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Mini-Review Article

Computational and Biological Investigations on Abl1 Tyrosine Kinase: A Review

Author(s): Masilamani Elizabeth Sobhia*, G. Siva Kumar, Antara Mallick, Harmanpreet Singh, Kranthi Kumar, Meenakshi Chaurasiya, Monica Singh, Narendra Gera, Sindhuja Deverakonda and Vinay Baghel

Volume 22, Issue 1, 2021

Published on: 13 October, 2020

Page: [38 - 51] Pages: 14

DOI: 10.2174/1389450121999201013152513

Price: $65

Abstract

Abl1 tyrosine kinase is a validated target for the treatment of chronic myeloid leukemia. It is a form of cancer that is difficult to treat and much research is being done to identify new molecular entities and to tackle drug resistance issues. In recent years, drug resistance of Abl1 tyrosine kinase has become a major healthcare concern. Second and third-generation TKI reported better responses against the resistant forms; still they had no impact on long-term survival prolongation. New compounds derived from natural products and organic small molecule inhibitors can lay the foundation for better clinical therapies in the future. Computational methods, experimental and biological studies can help us understand the mechanism of drug resistance and identify novel molecule inhibitors. ADMET parameters analysis of reported drugs and novel small molecule inhibitors can also provide valuable insights. In this review, available therapies, point mutations, structure-activity relationship and ADMET parameters of reported series of Abl1 tyrosine kinase inhibitors and drugs are summarised. We summarise in detail recent computational and molecular biology studies that focus on designing drug molecules, investigation of natural product compounds and organic new chemical entities. Current ongoing research suggests that selective targeting of Abl1 tyrosine kinase at the molecular level to combat drug resistance in chronic myeloid leukemia is promising.

Keywords: Abl1 tyrosine kinase, Chronic myeloid leukemia, ADMET properties, Drug resistance, 3D-QSAR, Molecular docking, Molecular dynamics, Biological inhibitory studies.

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[1]
Abelson HT, Rabstein LS. Lymphosarcoma: virus-induced thymic-independent disease in mice. Cancer Res 1970; 30(8): 2213-22.
[PMID: 4318922]
[2]
Sefton BM, Hunter T, Raschke WC. Evidence that the Abelson virus protein functions in vivo as a protein kinase that phosphorylates tyrosine. Proc Natl Acad Sci USA 1981; 78(3): 1552-6.
[http://dx.doi.org/10.1073/pnas.78.3.1552] [PMID: 6262813]
[3]
Goff SP, Gilboa E, Witte ON, Baltimore D. Structure of the Abelson murine leukemia virus genome and the homologous cellular gene: studies with cloned viral DNA. Cell 1980; 22(3): 777-85.
[http://dx.doi.org/10.1016/0092-8674(80)90554-1] [PMID: 6257398]
[4]
Kruh GD, King CR, Kraus MH, et al. A novel human gene closely related to the abl proto-oncogene. Science 1986; 234(4783): 1545-8.
[http://dx.doi.org/10.1126/science.3787260] [PMID: 3787260]
[5]
Kruh GD, Perego R, Miki T, Aaronson SA. The complete coding sequence of arg defines the Abelson subfamily of cytoplasmic tyrosine kinases. Proc Natl Acad Sci USA 1990; 87(15): 5802-6.
[http://dx.doi.org/10.1073/pnas.87.15.5802] [PMID: 2198571]
[6]
Ben-Neriah Y, Bernards A, Paskind M, Daley GQ, Baltimore D. Alternative 5′ exons in c-abl mRNA. Cell 1986; 44(4): 577-86.
[http://dx.doi.org/10.1016/0092-8674(86)90267-9] [PMID: 3512096]
[7]
Wang JY. The capable ABL: what is its biological function? Mol Cell Biol 2014; 34(7): 1188-97.
[http://dx.doi.org/10.1128/MCB.01454-13] [PMID: 24421390]
[8]
Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001; 344(14): 1031-7.
[http://dx.doi.org/10.1056/NEJM200104053441401] [PMID: 11287972]
[9]
Brahmachari S, Ge P, Lee SH, et al. Activation of tyrosine kinase c-Abl contributes to α-synuclein-induced neurodegeneration. J Clin Invest 2016; 126(8): 2970-88.
