Abstract 6502.
  • 71
    Cortes-Franco J, Khoury HJ, Nicolini FE, et al. Safety and efficacy of subcutaenous-administered omacetaxine mepesuccinate in imatinib-resistant chronic myeloid leukemia (CML) patients who harbor the bcr-abl T315I mutation—results of an ongoing multicenter phase 2/3 study [abstract]. Blood (ASH Annual Meeting Abstracts). 2009; 114: 267. Abstract 644.
  • 72
    O'Hare T, Shakespeare WC, Zhu X, et al. AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell. 2009; 16: 401-412.
  • 73
    Cortes J, Talpaz M, Denininger M, et al. A phase 1 trial of oral AP24534 in patients with refractory chronic myeloid leukemia and other hematologic malignancies: first results of safety and clinical activity against T315I and resistant mutations [abstract]. Blood (ASH Annual Meeting Abstracts). 2009; 114: 267. Abstract 643.
  • 74
    Talpaz M, Cortes JE, Deininger MW, et al. Phase I trial of AP24534 in patients with refractory chronic myeloid leukemia (CML) and hematologic malignancies [abstract]. J Clin Oncol. 2010; 28( 15S): 489s. Abstract 6511.
  • 75
    Cortes JE, Paquette R, Talpaz M, et al. Preliminary clinical activity in a phase 1 trial of the BCR-ABL/IGF-1R/aurora kinase inhibitor XL228 in patients with Ph+ leukemias with either failure to multiple TKI therapies or with T315I mutation [abstract]. Blood (ASH Annual Meeting Abstracts). 2008; 112: 1109. Abstract 3232.
  • 76
    Gontarewicz A, Balabanov S, Keller G, et al. Simultaneous targeting of aurora kinases and bcr-abl kinase by the small molecule inhibitor PHA-739358 is effective against imatinib-resistant BCR-ABL mutations including T315I. Blood. 2008; 111: 4355-4364.
  • 77
    Van Etten RA, Chan WW, Zaleskas VM, et al. DCC-2036: a novel switch pocket inhibitor of ABL tyrosine kinases with therapeutic efficacy against BCR-ABL T315I in vitro and in a CML mouse model [abstract]. Blood (ASH Annual Meeting Abstracts). 2007;110:142a. Abstract 463.
  • 78
    Agency for Healthcare Research and Quality (AHRQ). Technology Assessment: Report on the Relative Efficacy of Oral Cancer Therapy for Medicare Beneficiaries Versus Currently Covered Therapy. Part 3. Imatinib for Chronic Myeloid Leukemia (CML). Rockville, MD: AHRQ; 2009. http://www.ahrq.gov/clinic/ta/cml/cml.pdf. Accessed October 26, 2010.
  • 79
    Branford S, Melo JV, Hughes TP. 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: 5426-5435.
  • 80
    Lipton JH, Sriharsha L, Bogomilsky S, et al. Pleural effusions in patients treated with dasatinib: results from 2 institutions, risk factors and management [abstract]. J Clin Oncol. 2007; 25(18S). Abstract 17503.
  • 81
    Quintas-Cardama A, Kantarjian HM, O'Brien S, et al. Association of pleural effusion and bleeding in patients with chronic myelogenous leukemia receiving dasatinib. Blood. 2008; 112: 735. Abstract 2112.
  • 82
    Quintas-Cardama A, Kantarjian H, Ravandi F, et al. Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy. Cancer. 2009; 115: 2482-2490.
  • 83
    Quintas-Cardama A, Han X, Kantarjian H, Cortes, J. Dasatinib-induced platelet dysfunction [abstract]. Blood (ASH Annual Meeting Abstracts). 2007; 110: 864a. Abstract 2941.
  • 84
    Sillaber C, Herrmann H, Bennett K, et al. Immunosuppression and atypical infections in CML patients treated with dasatinib at 140 mg daily. Eur J Clin Invest. 2009; 39: 1098-1109.
  • 85
    Bradeen HA, Eide CA, O'Hare T, 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. Blood. 2006; 108: 2332-2338.
  • 86
    Jabbour E, Hochhaus A, Cortes J, Louisiana Rosee P, Kantarjian HM. Choosing the best treatment strategy for chronic myeloid leukemia patients resistant to imatinib: weighing the efficacy and safety of individual drugs with BCR-ABL mutations and patient history. Leukemia. 2010; 24: 6-12.
  • 87
    Kantarjian HM, Jabbour E, Giles FJ, et al. Prognostic factors for progression-free survival in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase (CML-CP) treated with nilotinib based on 24 month data [abstract]. Blood (ASH Annual Meeting Abstracts) 2009;114:1278-1279. Abstract 3298.
  • 88
    Milojkovic D, Nicholson E, Apperley JF, et al. Early prediction of success or failure of treatment with second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukemia. Hematologica. 2010; 95: 224-231.
  • 89
    Jabbour E, Kantarjian H, O'Brien S, et al. Predictive factors for response and outcome in patients (pts) treated with second generation tyrosine kinase inhibitors (2-TKI) for chronic myeloid leukemia in chronic phase (CML-CP) post imatinib failure [abstract]. Blood (ASH Annual Meeting Abstracts) 2009;114:210-211. Abstract 509.
  • 90
    O'Hare T, Walters DK, Stoffregen EP, et al. In vitro activity of bcr-abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant abl kinase domain mutants. Cancer Res. 2005; 65: 4500-4505.
  • 91
    Puttini M, Coluccia AM, Boschelli F, et al. In vitro and in vivo activity of SKI-606, a novel src-abl inhibitor, against imatinib-resistant bcr-abl+ neoplastic cells. Cancer Res. 2006; 66: 11314-11322.