文献リスト

1）Quintas-Cardama A, Cortes J. Molecular biology of bcr-abl1-positive chronic myeloid leukemia. Blood. 2009; 113: 1619-30

2）Van Etten RA. Oncogenic signaling: new insights and controversies from chronic myeloid leukemia. J Exp Med. 2007; 204: 461-5

3）Kantarjian HM, Baccarani M, Jabbour E, et al. Second-generation tyrosine kinase inhibitors: the future of frontline CML therapy. Clin Cancer Res. 2011; 17: 1674-83

4）Mahon FX, Rea D, Guilhot J, et al. Intergroupe Français des Leucemies Myeloides Chroniques. Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial. Lancet Oncol. 2010; 11: 1029-35

5）Ross DM, Branford S, Seymour JF, et al. Patients with chronic myeloid leukemia who maintain a complete molecular response after stopping imatinib treatment have evidence of persistent leukemia by DNA PCR. Leukemia. 2010; 24: 1719-24

6）Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplifi-cation. Science. 2001; 293: 876-80

7）Ernst T, La Rosee P, Muller MC, et al. BCR-ABL mutations in chronic myeloid leukemia. Hematol Oncol Clin North Am. 2011; 25: 997-1008, v-vi

8）OHare 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 resis-tance. Cancer Cell. 2009; 16: 401-12

9）Greenhalgh CJ, Alexander WS. Suppressors of cytokine signalling and regulation of growth hormone action. Growth Horm IGF Res. 2004; 14: 200-6

10）Yoshimura, A. Negative regulation of cytokine signaling. Clin Rev Allergy Immunol. 2005; 28: 205-20

11）Schultheis B, Carapeti-Marootian M, Hochhaus A, et al. Overexpression of SOCS-2 in advanced stages of chronic myeloid leukemia: possible inadequacy of a negative feedback mechanism. Blood. 2002; 99: 1766-75

12）Sakai I, Takeuchi K, Yamauchi H, et al. Constitutive expression of SOCS3 confers resis-tance to IFN-alpha in chronic myelogenous leukemia cells. Blood. 2002; 100: 2926-31

13）Roman-Gomez J, Jimenez-Velasco A, Castillejo JA, et al. The suppressor of cytokine signaling-1 is constitutively expressed in chronic myeloid leukemia and correlates with poor cytogenetic response to interferon-alpha. Haematologica. 2004; 89: 42-8

14）Belloc F, Airiau K, Jeanneteau M, et al. The stem cell factor-c-KIT pathway must be inhibited to enable apoptosis induced by BCR-ABL inhibitors in chronic myelogenous leukemia cells. Leukemia. 2009; 23: 679-85

15）Kuroda J, Taniwaki M. Involvement of BH3-only proteins in hematologic malignancies. Crit Rev Oncol Hematol. 2009; 71: 89-101

16）Kuroda J, Puthalakath H, Cragg MS, et al. Bim and Bad mediate imatinib-induced killing of Bcr/Abl＋ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic. Proc Natl Acad Sci U S A. 2006; 103: 14907-12

17）Kuroda J, Kimura S, Strasser A, et al. Apoptosis-based dual molecular targeting by INNO-406, a second-generation Bcr-Abl inhibitor, and ABT-737, an inhibitor of antiapoptotic Bcl-2 proteins, against Bcr-Abl-positive leukemia. Cell Death Differ. 2007; 14: 1667-77

18）Shah NP, Kasap C, Weier C, et al. Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis. Cancer Cell. 2008; 14: 485-93

19）Belloc F, Moreau-Gaudry F, Uhalde M, et al. Imatinib and nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines. Cancer Biol Ther. 2007; 6: 912-9

20）San Jose-Eneriz E, Agirre X, Jimenez-Velasco A, et al. Epigenetic down-regulation of BIM expression is associated with reduced optimal responses to imatinib treatment in chronic myeloid leukaemia. Eur J Cancer. 2009; 45: 1877-89