[http://dx.doi.org/10.1172/JCI85456] [PMID: 27348587]
[10]
Cancer Stat Facts: Leukemia - Chronic Myeloid Leukemia (CML): National Cancer Institute 2018. Available from: https://seer.cancer.gov/statfacts/html/cmyl.html
[11]
Key Statistics for Chronic Myeloid Leukemia: American Chemical Society 2018. Available from: https://www.cancer.org/cancer/chronic-myeloid-leukemia/about/statistics.html
[12]
Tadwalkar S. The global incidence and prevalence of chronic myeloid leukemia over the next ten years. International Conference on Hematology and Oncology. June 29-July 01, 2017; Bangkok, Thailand. 2017.
[13]
Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2018 update on diagnosis, therapy and monitoring. Am J Hematol 2018; 93(3): 442-59.
[http://dx.doi.org/10.1002/ajh.25011] [PMID: 29411417]
[14]
Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973; 243(5405): 290-3.
[http://dx.doi.org/10.1038/243290a0] [PMID: 4126434]
[15]
Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid cells. Blood 1993; 82(6): 1838-47.
[http://dx.doi.org/10.1182/blood.V82.6.1838.1838] [PMID: 7691239]
[16]
Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med 1996; 183(3): 811-20.
[http://dx.doi.org/10.1084/jem.183.3.811] [PMID: 8642285]
[17]
Esteva A, Kuprel B, Novoa RA, et al. Dermatologist-level classification of skin cancer with deep neural networks. Nature 2017; 542(7639): 115-8.
[http://dx.doi.org/10.1038/nature21056] [PMID: 28117445]
[18]
Hernández SE, Krishnaswami M, Miller AL, Koleske AJ. How do Abl family kinases regulate cell shape and movement? Trends Cell Biol 2004; 14(1): 36-44.
[http://dx.doi.org/10.1016/j.tcb.2003.11.003] [PMID: 14729179]
[19]
Koleske AJ, Gifford AM, Scott ML, et al. Essential roles for the Abl and Arg tyrosine kinases in neurulation. Neuron 1998; 21(6): 1259-72.
[http://dx.doi.org/10.1016/S0896-6273(00)80646-7] [PMID: 9883720]
[20]
Gambacorti-Passerini C, le Coutre P, Mologni L, et al. Inhibition of the ABL kinase activity blocks the proliferation of BCR/ABL+ leukemic cells and induces apoptosis. Blood Cells Mol Dis 1997; 23(3): 380-94.
[http://dx.doi.org/10.1006/bcmd.1997.0155] [PMID: 9446752]
[21]
Pendergast AM. The Abl family kinases: mechanisms of regulation and signaling. Adv Cancer Res 2002; 85: 51-100.
[http://dx.doi.org/10.1016/S0065-230X(02)85003-5] [PMID: 12374288]
[22]
Saglio G, Cilloni D. Abl: the prototype of oncogenic fusion proteins. Cell Mol Life Sci 2004; 61(23): 2897-911.
[http://dx.doi.org/10.1007/s00018-004-4271-0] [PMID: 15583852]
[23]
Buffa P, Manzella L, Consoli ML, Messina A, Vigneri P. Modelling of the ABL and ARG proteins predicts two functionally critical regions that are natively unfolded. Proteins 2007; 67(1): 1-11.
[http://dx.doi.org/10.1002/prot.21161] [PMID: 17211892]
[24]
Hantschel O. Structure, regulation, signaling, and targeting of abl kinases in cancer. Genes Cancer 2012; 3(5-6): 436-46.
[http://dx.doi.org/10.1177/1947601912458584] [PMID: 23226581]
[25]
Dölker N, Górna MW, Sutto L, Torralba AS, Superti-Furga G, Gervasio FL. The SH2 domain regulates c-Abl kinase activation by a cyclin-like mechanism and remodulation of the hinge motion. PLOS Comput Biol 2014; 10(10): e1003863.
[http://dx.doi.org/10.1371/journal.pcbi.1003863] [PMID: 25299346]
[26]
Nagar B, Hantschel O, Seeliger M, et al. Organization of the SH3-SH2 unit in active and inactive forms of the c-Abl tyrosine kinase. Mol Cell 2006; 21(6): 787-98.
[http://dx.doi.org/10.1016/j.molcel.2006.01.035] [PMID: 16543148]
[27]
Weng Z, Rickles RJ, Feng S, et al. Structure-function analysis of SH3 domains: SH3 binding specificity altered by single amino acid substitutions. Mol Cell Biol 1995; 15(10): 5627-34.
