Regulation of mammalian target of rapamycin and mitogen activated protein kinase pathways by BCR–ABL

References

• Druker BJ. Translation of the Philadelphia chromosome into therapy for CML. Blood 2008;112:4808–4817.
   PubMed Web of Science ®Google Scholar
• Sherbenou DW, Druker BJ. Applying the discovery of the Philadelphia chromosome. J Clin Invest 2007;117:2067–2074.
   PubMed Web of Science ®Google Scholar
• Nowell PC, Hungerford DA. Chromosome studies on normal and leukemic human leukocytes. J Natl Cancer Inst 1960;25:85–109.
   PubMed Web of Science ®Google Scholar
• Stock W. Current treatment options for adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia. Leuk Lymphoma 2010;51:188–198.
   PubMed Web of Science ®Google Scholar
• Soupir CP, Vergilio JA, Dal Cin P, et al. Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis. Am J Clin Pathol 2007;127:642–650.
   PubMed Web of Science ®Google Scholar
• Platanias LC. Map kinase signaling pathways and hematologic malignancies. Blood 2003;101:4667–4679.
   PubMed Web of Science ®Google Scholar
• Morrison DK, Davis RJ. Regulation of MAP kinase signaling modules by scaffold proteins in mammals. Annu Rev Cell Dev Biol 2003;19:91–118.
   PubMed Web of Science ®Google Scholar
• Strniskova M, Barancik M, Ravingerova T. Mitogen-activated protein kinases and their role in regulation of cellular processes. Gen Physiol Biophys 2002;21:231–255.
   PubMed Web of Science ®Google Scholar
• Rincón M, Flavell RA, Davis RJ. Signal transduction by MAP kinases in T lymphocytes. Oncogene 2001;20:2490–2497.
   PubMed Web of Science ®Google Scholar
• Dong C, Davis RJ, Flavell RA. MAP kinases in the immune response. Annu Rev Immunol 2002;20:55–72.
   PubMed Web of Science ®Google Scholar
• Rincón M, Davis RJ. Regulation of the immune response by stress-activated protein kinases. Immunol Rev 2009;228:212–224.
   PubMed Web of Science ®Google Scholar
• Deininger MW, Goldman JM, Melo JV. The molecular biology of chronic myeloid leukemia. Blood 2000;96:3343–3356.
   PubMed Web of Science ®Google Scholar
• Chen KC, Liu WH, Chang LS. Suppression of ERK signaling evokes autocrine Fas-mediated death in arachidonic acid-treated human chronic myeloid leukemia K562 cells. J Cell Physiol 2010;222:625–634.
   PubMed Web of Science ®Google Scholar
• Aceves-Luquero CI, Agarwal A, Callejas-Valera JL, et al. ERK2, but not ERK1, mediates acquired and ‘de novo’ resistance to imatinib mesylate: implication for CML therapy. PLoS One 2009;4:e6124.
   PubMed Web of Science ®Google Scholar
• Coppo P, Dusanter-Fourt I, Vainchenker W, Turhan AG. BCR-ABL induces opposite phenotypes in murine ES cells according to STAT3 activation levels. Cell Signal 2009;21:52–60.
   PubMed Web of Science ®Google Scholar
• McCubrey JA, Steelman LS, Abrams SL, et al. Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy. Leukemia 2008;22:708–722.
   PubMed Web of Science ®Google Scholar
• Liu XY, Yang YF, Wu CT, et al. Spred2 is involved in imatinib-induced cytotoxicity in chronic myeloid leukemia cells. Biochem Biophys Res Commun 2010;393:637–642.
   PubMed Web of Science ®Google Scholar
• McCallum L, Lu W, Price S, Lazar N, Perbal B, Irvine AE. CCN3: a key growth regulator in chronic myeloid leukaemia. J Cell Commun Signal 2009;3:115–124.
   PubMedGoogle Scholar
• Jin A, Kurosu T, Tsuji K, et al. BCR/ABL and IL-3 activate Rap1 to stimulate the B-Raf/MEK/Erk and Akt signaling pathways and to regulate proliferation, apoptosis, and adhesion. Oncogene 2006; 25:4332–4340.
