References
- O’Hare T, Deninger MW, Eide CA, et al. Targeting the BCR-ABL signaling pathway in therapy-resistant Philadelphia chromosome-positive leukemia. Clin Cancer Res 2011;17:212–221.
- Chen Y, Fu L. Mechanisms of acquired resistance to tyrosine kinase inhibitors. Acta Pharm Sin B 2011;1:197–207.
- Bixby DL. Managing inadequate responses to frontline treatment of chronic myeloid leukemia:a case-based review. Cancer Treat Rev 2013;39:241–251.
- Milojkovic D, Apperley J. Mechanisms of resistance to imatinib and second-generation tyrosine inhibitors in chronic myeloid leukemia. Clin Cancer Res 2009;15:7519–7527.
- Goldman JM, Melo JV. Chronic myeloid leukemia—advances in biology and new approaches to treatment. N Engl J Med 2003 ; 349:1451–1464.
- Lange T, Park B, Willis SG, et al. BCR-ABL kinase domain mutations in chronic myeloid leukemia not quite enough to cause resistance to imatinib therapy? Cell Cycle 2005;4:1761–1766.
- Agarwal MB, Rathi SA. Will kinase domain mutations dictate the terms. Indian J Med Paediatr Oncol 2013;34:151–153.
- Marin D, Bazeos A, Mahon FX, et al. Adherence is the critical factor for achieving molecular responses in patients with chronic myeloid leukemia who achieve complete cytogenetic responses on imatinib. J Clin Oncol 2010;28:2381–2388.
- Ibrahim AR, Eliasson L, Apperley JF, 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;117:3733–3736.
- Jorgensen HG, Holyoake TL. Characterization of cancer stem cells in chronic myeloid leukaemia. Biochem Soc Trans 2007;35:1347–1351.
- Bhatia R, Holtz M, Niu N, et al. Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. Blood 2003;101:4701–4707.
- Graham SM, Jorgensen HG, Allan E, et al. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood 2002;99:319–325.
- Huang WS, Metcalf CA, Sundaramoorthi R, et al. Discovery of 3-[2-(imidazo[1,2-b]pyridazin-3-yl)ethynyl]-4-methyl-N-{4-[(4-methylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl}benzamide (AP24534), a potent, orally active pan-inhibitor of breakpoint cluster region-abelson (BCR-ABL) kinase including the T315I gatekeeper mutant. J Med Chem 2010;53:4701–4719.
- 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.
- Cortes JE, Kim D-W, Pinilla-Ibarz J, et al. A phase 2 trial of ponatinib in philadelphia chromosome-positive leukemias. N Engl J Med 2013;369:1783–1796.
- National Cancer Institue. FDA approval for ponatinib hydrochloride. Available from: www.cancer.gov/cancertopics/druginfo/fda-ponatinibhydrochloride
- Wetzler M, Segal D. Omacetaxine as an anticancer therapeutic: what is old is new again. Curr Pharm Design 2011;17:59–64.
- National Cancer Institute. FDA approval for omacetaxine mepesuccinate. Available from: www.cancer.gov/cancertopics/druginfo/fda-omacetaxinemepesuccinate
- Quintás-Cardama A, Kantarjian H, Cortes J. Homoharringtonine, omacetaxine mepesuccinate, and chronic myeloid leukemia circa 2009. Cancer 2009:115:5382–5393.
- Yin Y, Sun H, Xu J, et al. Kinesin spindle protein inhibitor SB743921 induces mitotic arrest and apoptosis and overcomes imatinib resistance of chronic myeloid leukemia cells. Leuk Lymphoma 2015;56:1813–1820.
- Sarli V, Giannis A. Targeting the kinesin spindle protein: basic principles and clinical implications. Clin Cancer Res 2008;14: 7583–7587.