[http://dx.doi.org/10.1128/MCB.15.10.5627] [PMID: 7565714]
[28]
Panjarian S, Iacob RE, Chen S, Engen JR, Smithgall TE. Structure and dynamic regulation of Abl kinases. J Biol Chem 2013; 288(8): 5443-50.
[http://dx.doi.org/10.1074/jbc.R112.438382] [PMID: 23316053]
[29]
Nagar B, Hantschel O, Young MA, et al. Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell 2003; 112(6): 859-71.
[http://dx.doi.org/10.1016/S0092-8674(03)00194-6] [PMID: 12654251]
[30]
Imam SZ, Zhou Q, Yamamoto A, et al. Novel regulation of parkin function through c-Abl-mediated tyrosine phosphorylation: implications for Parkinson’s disease. J Neurosci 2011; 31(1): 157-63.
[http://dx.doi.org/10.1523/JNEUROSCI.1833-10.2011] [PMID: 21209200]
[31]
Lonskaya I, Hebron ML, Algarzae NK, Desforges N, Moussa CE. Decreased parkin solubility is associated with impairment of autophagy in the nigrostriatum of sporadic Parkinson’s disease. Neuroscience 2013; 232: 90-105.
[http://dx.doi.org/10.1016/j.neuroscience.2012.12.018] [PMID: 23262240]
[32]
Khatri A, Wang J, Pendergast AM. Multifunctional Abl kinases in health and disease. J Cell Sci 2016; 129(1): 9-16.
[http://dx.doi.org/10.1242/jcs.175521] [PMID: 26729027]
[33]
Gaki GS, Papavassiliou AG. Oxidative stress-induced signaling pathways implicated in the pathogenesis of Parkinson’s disease. Neuromolecular Med 2014; 16(2): 217-30.
[http://dx.doi.org/10.1007/s12017-014-8294-x] [PMID: 24522549]
[34]
Schlatterer SD, Acker CM, Davies P. c-Abl in neurodegenerative disease. J Mol Neurosci 2011; 45(3): 445-52.
[http://dx.doi.org/10.1007/s12031-011-9588-1] [PMID: 21728062]
[35]
Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Grosveld G. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell 1984; 36(1): 93-9.
[http://dx.doi.org/10.1016/0092-8674(84)90077-1] [PMID: 6319012]
[36]
Heisterkamp N, Stam K, Groffen J, de Klein A, Grosveld G. Structural organization of the bcr gene and its role in the Ph’ translocation. Nature 1985; 315(6022): 758-61.
[http://dx.doi.org/10.1038/315758a0] [PMID: 2989703]
[37]
Raponi S, De Propris MS, Wai H, et al. An accurate and rapid flow cytometric diagnosis of BCR-ABL positive acute lymphoblastic leukemia. Haematologica 2009; 94(12): 1767-70.
[http://dx.doi.org/10.3324/haematol.2009.010900] [PMID: 19608682]
[38]
Burton EA, Plattner R, Pendergast AM. Abl tyrosine kinases are required for infection by Shigella flexneri. EMBO J 2003; 22(20): 5471-9.
[http://dx.doi.org/10.1093/emboj/cdg512] [PMID: 14532119]
[39]
Selbach M, Moese S, Hurwitz R, Hauck CR, Meyer TF, Backert S. The Helicobacter pylori CagA protein induces cortactin dephosphorylation and actin rearrangement by c-Src inactivation. EMBO J 2003; 22(3): 515-28.
[http://dx.doi.org/10.1093/emboj/cdg050] [PMID: 12554652]
[40]
Haraga A, Ohlson MB, Miller SI. Salmonellae interplay with host cells. Nat Rev Microbiol 2008; 6(1): 53-66.
[http://dx.doi.org/10.1038/nrmicro1788] [PMID: 18026123]
[41]
Wessler S, Backert S. Abl family of tyrosine kinases and microbial pathogenesis. Int Rev Cell Mol Biol 2011; 286: 271-300.
[http://dx.doi.org/10.1016/B978-0-12-385859-7.00006-9] [PMID: 21199784]
[42]
Wahiduzzaman M, Ota A, Karnan S, et al. Novel combined Ato-C treatment synergistically suppresses proliferation of Bcr-Abl-positive leukemic cells in vitro and in vivo. Cancer Lett 2018; 433: 117-30.
[http://dx.doi.org/10.1016/j.canlet.2018.06.027] [PMID: 29944906]
[43]
Du Y, Wang K, Fang H, et al. Coordination of intrinsic, extrinsic, and endoplasmic reticulum-mediated apoptosis by imatinib mesylate combined with arsenic trioxide in chronic myeloid leukemia. Blood 2006; 107(4): 1582-90.
