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1482 Part X: Malignant Myeloid Diseases Chapter 89: Chronic Myelogenous Leukemia and Related Disorders 1483

527. Michor F, Hughes TP, Iwasa Y, et al: Dynamics of chronic myeloid leukaemia. Nature 555. Carter BZ, Mak DH, Schober WD, et al: Regulation of survivin expression through
435:1267, 2005. Bcr-Abl/MAPK cascade: Targeting survivin overcomes imatinib resistance and
528. Zhang WW, Cortes JE, Yao H, et al: Predictors of primary imatinib resistance in increases imatinib sensitivity in imatinib-responsive CML cells. Blood 107:1555, 2006.
chronic myelogenous leukemia are distinct from those in secondary imatinib resis- 556. Wu J, Meng F, Kong LY, et al: Association between imatinib-resistant BCR-ABL
tance. J Clin Oncol 27:3642, 2009. mutation-negative leukemia and persistent activation of LYN kinase. J Natl Cancer
529. White DL, Saunders VA, Dang P, et al: OCT-1-mediated influx is a key determinant Inst 100:926, 2008.
of the intracellular uptake of imatinib but not nilotinib (AMN107): Reduced OCT-1 557. Hochhaus A, Erben P, Ernst T, Mueller MC: Resistance to targeted therapy in chronic
activity is the cause of low in vitro sensitivity to imatinib. Blood 108:697, 2006. myelogenous leukemia. Semin Hematol 44:S15, 2007.
530. Hiwase DK, Saunders V, Hewett D, et al: Dasatinib cellular uptake and efflux in 558. Feller SM, Tuchscherer G, Voss J: High affinity molecular disruption of GRB2 protein
chronic myeloid leukemia cells: Therapeutic implications. Clin Cancer Res 14:3881, complexes as a therapeutic strategy for chronic myelogenous leukemia. Leuk Lym-
2008. phoma 44:411, 2003.
531. White DL, Dang P, Engler J, et al: Functional activity of the OCT-1 protein is predic- 559. Hochhaus A: Cytogenetic and molecular mechanisms of resistance to imatinib. Semin
tive of long-term outcome in patients with chronic-phase chronic myeloid leukemia Hematol 40:69, 2003.
treated with imatinib. J Clin Oncol 28:2761, 2010. 560. Ohno R, Nakamura Y: Prediction of response to imatinib by cDNA microarray analy-
532. Jordanides NE, Jorgensen HG, Holyoake TL, et al: Functional ABCG2 is overex- sis. Semin Hematol 40:42, 2003.
pressed on primary CML CD34+ cells and is inhibited by imatinib mesylate. Blood 561. Cortes J, Kantarjian H: Beyond dose escalation: Clinical options for relapse or resis-
108:1370, 2006. tance in chronic myelogenous leukemia. J Natl Compr Canc Netw 6 Suppl 2:S22, 2008.
533. Ossard-Receveur A, Bernheim A, Clausse B, et al: Duplication of the Ph-chromosome 562. Soverini S, Hochhaus A, Nicolini FE, et al: BCR-ABL kinase domain mutation analysis
as a possible mechanism of resistance to imatinib mesylate in patients with chronic in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: Rec-
myelogenous leukemia. Cancer Genet Cytogenet 163:189, 2005. ommendations from an expert panel on behalf of European LeukemiaNet. Blood
534. Szych CM, Liesveld JL, Iqbal MA, et al: Isodicentric Philadelphia chromosomes in 118:1208, 2011.
imatinib mesylate (Gleevec)-resistant patients. Cancer Genet Cytogenet 174:132, 563. Jabbour E, Kantarjian HM, Saglio G, et al: Early response with dasatinib or imatinib in
2007. chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASI-
535. Khorashad JS, Kelley TW, Szankasi P, et al: BCR-ABL1 Compound mutations in SION). Blood 123:494, 2014.
tyrosine kinase inhibitor-resistant CML: Frequency and clonal relationships. Blood 564. Martinelli G, Soverini S, Rosti G, Baccarani M: Dual tyrosine kinase inhibitors in
121:489, 2013. chronic myeloid leukemia. Leukemia 19:1872, 2005.
