1)Druker BJ, Guilhot F, OʼBrien SG, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med. 2006; 355: 2408-17
|
|
|
2)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: 2260-70
|
|
|
3)Saglio G, Kim DW, Issaragrisil S, et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med. 2010; 362: 2251-9
|
|
|
4)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: 276-83
|
|
|
5)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: 7374-9
|
|
|
6)Nicolini FE, Corm S, Lê 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: 1061-6
|
|
|
7)OʼHare T, Eide CA, Deininger MW. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood. 2007; 110: 2242-9
|
|
|
8)Eghtedar A, Kantarjian H, Jabbour E, et al. Outcome after failure of second generation tyrosine kinase inhibitors treatment as first-line therapy for patients with chronic myeloid leukemia. Clin Lymphoma, Myeloma Leukemia. 2003; 13: 477-84
|
|
|
9)Garg RJ, Kantarjian H, OʼBrien S, et al. The use of nilotinib or dasatinib after failure to 2 prior tyrosine kinase inhibitors: long-term follow-up. Blood. 2009; 114: 4361-8
|
|
|
10)Nicolini FE, Mauro MJ, Martinelli G, et al. Epidemiologic study on survival of chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia patients with BCR-ABL T315I mutation. Blood. 2009; 114: 5271-8
|
|
|
11)OʼHare 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: 401-12
|
|
|
12)Cortes J. A phase 1 trial of oral ponatinib (AP24534) in patients with refractory chronic myelogenous leukemia (CML) and other hematologic malignancies: Emerging safety and clinical response findings. ASH2010; #210
|
|
|
13)Cortes J, Kantarjian H, Shah N, et al. Subset analysis of response to treatment of chronic phase CML in a phase 1 study of ponatinib in refractory hematologic malignancies. ASH2011; #602
|
|
|
14)Shah NP, Talpaz M, Deininger MWN, et al. Ponatinib in patients with refractory acute myeloid leukaemia: findings from a phase 1 study. Br J Haematol. 2013; 62: 548-52
|
|
|
15)Cortes JE. A pivotal phase 2 trial of ponatinib in patients with CML and Ph+ ALL resistant or intolerant to dasatinib or nilotinib, or with the T315I BCR-ABL mutation: 12-month follow-up of the PACE trial. ASH2012; #163
|
|
|
16)Cortes JE. PACE: A pivotal phase I trial of ponatinib in patients with CML and Ph+ALL resistant or intolerant to dasatinib or nilotinib, or with the T315I mutation. ASCO, #6503
|
|
|
17)Cortes JE, Kantarjian H, Shah, NP, et al. Ponatinib in refractory Philadelphia chromosome-positive Leukemias. N Engl J Med. 2012; 367: 2075-88
|
|
|
18)Kantarjian HM. Efficacy and safety of ponatinib in patients with AP-CML, BP-CML or Ph+ALL: 12-month follow-up of the PACE trial. ASH2012; #915
|
|
|
19)Smith C, Elisabeth A, Xiaotian L, et al. Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD. Blood. 2013; 121: 3165-71
|
|
|