[http://dx.doi.org/10.1182/blood-2005-06-2318] [PMID: 16249384]
[44]
Porosnicu M, Nimmanapalli R, Nguyen D, Worthington E, Perkins C, Bhalla KN. Co-treatment with As2O3 enhances selective cytotoxic effects of STI-571 against Brc-Abl-positive acute leukemia cells. Leukemia 2001; 15(5): 772-8.
[http://dx.doi.org/10.1038/sj.leu.2402104] [PMID: 11368438]
[45]
de Araujo ED, Manaswiyoungkul P, Erdogan F, et al. A functional in vitro assay for screening inhibitors of STAT5B phosphorylation. J Pharm Biomed Anal 2019; 162: 60-5.
[http://dx.doi.org/10.1016/j.jpba.2018.08.036] [PMID: 30223143]
[46]
Levy DE, Darnell JE Jr. Stats: transcriptional control and biological impact. Nat Rev Mol Cell Biol 2002; 3(9): 651-62.
[http://dx.doi.org/10.1038/nrm909] [PMID: 12209125]
[47]
Gerboth S, Frittoli E, Palamidessi A, et al. Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis. Leukemia 2018; 32(3): 820-7.
[http://dx.doi.org/10.1038/leu.2017.267] [PMID: 28819285]
[48]
Deininger M, Buchdunger E, Druker BJ. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood 2005; 105(7): 2640-53.
[http://dx.doi.org/10.1182/blood-2004-08-3097] [PMID: 15618470]
[49]
Kalmanti L, Saussele S, Lauseker M, et al. Safety and efficacy of imatinib in CML over a period of 10 years: data from the randomized CML-study IV. Leukemia 2015; 29(5): 1123-32.
[http://dx.doi.org/10.1038/leu.2015.36] [PMID: 25676422]
[50]
Rea D. Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia. Ann Hematol 2015; 94(Suppl. 2): S149-58.
[http://dx.doi.org/10.1007/s00277-015-2318-y] [PMID: 25814081]
[51]
Barak AF, Bonstein L, Lauterbach R, Naparstek E, Tavor S. Tyrosine kinase inhibitors induced immune thrombocytopenia in chronic myeloid leukemia? Hematol Rep 2011; 3(3): e29.
[http://dx.doi.org/10.4081/hr.2011.e29] [PMID: 22593820]
[52]
Braun TP, Eide CA, Druker BJ. Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell 2020; 37(4): 530-42.
[http://dx.doi.org/10.1016/j.ccell.2020.03.006] [PMID: 32289275]
[53]
Gambacorti-Passerini C, Antolini L, Mahon FX, et al. Multicenter independent assessment of outcomes in chronic myeloid leukemia patients treated with imatinib. J Natl Cancer Inst 2011; 103(7): 553-61.
[http://dx.doi.org/10.1093/jnci/djr060] [PMID: 21422402]
[54]
Saglio G, Kim DW, Issaragrisil S, et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med 2010; 362(24): 2251-9.
[http://dx.doi.org/10.1056/NEJMoa0912614] [PMID: 20525993]
[55]
Kantarjian HM, Giles F, Gattermann N, 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(10): 3540-6.
[http://dx.doi.org/10.1182/blood-2007-03-080689] [PMID: 17715389]
[56]
Jabbour E, Kantarjian HM, Saglio G, 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(4): 494-500.
[http://dx.doi.org/10.1182/blood-2013-06-511592] [PMID: 24311723]
[57]
Kantarjian HM, Hochhaus A, Saglio G, et al. Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial. Lancet Oncol 2011; 12(9): 841-51.
[http://dx.doi.org/10.1016/S1470-2045(11)70201-7] [PMID: 21856226]
[58]
Shah NP, Tran C, Lee FY, Chen P, Norris D, Sawyers CL. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science 2004; 305(5682): 399-401.
[http://dx.doi.org/10.1126/science.1099480] [PMID: 15256671]
[59]
Hochhaus A, Kantarjian HM, Baccarani M, et al. Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Blood 2007; 109(6): 2303-9.
[http://dx.doi.org/10.1182/blood-2006-09-047266] [PMID: 17138817]
[60]
Talpaz M, Shah NP, Kantarjian H, et al. Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med 2006; 354(24): 2531-41.
[http://dx.doi.org/10.1056/NEJMoa055229] [PMID: 16775234]
[61]
Cortes JE, Saglio G, Kantarjian HM, 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(20): 2333-40.