   PubMed Web of Science ®Google Scholar
• Mizuchi D, Kurosu T, Kida A, et al. BCR/ABL activates Rap1 and B-Raf to stimulate the MEK/Erk signaling pathway in hematopoietic cells. Biochem Biophys Res Commun 2005;326:645–651.
   PubMed Web of Science ®Google Scholar
• Yasuda T, Shirakata M, Iwama A, et al. Role of Dok-1 and Dok-2 in myeloid homeostasis and suppression of leukemia. J Exp Med 2004;200:1681–1687.
   PubMed Web of Science ®Google Scholar
• Coppo P, Flamant S, De Mas V, et al. BCR-ABL activates STAT3 via JAK and MEK pathways in human cells. Br J Haematol 2006;134:171–179.
   PubMed Web of Science ®Google Scholar
• Nakamura Y, Yujiri T, Nawata R, Tagami K, Tanizawa Y. MEK kinase 1 is essential for Bcr-Abl-induced STAT3 and self-renewal activity in embryonic stem cells. Oncogene 2005;24:7592–7598.
   PubMed Web of Science ®Google Scholar
• Notari M, Neviani P, Santhanam R, et al. A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation. Blood 2006;107:2507–2516.
   Google Scholar
• Aichberger KJ, Mayerhofer M, Krauth MT, et al. Low-level expression of proapoptotic Bcl-2-interacting mediator in leukemic cells in patients with chronic myeloid leukemia: role of BCR/ABL, characterization of underlying signaling pathways, and reexpression by novel pharmacologic compounds. Cancer Res 2005;65:9436–9444.
   PubMed Web of Science ®Google Scholar
• Aichberger KJ, Mayerhofer M, Krauth MT, et al. Identification of mcl-1 as a BCR/ABL-dependent target in chronic myeloid leukemia (CML): evidence for cooperative antileukemic effects of imatinib and mcl-1 antisense oligonucleotides. Blood 2005;105:3303–3311.
   PubMed Web of Science ®Google Scholar
• Nguyen TK, Rahmani M, Harada H, Dent P, Grant S. MEK1/2 inhibitors sensitize Bcr/Abl+ human leukemia cells to the dual Abl/Src inhibitor BMS-354/825. Blood 2007;109:4006–4015.
   PubMed Web of Science ®Google Scholar
• Suzuki M, Abe A, Imagama S, et al. BCR-ABL-independent and RAS/MAPK pathway-dependent form of imatinib resistance in Ph-positive acute lymphoblastic leukemia cell line with activation of EphB4. Eur J Haematol 2010;84:229–238.
   PubMed Web of Science ®Google Scholar
• Bonhoure E, Lauret A, Barnes DJ, et al. Sphingosine kinase-1 is a downstream regulator of imatinib-induced apoptosis in chronic myeloid leukemia cells. Leukemia 2008;22:971–979.
   PubMed Web of Science ®Google Scholar
• Zhang M, Fu W, Prabhu S, et al. Inhibition of polysome assembly enhances imatinib activity against chronic myelogenous leukemia and overcomes imatinib resistance. Mol Cell Biol 2008;28:6496–6509.
   PubMed Web of Science ®Google Scholar
• Jorgensen HG, Holyoake TL. Characterization of cancer stem cells in chronic myeloid leukaemia. Biochem Soc Trans 2007;35:1347–1351.
   PubMed Web of Science ®Google Scholar
• Nguyen TK, Rahmani M, Gao N, et al. Synergistic interactions between DMAG and mitogen-activated protein kinase kinase 1/2 inhibitors in Bcr/abl+ leukemia cells sensitive and resistant to imatinib mesylate. Clin Cancer Res 2006;12:2239–2247.
   PubMed Web of Science ®Google Scholar
• Yu C, Dasmahapatra G, Dent P, Grant S. Synergistic interactions between MEK1/2 and histone deacetylase inhibitors in BCR/ABL+ human leukemia cells. Leukemia 2005;19:1579–1589.