21）Ng KP, Hillmer AM, Chuah CT, et al. A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer. Nat Med. 2012; 18: 521-8

22）Salomoni P, Condorelli F, Sweeney SM, et al. Versatility of BCR/ABL-expressing leukemic cells in circumventing proapoptotic BAD effects. Blood. 2000; 96: 676-84

23）Li QF, Huang WR, Duan HF, et al. Sphingosine kinase-1 mediates BCR/ABL-induced upregulation of Mcl-1 in chronic myeloid leukemia cells. Oncogene. 2007; 26: 7904-8

24）Horita M, Andreu EJ, Benito A, et al. Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL. J Exp Med. 2000; 191: 977-84

25）Rabinowitz JD, White, E. Autophagy and metabolism. Science. 2010; 330: 1344-8

26）Lum JJ, Bauer DE, Kong M, et al. Growth factor regulation of autophagy and cell survival in the absence of apoptosis. Cell. 2005; 120: 237-48

27）Kamitsuji Y, Kuroda J, Kimura S, et al. The Bcr-Abl kinase inhibitor INNO-406 induces autophagy and different modes of cell death execution in Bcr-Abl-positive leukemias. Cell Death Differ. 2008; 15: 1712-22

28）Yu Y, Yang L, Zhao M, et al. Targeting microRNA-30a-mediated autophagy enhances imatinib activity against human chronic myeloid leukemia cells. Leukemia. 2012; 26: 1752-60

29）Bellodi C, Lidonnici MR, Hamilton A, et al. Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells. J Clin Invest. 2009; 119: 1109-23

30）Crowley LC, Elzinga BM, OSullivan GC, et al. Autophagy induction by Bcr-Abl-expressing cells facilitates their recovery from a targeted or nontargeted treatment. Am J Hematol. 2011; 86: 38-47

31）Sheng Z, Ma L, Sun JE, et al. BCR-ABL suppresses autophagy through ATF5-mediated regulation of mTOR transcription. Blood. 2011; 118: 2840-8

32）Can G, Ekiz HA, Baran Y. Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells. Hematology. 2011; 16: 95-9

33）Burke BA, Carroll M. BCR-ABL: a multi-faceted promoter of DNA mutation in chronic myeloge-neous leukemia. Leukemia. 2010; 24: 1105-12

34）Skorski T. BCR/ABL, DNA damage and DNA repair: implications for new treatment concepts. Leuk Lymphoma. 2008; 49: 610-4

35）Slupianek A, Poplawski T, Jozwiakowski SK, et al. BCR/ABL stimulates WRN to promote survival and genomic instability. Cancer Res. 2011; 71: 842-51

36）Takeda N, Shibuya M, Maru Y. The BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B protein. Proc Natl Acad Sci U S A. 1999; 96: 203-7

37）Daboussi F, Dumay A, Delacote F, et al. DNA double-strand break repair signalling: the case of RAD51 post-translational regulation. Cell Signal. 2002; 14: 969-75

38）Poplawski T, Blasiak J. BCR/ABL downregulates DNA-PK(CS)-dependent and upregulates backup non-homologous end joining in leukemic cells. Mol Biol Rep. 2010; 37: 2309-15

39）Canitrot Y, Lautier D, Laurent G, et al. Mutator phenotype of BCR-ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA polymerase beta. Oncogene. 1999; 18: 2676-80

40）Nieborowska-Skorska M, Stoklosa T, Datta M, et al. ATR-Chk1 axis protects BCR/ABL leukemia cells from the lethal effect of DNA double-strand breaks. Cell Cycle. 2006; 5: 994-1000

41）Graham SM, Vass JK, Holyoake TL, et al. Transcriptional analysis of quiescent and proliferating CD34＋ human hemopoietic cells from normal and chronic myeloid leukemia sources. Stem Cells. 2007; 25: 3111-20

42）Villuendas R, Steegmann JL, Pollan M, et al. Identification of genes involved in imatinib resistance in CML: a gene-expression profiling approach. Leukemia. 2006; 20: 1047-54