[http://dx.doi.org/10.1200/JCO.2015.64.8899] [PMID: 27217448]
[62]
Ravandi F, O’Brien SM, Cortes JE, et al. Long-term follow-up of a phase 2 study of chemotherapy plus dasatinib for the initial treatment of patients with Philadelphia chromosome-positive acute lymphoblastic leukemia. Cancer 2015; 121(23): 4158-64.
[http://dx.doi.org/10.1002/cncr.29646] [PMID: 26308885]
[63]
Guignabert C, Phan C, Seferian A, et al. Dasatinib induces lung vascular toxicity and predisposes to pulmonary hypertension. J Clin Invest 2016; 126(9): 3207-18.
[http://dx.doi.org/10.1172/JCI86249] [PMID: 27482885]
[64]
Weatherald J, Chaumais MC, Savale L, et al. Long-term outcomes of dasatinib-induced pulmonary arterial hypertension: a population-based study. Eur Respir J 2017; 50(1): 1700217.
[http://dx.doi.org/10.1183/13993003.00217-2017] [PMID: 28751413]
[65]
Maiti A, Cortes JE, Patel KP, et al. Long-term results of frontline dasatinib in chronic myeloid leukemia. Cancer 2020; 126(7): 1502-11.
[http://dx.doi.org/10.1002/cncr.32627] [PMID: 31999839]
[66]
Shah NP, Rousselot P, Schiffer C, et al. Dasatinib in imatinib-resistant or -intolerant chronic-phase, chronic myeloid leukemia patients: 7-year follow-up of study CA180-034. Am J Hematol 2016; 91(9): 869-74.
[http://dx.doi.org/10.1002/ajh.24423] [PMID: 27192969]
[67]
Koinuma K, Sakairi T, Watanabe Y, et al. A case of long-term dasatinib-induced proteinuria and glomerular injury. CEN Case Rep 2020.
[http://dx.doi.org/10.1007/s13730-020-00484-8] [PMID: 32388829]
[68]
Ochiai S, Sato Y, Minakawa A, Fukuda A, Fujimoto S. Dasatinib-induced nephrotic syndrome in a patient with chronic myelogenous leukemia: a case report. BMC Nephrol 2019; 20(1): 87.
[http://dx.doi.org/10.1186/s12882-019-1273-6] [PMID: 30845905]
[69]
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(3): 469-71.
[http://dx.doi.org/10.1200/JCO.2008.19.8853] [PMID: 19075254]
[70]
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(23): 11314-22.
[http://dx.doi.org/10.1158/0008-5472.CAN-06-1199] [PMID: 17114238]
[71]
Cortes JE, Gambacorti-Passerini C, Deininger MW, et al. Bosutinib versus imatinib for newly diagnosed chronic myeloid leukemia: Results from the randomized BFORE trial. J Clin Oncol 2018; 36(3): 231-7.
[http://dx.doi.org/10.1200/JCO.2017.74.7162] [PMID: 29091516]
[72]
Cortes JE, Kantarjian HM, Brümmendorf TH, 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(17): 4567-76.
[http://dx.doi.org/10.1182/blood-2011-05-355594] [PMID: 21865346]
[73]
Hochhaus A, Gambacorti-Passerini C, Abboud C, et al. Bosutinib for pretreated patients with chronic phase chronic myeloid leukemia: primary results of the phase 4 BYOND study. Leukemia 2020; 34(8): 2125-37.
[http://dx.doi.org/10.1038/s41375-020-0915-9] [PMID: 32572189]
[74]
García-Gutiérrez V, Milojkovic D, Hernandez-Boluda JC, et al. Safety and efficacy of bosutinib in fourth-line therapy of chronic myeloid leukemia patients. Ann Hematol 2019; 98(2): 321-30.
[http://dx.doi.org/10.1007/s00277-018-3507-2] [PMID: 30446802]
[75]
Aghel N, Delgado DH, Lipton JH. Cardiovascular toxicities of BCR-ABL tyrosine kinase inhibitors in chronic myeloid leukemia: preventive strategies and cardiovascular surveillance. Vasc Health Risk Manag 2017; 13: 293-303.
[http://dx.doi.org/10.2147/VHRM.S108874] [PMID: 28831263]
[76]
Cortes JE, Jean Khoury H, Kantarjian H, et al. Long-term evaluation of cardiac and vascular toxicity in patients with Philadelphia chromosome-positive leukemias treated with bosutinib. Am J Hematol 2016; 91(6): 606-16.