   PubMed Web of Science ®Google Scholar
• Yu C, Subler M, Rahmani M, et al. Induction of apoptosis in BCR/ABL+ cells by histone deacetylase inhibitors involves reciprocal effects on the RAF/MEK/ERK and JNK pathways. Cancer Biol Ther 2003;2:544–551.
   PubMed Web of Science ®Google Scholar
• Sanchez-Arevalo Lobo VJ, Aceves Luquero CI, Alvarez-Vallina L, et al. Modulation of the p38 MAPK (mitogen-activated protein kinase) pathway through Bcr/Abl: implications in the cellular response to Ara-C. Biochem J 2005;387:231–238.
   PubMed Web of Science ®Google Scholar
• Bandyopadhyay G, Biswas T, Roy KC, et al. Chlorogenic acid inhibits Bcr-Abl tyrosine kinase and triggers p38 mitogen-activated protein kinase-dependent apoptosis in chronic myelogenous leukemic cells. Blood 2004;104:2514–2522.
   PubMed Web of Science ®Google Scholar
• Mayer IA, Verma A, Grumbach IM, et al. The p38 MAPK pathway mediates the growth inhibitory effects of interferon-alpha in BCR-ABL-expressing cells. J Biol Chem 2001;276:28570–28577.
   PubMed Web of Science ®Google Scholar
• Wong S, McLaughlin J, Cheng D, Witte ON. Cell context-specific effects of the BCR-ABL oncogene monitored in hematopoietic progenitors. Blood 2003;101:4088–4097.
   PubMed Web of Science ®Google Scholar
• Korus M, Mahon GM, Cheng L, Whitehead IP. p38 MAPK-mediated activation of NF-kappaB by the RhoGEF domain of Bcr. Oncogene 2002;21:4601–4612.
   PubMed Web of Science ®Google Scholar
• Iotti G, Ferrari-Amorotti G, Rosafio C, et al. Expression of CCL9/MIP-1gamma is repressed by BCR/ABL and its restoration suppresses in vivo leukemogenesis of 32D-BCR/ABL cells. Oncogene 2007;26:3482–3491.
   PubMed Web of Science ®Google Scholar
• Katsoulidis E, Sassano A, Majchrzak-Kita B, et al. Suppression of interferon (IFN)-inducible genes and IFN-mediated functional responses in BCR-ABL-expressing cells. J Biol Chem 2008;283:10793–10803.
   PubMed Web of Science ®Google Scholar
• Parmar S, Katsoulidis E, Verma A, et al. Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells. J Biol Chem 2004;279:25345–25352.
   PubMedGoogle Scholar
• Dumka D, Puri P, Carayol N, et al. Activation of the p38 Map kinase pathway is essential for the antileukemic effects of dasatinib. Leuk Lymphoma 2009;50:2017–2029.
   PubMed Web of Science ®Google Scholar
• Maia V, Sanz M, Gutierrez-Berzal J, et al. C3G silencing enhances STI-571-induced apoptosis in CML cells through p38 MAPK activation, but it antagonizes STI-571 inhibitory effect on survival. Cell Signal 2009;21:1229–1235.
   PubMed Web of Science ®Google Scholar
• Galan-Moya EM, Hernandez-Losa J, Aceves Luquero CI, et al. c-Abl activates p38 MAPK independently of its tyrosine kinase activity: implications in cisplatin-based therapy. Int J Cancer 2008;122:289–297.
   PubMed Web of Science ®Google Scholar
• Carter TA, Wodicka LM, Shah NP, et al. Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases. Proc Natl Acad Sci USA 2005;102:11011–11016.
   PubMed Web of Science ®Google Scholar
• Jacquel A, Colosetti P, Grosso S, et al. Apoptosis and erythroid differentiation triggered by Bcr-Abl inhibitors in CML cell lines are fully distinguishable processes that exhibit different sensitivity to caspase inhibition. Oncogene 2007;26:2445–2458.
