Nilotinib for the treatment of chronic myeloid leukemia: An evidence-based review

References

• Faderl S, Talpaz M, Estrov Z, O’Brien S, Kurzrock R, Kantarjian HM. The biology of chronic myeloid leukemia. N Engl J Med. 1999;341:164–172.
   PubMed Web of Science ®Google Scholar
• Goldman JM, Melo JV. Chronic myeloid leukemia – advances in biology and new approaches to treatment. N Engl J Med. 2003;349:1451–1464.
   PubMed Web of Science ®Google Scholar
• Kantarjian HM, Cortes JE, O’Brien S, et al. Long-term survival benefit and improved complete cytogenetic and molecular response rates with imatinib mesylate in Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia after failure of interferon-{alpha}. Blood. 2004;104:1979–1988.
   PubMed Web of Science ®Google Scholar
• Kantarjian H, Sawyers C, Hochhaus A, et al. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. N Engl J Med. 2002;346:645–652.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Kantarjian H, Talpaz M, O’Brien S, et al. High-dose imatinib mesylate therapy in newly diagnosed Philadelphia chromosome-positive chronic phase chronic myeloid leukemia. Blood. 2004;103:2873–2878.
   PubMed Web of Science ®Google Scholar
• Cortes J, Talpaz M, O’Brien S, et al. Molecular responses in patients with chronic myelogenous leukemia in chronic phase treated with imatinib mesylate. Clin Cancer Res. 2005;11:3425–3432.
   PubMed Web of Science ®Google Scholar
• Hughes TP, Kaeda J, Branford S, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003;349:1423–1432.
   PubMed Web of Science ®Google Scholar
• Manley PW, Cowan-Jacob SW, Mestan J. Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia. Biochim Biophys Acta. 2005;1754:3–13.
   PubMed Web of Science ®Google Scholar
• Hochhaus A, La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia. 2004;18:1–11.
   PubMed Web of Science ®Google Scholar
• Cowan-Jacob SW, Guez V, Griffin JD, et al. Imatinib (STI571) resistance in chronic myelogenous leukemia: molecular basis of the underlying mechanisms and potential strategies for treatment. Mini Rev Med Chem. 2004;4:285–299.
   PubMed Web of Science ®Google Scholar
• 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(varphi)-LMC GROUP). Leukemia. 2006;20:1061–1066.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Golemovic M, Verstovsek S, Giles F, et al. AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia. Clin Cancer Res. 2005;11:4941–4947.
   PubMed Web of Science ®Google Scholar
• Weisberg E, Manley PW, Breitenstein W, et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell. 2005;7:129–141.
   PubMed Web of Science ®Google Scholar
• Talpaz M, Shah N, Kantarjian HM, et al. Dasatinib in imatinibresistant Philadelphia chromosome-positive leukemias. N Engl J Med. 2006;354:2531–2541.
   PubMed Web of Science ®Google Scholar
• Grafone T, Mancini M, Ottaqviani E, et al. A novel 4-anilino- 3-quinolinecarbonitile dual SRC and ABL kinase inhibitor (SKI-606) has in vitro pro-apoptotic activity on CML Ph blast cells resistant to imatinib. Available at: http://www.parthen-impact.com/cgi-bin/pco/6_05EHA/public/index.cgi?unit+pub_search_results&doem_i.
   Google Scholar
• Kimura S, Naito H, Segawa H, et al. NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinibresistant leukemia. Blood. 2005;106:3948–3954.
   PubMed Web of Science ®Google Scholar
• O’Hare T, Walters DK, Deininger MW, Druker BJ. AMN107: tightening the grip of imatinib. Cancer Cell. 2005;7:117–119.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Weisberg E, Manley P, Mestan J, Cowan-Jacob S, Ray A, Griffin JD. AMN107 (nilotinib): A novel and selective inhibitor Bcr-Abl. Br J Cancer. 2006;7:129–141.