[http://dx.doi.org/10.1002/ajh.24360] [PMID: 26971533]
[77]
Gozgit JM, Wong MJ, Wardwell S, et al. Potent activity of ponatinib (AP24534) in models of FLT3-driven acute myeloid leukemia and other hematologic malignancies. Mol Cancer Ther 2011; 10(6): 1028-35.
[http://dx.doi.org/10.1158/1535-7163.MCT-10-1044] [PMID: 21482694]
[78]
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(5): 401-12.
[http://dx.doi.org/10.1016/j.ccr.2009.09.028] [PMID: 19878872]
[79]
Cortes JE, Kim DW, Pinilla-Ibarz J, et al. Ponatinib efficacy and safety in Philadelphia chromosome-positive leukemia: final 5-year results of the phase 2 PACE trial. Blood 2018; 132(4): 393-404.
[http://dx.doi.org/10.1182/blood-2016-09-739086] [PMID: 29567798]
[80]
Lipton JH, Chuah C, Guerci-Bresler A, et al. Ponatinib versus imatinib for newly diagnosed chronic myeloid leukaemia: an international, randomised, open-label, phase 3 trial. Lancet Oncol 2016; 17(5): 612-21.
[http://dx.doi.org/10.1016/S1470-2045(16)00080-2] [PMID: 27083332]
[81]
Cortes JE, Kantarjian H, Shah NP, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med 2012; 367(22): 2075-88.
[http://dx.doi.org/10.1056/NEJMoa1205127] [PMID: 23190221]
[82]
Cortes JE, Kim DW, Pinilla-Ibarz J, et al. A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias. N Engl J Med 2013; 369(19): 1783-96.
[http://dx.doi.org/10.1056/NEJMoa1306494] [PMID: 24180494]
[83]
Gainor JF, Chabner BA. Ponatinib: Accelerated Disapproval. Oncologist 2015; 20(8): 847-8.
[http://dx.doi.org/10.1634/theoncologist.2015-0253] [PMID: 26173838]
[84]
Cortes J, Talpaz M, Smith HP, et al. Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia. Haematologica 2017; 102(3): 519-28.
[http://dx.doi.org/10.3324/haematol.2016.152710] [PMID: 27927766]
[85]
Hughes TP, Mauro MJ, Cortes JE, et al. Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure. N Engl J Med 2019; 381(24): 2315-26.
[http://dx.doi.org/10.1056/NEJMoa1902328] [PMID: 31826340]
[86]
Eskazan AE, Keskin D. Radotinib and its clinical potential in chronic-phase chronic myeloid leukemia patients: an update. Ther Adv Hematol 2017; 8(9): 237-43.
[http://dx.doi.org/10.1177/2040620717719851] [PMID: 29051802]
[87]
Wishart DS, Feunang YD, Guo AC, et al. DrugBank 5.0: a major update to the DrugBank database for 2018. Nucleic Acids Res 2018; 46(D1): D1074-82.
[http://dx.doi.org/10.1093/nar/gkx1037] [PMID: 29126136]
[88]
Nagar B, Bornmann WG, Pellicena P, et al. Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571). Cancer Res 2002; 62(15): 4236-43.
[PMID: 12154025]
[89]
Asaki T, Sugiyama Y, Hamamoto T, et al. Design and synthesis of 3-substituted benzamide derivatives as Bcr-Abl kinase inhibitors. Bioorg Med Chem Lett 2006; 16(5): 1421-5.
[http://dx.doi.org/10.1016/j.bmcl.2005.11.042] [PMID: 16332440]
[90]
Zimmermann J, Caravatti G, Mett H, et al. Phenylamino-pyrimidine (PAP) derivatives: a new class of potent and selective inhibitors of protein kinase C (PKC). Arch Pharm (Weinheim) 1996; 329(7): 371-6.
[http://dx.doi.org/10.1002/ardp.19963290707] [PMID: 8764886]
[91]
Manetti F, Locatelli GA, Maga G, et al. A combination of docking/dynamics simulations and pharmacophoric modeling to discover new dual c-Src/Abl kinase inhibitors. J Med Chem 2006; 49(11): 3278-86.
[http://dx.doi.org/10.1021/jm060236z] [PMID: 16722646]
[92]
Tokarski JS, Newitt JA, Chang CY, et al. The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Cancer Res 2006; 66(11): 5790-7.