   PubMed Web of Science ®Google Scholar
• Merkerova M, Klamova H, Brdicka R, Bruchova H. Targeting of gene expression by siRNA in CML primary cells. Mol Biol Rep 2007;34:27–33.
   PubMed Web of Science ®Google Scholar
• Mancini M, Veljkovic N, Corradi V, et al. 14–3–3 Ligand prevents nuclear import of c-ABL protein in chronic myeloid leukemia. Traffic 2009;10:637–647.
   PubMed Web of Science ®Google Scholar
• Hess P, Pihan G, Sawyers CL, Flavell RA, Davis RJ. Survival signaling mediated by c-Jun NH(2)-terminal kinase in transformed B lymphoblasts. Nat Genet 2002;32:201–205.
   PubMed Web of Science ®Google Scholar
• Hoornaert I, Marynen P, Goris J, Sciot R, Baens M. MAPK phosphatase DUSP16/MKP-7, a candidate tumor suppressor for chromosome region 12p12–13, reduces BCR-ABL-induced transformation. Oncogene 2003;22:7728–7736.
   PubMed Web of Science ®Google Scholar
• Puissant A, Robert G, Fenouille N, et al. Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation. Cancer Res 2010;70:1042–1052.
   PubMed Web of Science ®Google Scholar
• Nica AF, Tsao CC, Watt JC, et al. Ceramide promotes apoptosis in chronic myelogenous leukemia-derived K562 cells by a mechanism involving caspase-8 and JNK. Cell Cycle 2008;7:3362–3370.
   PubMed Web of Science ®Google Scholar
• Mao X, Yu CR, Li WH, Li WX. Induction of apoptosis by shikonin through a ROS/JNK-mediated process in Bcr/Abl-positive chronic myelogenous leukemia (CML) cells. Cell Res 2008;18:879–888.
   PubMed Web of Science ®Google Scholar
• Potin S, Bertoglio J, Bréard J. Involvement of a Rho-ROCK-JNK pathway in arsenic trioxide-induced apoptosis in chronic myelogenous leukemia cells. FEBS Lett 2007;581:118–124.
   PubMed Web of Science ®Google Scholar
• Gingras AC, Raught B, Sonenberg N. Regulation of translation initiation by FRAP/mTOR. Genes Dev 2001;15:807–826.
   PubMed Web of Science ®Google Scholar
• Hay N, Sonenberg N. Upstream and downstream of mTOR. Genes Dev 2004;18:1926–1945.
   PubMed Web of Science ®Google Scholar
• Hay N. The Akt-mTOR tango and its relevance to cancer. Cancer Cell 2005;8:179–183.
   PubMed Web of Science ®Google Scholar
• Platanias LC. Mechanisms of type I and II interferon signaling. Nat Rev Immunol 2005;5: 375–386.
   PubMed Web of Science ®Google Scholar
• Bjornsti MA, Houghton PJ. The TOR pathway: a target for cancer therapy. Nat Rev Cancer 2004;4: 335–348.
   PubMed Web of Science ®Google Scholar
• Fingar DC, Blenis J. Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression. Oncogene 2004;23:3151–3171.
   PubMed Web of Science ®Google Scholar
• Guertin DA, Sabatini DM. Defining the role of mTOR in cancer. Cancer Cell 2007;12:9–22.
   PubMed Web of Science ®Google Scholar
• Altman JK, Platanias LC. Exploiting the mammalian target of rapamycin pathway in hematologic malignancies. Curr Opin Hematol 2008;15:88–94.
   PubMed Web of Science ®Google Scholar
• Kroczynska B, Kaur S, Platanias LC. Growth suppressive cytokines and the AKT/mTOR pathway. Cytokine 2009;48:138–143.
   PubMed Web of Science ®Google Scholar
• Ma XM, Blenis J. Molecular mechanisms of mTOR mediated translational control. Nat Rev Mol Cell Biol 2009;10:307–318.