536. Roche-Lestienne C, Preudhomme C: Mutations in the ABL kinase domain pre-exist 565. Kantarjian H, Pasquini R, Hamerschlak N, et al: Dasatinib or high-dose imatinib for
the onset of imatinib treatment. Semin Hematol 21:80, 2003. chronic-phase chronic myeloid leukemia after failure of first-line imatinib: A random-
537. Corbin AS, La Rosee P, Stoffregen EP, et al: Several Bcr-Abl kinase domain mutants ized phase 2 trial. Blood 109:5143, 2007.
associated with imatinib mesylate resistance remain sensitive to imatinib. Blood 566. Porkka K, Koskenvesa P, Lundán T, et al: Dasatinib crosses the blood–brain barrier
101:4611, 2003. and is an efficient therapy for central nervous system Philadelphia chromosome-pos-
538. Khorashad JS, Anand M, Marin D, et al: The presence of a BCR-ABL mutant allele in itive leukemia. Blood 112:1005, 2008.
CML does not always explain clinical resistance to imatinib. Leukemia 20:658, 2006. 567. Shah NP, Guilhot F, Cortes JE, et al: Long-term outcome with dasatinib after ima-
539. Wei Y, Hardling M, Olsson B, et al: Not all imatinib resistance in CML are BCR-ABL tinib failure in chronic-phase chronic myeloid leukemia: Follow-up of a phase 3 study.
kinase domain mutations. Ann Hematol 85:841, 2006. Blood 123:2317, 2014.
540. Soverini S, Colarossi S, Gnani A, et al: Contribution of ABL kinase domain mutations 568. Khoury HJ, Cortes JE, Kantarjian HM, et al: Bosutinib is active in chronic phase
to imatinib resistance in different subsets of Philadelphia-positive patients: By the chronic myeloid leukemia after imatinib and dasatinib and/or nilotinib therapy fail-
GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res 12:7374, ure. Blood 119:343, 2012.
2006. 569. Ibrahim AR, Pallompeis C, Bua M, et al: Efficacy of tyrosine kinase inhibitors (TKIs)
541. Sherbenou DW, Wong MJ, Humayun A, et al: Mutations of the BCR-ABL-kinase as third-line therapy in patients with chronic myeloid leukemia in chronic phase who
domain occur in a minority of patients with stable complete cytogenetic response to have failed 2 prior lines of TKI therapy. Blood 116:5497, 2010.
imatinib. Leukemia 21:489, 2007. 570. Cortes JE, Nicolini FE, Wetzler M, et al: Subcutaneous omacetaxine mepesuccinate
542. Miething C, Mugler C, Grundler R, et al: Phosphorylation of tyrosine 393 in the in patients with chronic-phase chronic myeloid leukemia previously treated with 2 or
kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo. Leuke- more tyrosine kinase inhibitors including Imatinib. Clin Lymphoma Myeloma Leuk
mia 17:1695, 2003. 13:584, 2013.
543. Branford S, Rudzki Z, Walsh S, et al: Detection of BRC-ABL mutations in patients 571. Cortes J, Digumatri R, Parikh PM, et al: Phase 2 study of subcutaneous omacetaxine
with CML treated with imatinib is virtually always accompanied by clinical resistance, mepesuccinate for chronic-phase chronic myeloid leukemia patients resistant to or
and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor intolerant of tyrosine kinase inhibitors. Am J Hematol 88:350, 2013.
prognosis. Blood 102:276, 2003. 572. Sun X, Layton JE, Elefanty A, Lieschke GJ: Comparison of effects of the tyrosine
544. Nicolini FE, Corm S, Lê QH, et al: Mutation status and clinical outcome of 89 imatinib kinase inhibitors AG957, AG490, and STI571 on BCR-ABL-expressing cells, demon-
mesylate-resistant chronic myelogenous leukemia patients: A retrospective analysis strating synergy between AG490 and STI571. Blood 97:2008, 2001.
from the French intergroup of CML (Fi(phi)-LMC GROUP). Leukemia 20:1061, 573. Mohi MG, Boulton C, Gu TL, et al: Combination of rapamycin and protein tyrosine
2006. kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs.