[http://dx.doi.org/10.1158/0008-5472.CAN-05-4187] [PMID: 16740718]
[93]
Radi M, Crespan E, Botta G, et al. Discovery and SAR of 1,3,4-thiadiazole derivatives as potent Abl tyrosine kinase inhibitors and cytodifferentiating agents. Bioorg Med Chem Lett 2008; 18(3): 1207-11.
[http://dx.doi.org/10.1016/j.bmcl.2007.11.112] [PMID: 18078752]
[94]
Schindler T, Bornmann W, Pellicena P, Miller WT, Clarkson B, Kuriyan J. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000; 289(5486): 1938-42.
[http://dx.doi.org/10.1126/science.289.5486.1938] [PMID: 10988075]
[95]
Manley PW, Cowan-Jacob SW, Buchdunger E, et al. Imatinib: a selective tyrosine kinase inhibitor. Eur J Cancer 2002; 38(Suppl. 5): S19-27.
[http://dx.doi.org/10.1016/S0959-8049(02)80599-8] [PMID: 12528769]
[96]
Manley PW, Breitenstein W, Brüggen J, et al. Urea derivatives of STI571 as inhibitors of Bcr-Abl and PDGFR kinases. Bioorg Med Chem Lett 2004; 14(23): 5793-7.
[http://dx.doi.org/10.1016/j.bmcl.2004.09.042] [PMID: 15501042]
[97]
O’Hare 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(7): 2242-9.
[http://dx.doi.org/10.1182/blood-2007-03-066936] [PMID: 17496200]
[98]
Razga F, Jurcek T, Zackova D, et al. Role of treatment in the appearance and selection of BCR-ABL1 kinase domain mutations. Mol Diagn Ther 2012; 16(4): 251-9.
[http://dx.doi.org/10.1007/BF03262214] [PMID: 22873741]
[99]
Donato NJ, Wu JY, Stapley J, et al. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood 2003; 101(2): 690-8.
[http://dx.doi.org/10.1182/blood.V101.2.690] [PMID: 12509383]
[100]
Zhou LL, Zhao Y, Ringrose A, et al. AHI-1 interacts with BCR-ABL and modulates BCR-ABL transforming activity and imatinib response of CML stem/progenitor cells. J Exp Med 2008; 205(11): 2657-71.
[http://dx.doi.org/10.1084/jem.20072316] [PMID: 18936234]
[101]
Warsch W, Kollmann K, Eckelhart E, et al. High STAT5 levels mediate imatinib resistance and indicate disease progression in chronic myeloid leukemia. Blood 2011; 117(12): 3409-20.
[http://dx.doi.org/10.1182/blood-2009-10-248211] [PMID: 21220747]
[102]
Gioia R, Leroy C, Drullion C, et al. Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells. Blood 2011; 118(8): 2211-21.
[http://dx.doi.org/10.1182/blood-2010-10-313692] [PMID: 21730355]
[103]
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(2): 117-25.
[http://dx.doi.org/10.1016/S1535-6108(02)00096-X] [PMID: 12204532]
[104]
Redaelli S, Mologni L, Rostagno R, et al. Three novel patient-derived BCR/ABL mutants show different sensitivity to second and third generation tyrosine kinase inhibitors. Am J Hematol 2012; 87(11): E125-8.
[http://dx.doi.org/10.1002/ajh.23338] [PMID: 23044928]
[105]
Chang BH, Willis SG, Stork L, et al. Imatinib resistant BCR-ABL1 mutations at relapse in children with Ph+ ALL: a Children’s Oncology Group (COG) study. Br J Haematol 2012; 157(4): 507-10.
[http://dx.doi.org/10.1111/j.1365-2141.2012.09039.x] [PMID: 22299775]
[106]
Marcé S, Zamora L, Cabezón M, et al. Frequency of ABL gene mutations in chronic myeloid leukemia patients resistant to imatinib and results of treatment switch to second-generation tyrosine kinase inhibitors. Med Clin (Barc) 2013; 141(3): 95-9.
[http://dx.doi.org/10.1016/j.medcli.2012.10.028] [PMID: 23433665]
[107]
Parker WT, Lawrence RM, Ho M, et al. Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after imatinib resistance is predictive of outcome during subsequent therapy. J Clin Oncol 2011; 29(32): 4250-9.
[http://dx.doi.org/10.1200/JCO.2011.35.0934] [PMID: 21990409]
[108]
Khoury HJ, Cortes JE, Kantarjian HM, et al. Bosutinib is active in chronic phase chronic myeloid leukemia after imatinib and dasatinib and/or nilotinib therapy failure. Blood 2012; 119(15): 3403-12.