   PubMed Web of Science ®Google Scholar
• Peng T, Golub TR, Sabatini DM. The immunosuppressant rapamycin mimics a starvation-like signal distinct from amino acid and glucose deprivation. Mol Cell Biol 2002;22:5575–5584.
   PubMed Web of Science ®Google Scholar
• Martelli AM, Nyakern M, Tabellini G, et al. Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia 2006;20:911–928.
   PubMed Web of Science ®Google Scholar
• Martelli AM, Evangelisti C, Chiarini F, Grimaldi C, Manzoli L, McCubrey JA. Targeting the PI3′K/AKT/mTOR signaling network in acute myelogenous leukemia. Expert Opin Investig Drugs 2009;18:1333–1349.
   PubMed Web of Science ®Google Scholar
• Bhaskar PT, Hay N. The two TORCs and Akt. Dev Cell 2007;12:487–502.
   PubMed Web of Science ®Google Scholar
• Kim DH, Sarbassov DD, Ali SM, et al. mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery. Cell 2002;110:163–175.
   PubMed Web of Science ®Google Scholar
• Hoeffer CA, Klann E. mTOR signaling: at the crossroads of plasticity, memory and disease. Trends Neurosci 2010;33:67–75.
   PubMed Web of Science ®Google Scholar
• Long X, Lin Y, Ortiz-Vega S, Yonezawa K, Avruch J. Rheb binds and regulates the mTOR kinase. Curr Biol 2005;15:702–713.
   PubMed Web of Science ®Google Scholar
• Sarbassov DD, Ali SM, Kim DH, et al. Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton. Curr Biol 2004;14:1296–1302.
   PubMed Web of Science ®Google Scholar
• Mayerhofer M, Valent P, Sperr WR, Griffin JD, Sillaber C. BCR/ABL induces expression of vascular endothelial growth factor and its transcriptional activator, hypoxia inducible factor-1alpha, through a pathway involving phosphoinositide 3-kinase and the mammalian target of rapamycin. Blood 2002;100:3767–3775.
   PubMed Web of Science ®Google Scholar
• Mayerhofer M, Aichberger KJ, Florian S, et al. Identification of mTOR as a novel bifunctional target in chronic myeloid leukemia: dissection of growth-inhibitory and VEGF-suppressive effects of rapamycin in leukemic cells. FASEB J 2005;19:960–962.
   PubMed Web of Science ®Google Scholar
• Ly C, Arechiga AF, Melo JV, Walsh CM, Ong ST. Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin. Cancer Res 2003;63:5716–5722.
   PubMed Web of Science ®Google Scholar
• Mohi MG, Boulton C, Gu TL, et al. Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs. Proc Natl Acad Sci USA 2004;101:3130–3135.
   PubMed Web of Science ®Google Scholar
• Parmar S, Smith J, Sassano A, et al. Differential regulation of the p70 S6 kinase pathway by interferon alpha (IFNalpha) and imatinib mesylate (STI571) in chronic myelogenous leukemia cells. Blood 2005;106:2436–2443.
   PubMed Web of Science ®Google Scholar
• Markova B, Albers C, Breitenbuecher F, et al. Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-gamma1-driven activation of mTOR/p70S6-kinase pathway. Oncogene 2010;29:739–751.
   PubMed Web of Science ®Google Scholar
• Kim JH, Chu SC, Gramlich JL, et al. Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen species. Blood 2005;105:1717–1723.
   PubMed Web of Science ®Google Scholar
• Carayol N, Katsoulidis E, Sassano A, Altman JK, Druker BJ, Platanias LC. Suppression of programmed cell death 4 (PDCD4) protein expression by BCR-ABL-regulated engagement of the mTOR/p70 S6 kinase pathway. J Biol Chem 2008;283:8601–8610.
   PubMed Web of Science ®Google Scholar
• Cmarik JL, Min H, Hegamyer G, et al. Differentially expressed protein Pdcd4 inhibits tumor promoter-induced neoplastic transformation. Proc Natl Acad Sci USA 1999;96:14037–14042.