   Google Scholar
• von Bubnoff N, Manley PW, Mestan J, Sanger J, Peschel C, Duyster J. Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107). Blood. 2006;108:1328–1333.
   PubMed Web of Science ®Google Scholar
• Ray A, Cowan-Jacob SW, Manley PW, Mestan J, Griffin JD. Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study. Blood. 2007;109:5011–5015.
   PubMed Web of Science ®Google Scholar
• Weisberg E, Catley L, Wright RD, et al. Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias. Blood. 2007;109:2112–2120.
   PubMed Web of Science ®Google Scholar
• Kantarjian H, Giles F, Wunderle L, et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med. 2006;354:2542–2551.
   PubMed Web of Science ®Google Scholar
• Kantarjian H, Hochhaus A, Bhalla K, et al. Nilotinib in patients with imatinib-resistant or -intolerant chronic myelogenous leukemia in chronic phase (CML-CP): Updated phase II results [abstract]. J Clin Oncol. 2008;26:7010.
   Web of Science ®Google Scholar
• le Coutre P, Apperley J, Ottmann OG, et al. Nilotinib in accelerated phase chronic myelogenous leukemia (CML-AP) patients with imatinibresistance or -intolerance: Update of a phase II study [abstract]. J Clin Oncol. 2008;26:7050.
   Web of Science ®Google Scholar
• Giles F, Kantarjian H, le Coutre P, et al. Nilotinib in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in blast crisis (CML-BC) who are resistant or intolerant to imatinib [abstract]. J Clin Oncol. 2008;26:7017.
   Web of Science ®Google Scholar
• Ottmann OG, Larson RA, Kantarjian HM, et al. Nilotinib in patients (pts) with relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) who are resistant or intolerant to imatinib [abstract]. Blood. 2007;2815.
   Google Scholar
• Jabbour E, le Coutre P, Rosti G, et al. Minimal cross-intolerance between nilotinib and imatinib in patients with imatinib-intolerant chronic myelogenous leukemia (CML) in chronic phase (CP) or accelerated phase (AP) [abstract]. J Clin Oncol. 2008;26:7063.
   Web of Science ®Google Scholar
• Cortes J, Ferrajoli A, Borthakur G, et al. Efficacy of nilotinib (AMN107) in patients (Pts) with newly diagnosed, previously untreated philadelphia chromosome (Ph)- positive chronic myelogenous leukemia in early chronic phase (CML-CP) [abstract]. J Clin Oncol. 2008;26:7016.
   Web of Science ®Google Scholar
• Shah N, Nicoll J, Branford S, et al. Molecular analysis of dasatinib resistance mechanisms in CML patients identifies novel BCR-ABL mutations predicted to retain sensitivity to imatinib: rationale for combination tyrosine kinase inhibitor therapy [abstract]. Blood. 2005;106:318a.
   PubMed Web of Science ®Google Scholar
• Brendel C, Scharenberg C, Dohse M, et al. Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells. Leukemia. 2007;21:1267–1275.
   PubMed Web of Science ®Google Scholar
• White DL, Saunders VA, Dang P, 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. i. 2006;108:697–704.
   Google Scholar
• Jabbour E, Cortes J, Kantarjian H. Dasatinib for the treatment of Philadelphia chromosome-positive leukaemias. Expert Opin Investig Drugs. 2007;16(5):679–687.
   PubMed Web of Science ®Google Scholar
• Talpaz M, Shah NP, Kantarjian H, et al. Dasatinib in imatinibresistant Philadelphia chromosome-positive leukemias. N Engl J Med. 2006;354:2531–2541.
   PubMed Web of Science ®Google Scholar
• O’Hare T, Eide CA, Tyner JW, et al. SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib. Proc Natl Acad Sci U S A. 2008;105:5507–5512.
   PubMed Web of Science ®Google Scholar
• Fiskus W, Pranpat M, Bali P, et al. Combined effects of novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing human leukemia cells. Blood. 2006;108:645–652.
   PubMed Web of Science ®Google Scholar