[http://dx.doi.org/10.1182/blood-2011-11-390120] [PMID: 22371878]
[109]
Quintás-Cardama A, Kantarjian H, O’Brien S, et al. Outcome of patients with chronic myeloid leukemia with multiple ABL1 kinase domain mutations receiving tyrosine kinase inhibitor therapy. Haematologica 2011; 96(6): 918-21.
[http://dx.doi.org/10.3324/haematol.2010.039321] [PMID: 21357704]
[110]
Sakai K, Ishikawa Y, Mori Y, et al. A novel insertion mutation of K294RGG within BCR-ABL kinase domain confers imatinib resistance: sequential analysis of the clonal evolution in a patient with chronic myeloid leukemia in blast crisis. Int J Hematol 2011; 93(2): 237-42.
[http://dx.doi.org/10.1007/s12185-011-0766-2] [PMID: 21264552]
[111]
Jabbour E, Morris V, Kantarjian H, Yin CC, Burton E, Cortes J. Characteristics and outcomes of patients with V299L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors. Blood 2012; 120(16): 3382-3.
[http://dx.doi.org/10.1182/blood-2012-04-424192] [PMID: 23086624]
[112]
Jabbour E, Jones D, Kantarjian HM, et al. Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations. Blood 2009; 114(10): 2037-43.
[http://dx.doi.org/10.1182/blood-2009-01-197715] [PMID: 19567878]
[113]
Press RD, Willis SG, Laudadio J, Mauro MJ, Deininger MW. Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib. Blood 2009; 114(13): 2598-605.
[http://dx.doi.org/10.1182/blood-2008-08-173674] [PMID: 19625707]
[114]
Xu HL, Wang ZJ, Liang XM, et al. In silico identification of novel kinase inhibitors targeting wild-type and T315I mutant ABL1 from FDA-approved drugs. Mol Biosyst 2014; 10(6): 1524-37.
[http://dx.doi.org/10.1039/c3mb70577c] [PMID: 24691568]
[115]
Gibbons DL, Pricl S, Posocco P, et al. Molecular dynamics reveal BCR-ABL1 polymutants as a unique mechanism of resistance to PAN-BCR-ABL1 kinase inhibitor therapy. Proc Natl Acad Sci USA 2014; 111(9): 3550-5.
[http://dx.doi.org/10.1073/pnas.1321173111] [PMID: 24550512]
[116]
Guglielmetti L, Barkane L, Le Dû D, et al. Safety and efficacy of exposure to bedaquiline-delamanid in multidrug-resistant tuberculosis: a case series from France and Latvia. Eur Respir J 2018; 51(3): 1702550.
[http://dx.doi.org/10.1183/13993003.02550-2017] [PMID: 29419439]
[117]
Kamasani S, Akula S, Sivan SK, et al. Computational analysis of ABL kinase mutations allows predicting drug sensitivity against selective kinase inhibitors. Tumour Biol 2017; 39(5): 1010428317701643.
[http://dx.doi.org/10.1177/1010428317701643] [PMID: 28475010]
[118]
Raghi KR, Sherin DR, Saumya MJ, Arun PS, Sobha VN, Manojkumar TK. Computational study of molecular electrostatic potential, docking and dynamics simulations of gallic acid derivatives as ABL inhibitors. Comput Biol Chem 2018; 74: 239-46.
[http://dx.doi.org/10.1016/j.compbiolchem.2018.04.001] [PMID: 29660671]
[119]
Kumar H, Raj U, Gupta S, Varadwaj PK. In-silico identification of inhibitors against mutated BCR-ABL protein of chronic myeloid leukemia: a virtual screening and molecular dynamics simulation study. J Biomol Struct Dyn 2016; 34(10): 2171-83.
[http://dx.doi.org/10.1080/07391102.2015.1110046] [PMID: 26479578]
[120]
Subramanian V, Muhammad SA, Sundaram K, Ravi S. Novel thiadiazole derivatives as Bcr-Abl tyrosine kinase inhibitors. Journal of Applied Pharmaceutical Science 2017; 7(03): 068-76.
[121]
Kanimozi K, Muhammad KA, Kumar R, Ravi S. Synthesis and molecular docking studies of novel phenothiazine chalcone derivatives as T3151 mutated Bcr-Abl kinase inhibitors. J Chem Pharm Res 2016; 9(3): 1139-43.
[122]
Studio D. Version 25. San Diego: Accelrys Inc. 2009.

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