   PubMed Web of Science ®Google Scholar
• Yang HS, Knies JL, Stark C, Colburn N. Pdcd4 suppresses tumor phenotype in JB6 cells by inhibiting AP-1 transactivation. Oncogene 2003;22:3712–3720.
   PubMedGoogle Scholar
• Yang HS, Jansen AP, Komar AA, et al. The transformation suppressor Pdcd4 is a novel eukaryotic translation initiation factor 4A binding protein that inhibits translation. Mol Cell Biol 2003;23:26–37.
   PubMed Web of Science ®Google Scholar
• Yang HS, Cho MH, Zakowicz H, Hegamyer G, Sonenberg N, Colburn NH. A novel function of the MA-3 domains in transformation and translation suppressor Pdcd4 is essential for its binding to eukaryotic translation initiation factor 4A. Mol Cell Biol 2004;24:3894–3906.
   PubMed Web of Science ®Google Scholar
• Dorrello NV, Peschiaroli A, Guardavaccaro D, Colburn NH, Sherman NE, Pagano M. S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth. Science 2006;314:467–471.
   PubMed Web of Science ®Google Scholar
• Sonenberg N, Pause A. Signal transduction. Protein synthesis and oncogenesis meet again. Science 2006;314:428–429.
   PubMed Web of Science ®Google Scholar
• Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development. Leukemia 2005;19:1774–1782.
   PubMed Web of Science ®Google Scholar
• Sillaber C, Mayerhofer M, Bohm A, et al. Evaluation of antileukaemic effects of rapamycin in patients with imatinib-resistant chronic myeloid leukaemia. Eur J Clin Invest 2008;38:43–52.
   PubMed Web of Science ®Google Scholar
• Hirase C, Maeda Y, Takai S, Kanamaru A. Hypersensitivity of Ph-positive lymphoid cell lines to rapamycin: possible clinical application of mTOR inhibitor. Leuk Res 2009;33:450–459.
   PubMed Web of Science ®Google Scholar
• Mancini M, Corradi V, Petta S, Martinelli G, Barbieri E, Santucci MA. mTOR inhibitor RAD001 (everolimus) enhances the effects of imatinib in chronic myeloid leukemia by raising the nuclear expression of c-ABL protein. Leuk Res 2010;34:641–648.
   PubMed Web of Science ®Google Scholar
• Mancini M, Petta S, Martinelli G, Barbieri E, Santucci MA. RAD 001 (everolimus) prevents mTOR and Akt late re-activation in response to imatinib in chronic myeloid leukemia. J Cell Biochem 2010;109:320–328.
   PubMed Web of Science ®Google Scholar
• Weisberg E, Banerji L, Wright RD, et al. Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells. Blood 2008;111:3723–3734.
   PubMed Web of Science ®Google Scholar
• Kharas MG, Janes MR, Scarfone VM, et al. Ablation of PI3K blocks BCR-ABL leukemogenesis in mice, and a dual PI3K/mTOR inhibitor prevents expansion of human BCR-ABL+ leukemia cells. J Clin Invest 2008;118:3038–3050.
   PubMed Web of Science ®Google Scholar
• Janes MR, Limon JJ, So L, et al. Effective and selective targeting of leukemia cells using a TORC1/2 kinase inhibitor. Nat Med 2010;16:205–213.
   PubMed Web of Science ®Google Scholar
• Carayol N, Vakana E, Sassano A, et al. Critical roles for mTORC2 and rapamycin-insensitive mTORC1 complexes in growth and survival of BCR-ABL expressing cells. Proc Natl Acad Sci USA 2010;107:12469–12474.
   PubMed Web of Science ®Google Scholar
• Kantarjian HM, Talpaz M, Giles F, O'Brien S, Cortes J. New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance. Ann Intern Med 2006;145:913–923.
   PubMed Web of Science ®Google Scholar
• Melo JV, Chuah C. Resistance to imatinib mesylate in chronic myeloid leukaemia. Cancer Lett 2007;249:121–132.
   PubMed Web of Science ®Google Scholar