545. Soverini S, De Benedittis C, Machova Polakova K, et al: Unraveling the complexity of Proc Natl Acad Sci U S A 101:3130, 2004.
tyrosine kinase inhibitor-resistant populations by ultra-deep sequencing of the BCR- 574. Gatto S, Scappini B, Pham L, et al: The proteasome inhibitor PS-341 inhibits growth
ABL kinase domain. Blood 122:1634, 2013. and induces apoptosis in Bcr/Abl-positive cell lines sensitive and resistant to imatinib
546. Parker WT, Lawrence RM, Ho M, et al: Sensitive detection of BDR-ABL! Mutations mesylate. Haematologica 88:853, 2003.
in patients with chronic myeloid leukemia after imatinib resistance is predictive of 575. Dai Y, Rahmani M, Pei XY, et al: Bortezomib and flavopiridol interact synergistically
outcome during subsequent therapy. J Clin Oncol 29:4250, 2011. to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate
547. Vainstein V, Eide CA, O’Hare T, et al: Integrating in vitro sensitivity and dose-response through both Bcr/Abl-dependent and -independent mechanisms. Blood 104:509,
slope is predictive of clinical response to ABL kinase inhibitors in chronic myeloid 2004.
leukemia. Blood 122:3331, 2013. 576. Yu C, Rahmani M, Conrad D, et al: The proteasome inhibitor bortezomib interacts
548. Cortes JE, Kim DW, Pinilla-Ibarz J, et al: A phase 2 trial of ponatinib in Philadelphia synergistically with histone deacetylase inhibitors to induce apoptosis in Bcr/Abl+
chromosome-positive leukemias. N Engl J Med 369:1783, 2013. cells sensitive and resistant to STI571. Blood 102:3765, 2003.
549. Khorashad JS, Kelley TW, Szankasi P, et al: BCR-ABL1 compound mutations in 577. Fiskus W, Pranpat M, Bali P, et al: Combined effects of novel tyrosine kinase inhib-
tyrosine kinase inhibitor-resistant CML: Frequency and clonal relationships. Blood itor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing
121;489, 2013. human leukemia cells. Blood 108:645, 2006.
550. Quintás-Cardama A, Cortes J: Therapeutic options against BCR-ABL1 T315I-positive 578. Sawyers CL, Hochhaus A, Feldman E, et al: Imatinib induces hematologic and cytoge-
chronic myelogenous leukemia. Clin Cancer Res 14:4392, 2008. netic responses in patients with chronic myelogenous leukemia in myeloid blast crisis:
551. Jabbour E, Kantarjian H, Jones D, et al: Characteristics and outcomes of patients with Results of a phase II study. Blood 99:3530, 2002.
chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate 579. Gorre ME, Ellwood-Yen K, Chiosis G, et al: BCR-ABL point mutants isolated from
therapy. Blood 112:53, 2008. patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive
552. de Lavallade H, Khorashad JS, Davis HP, et al: Interferon-alpha or homoharringtonine to inhibitors of the BCR-ABL chaperone heat shock protein 90. Blood 100:3041, 2002.
as salvage treatment for chronic myeloid leukemia patients who acquire the T315I 580. Zhao C, Chen A, Jamieson CH, et al: Hedgehog signaling is essential for maintenance
BCR-ABL mutation. Blood 110:2779, 2007. of cancer stem cells in myeloid leukaemia. Nature 458:776, 2009.
553. Jilani I, Kantarjian H, Gorre M, et al: Phosphorylation levels of BCR-ABL, CrkL, AKT 581. Tipping AJ, Mahon FX, Zafirides G, et al: Drug responses of imatinib mesylate-
and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative resistant cells: Synergism of imatinib with other chemotherapeutic drugs. Leukemia
pathway usage as a survival strategy. Leuk Res 32:643, 2008. 16:2349, 2002.
554. Pocaly M, Lagarde V, Etienne G, et al: Overexpression of the heat-shock protein 70 is 582. Tipping AJ, Melo JV: Imatinib mesylate in combination with other hemotherapeutic
associated to imatinib resistance in chronic myeloid leukemia. Leukemia 21:93, 2007. drugs: In vitro studies. Semin Hematol 40:83, 2003.

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