43）Frank O, Brors B, Fabarius A, et al. Gene expression signature of primary imatinib-resistant chronic myeloid leukemia patients. Leukemia. 2006; 20: 1400-7

44）Skorski T. Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state. Leuk Lymphoma. 2011; 52 Suppl 1: 23-9

45）Perrotti D, Jamieson C, Goldman J, et al. Chronic myeloid leukemia: mechanisms of blastic transformation. J Clin Invest. 2010; 120: 2254-64

46）Saglio G, Kim DW, Issaragrisil S, et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med. 2010; 362: 2251-9

47）Kantarjian H, Shah NP, Hochhaus A, et al. Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med. 2010; 362: 2260-70

48）Kim TD, Turkmen S, Schwarz M, et al. Impact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia. Haematologica. 2010; 95: 582-8

49）Ahn JS, Kim YK, Lee SR, et al. Coexisting with clonal evolution and BCR-ABL mutant in CML patients treated with second-generation tyrosine kinase inhibitors predict the discrepancy of in vitro drug sensitivity. Cancer Res Treat. 2010; 42: 37-41

50）Milojkovic D, Nicholson E, Apperley JF, et al. Early prediction of success or failure of treatment with second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukemia. Haematologica. 2010; 95: 224-31

51）Nair RR, Tolentino J, Hazlehurst LA. The bone marrow microenvironment as a sanctuary for minimal residual disease in CML. Biochem Pharmacol. 2010; 80: 602-12

52）Colmone A, Amorim M, Pontier AL, et al. Leukemic cells create bone marrow niches that disrupt the behavior of normal hematopoietic progenitor cells. Science. 2008; 322: 1861-5

53）Ishikawa F, Yoshida S, Saito Y, et al. Chemo-therapy-resistant human AML stem cells home to and engraft within the bone-marrow endosteal region. Nat Biotechnol. 2007; 25: 1315-21

54）Ninomiya M, Abe A, Katsumi A, et al. Homing, proliferation and survival sites of human leukemia cells in vivo in immunodeficient mice. Leukemia. 2007; 21: 136-42

55）Lundell BI, McCarthy JB, Kovach NL, et al. Activation of beta1 integrins on CML progenitors reveals cooperation between beta1 integrins and CD44 in the regulation of adhesion and pro-liferation. Leukemia. 1997; 11: 822-9

56）Damiano JS, Hazlehurst LA, Dalton WS. Cell adhesion-mediated drug resistance (CAM-DR) protects the K562 chronic myelogenous leukemia cell line from apoptosis induced by BCR/ABL inhibition, cytotoxic drugs, and gamma-irradiation. Leukemia. 2001; 15: 1232-9

57）Jin L, Tabe Y, Konoplev S, et al. CXCR4 up-regulation by imatinib induces chronic myelo-genous leukemia (CML) cell migration to bone marrow stroma and promotes survival of quiescent CML cells. Mol Cancer Ther. 2008; 7: 48-58

58）Tabe Y, Jin L, Tsutsumi-Ishii Y, et al. Activation of integrin-linked kinase is a critical prosurvival pathway induced in leukemic cells by bone marrow-derived stromal cells. Cancer Res. 2007; 67: 684-94

59）Bewry NN, Nair RR, Emmons MF, et al. Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistance. Mol Cancer Ther. 2008; 7: 3169-75

60）Wang Y, Cai D, Brendel C, et al. Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL＋ progenitors via JAK-2/STAT-5 pathway activation. Blood. 2007; 109: 2147-55

61）Hazlehurst LA, Argilagos RF, Dalton WS. Beta1 integrin mediated adhesion increases Bim protein degradation and contributes to drug resistance in leukaemia cells. Br J Haematol. 2007; 136: 269-75

62）Yamamoto-Sugitani M, Kuroda J, Ashihara E, et al. Galectin-3 induced by leukemia micro-environment promotes drug resistance and bone marrow lodgment in chronic myelogenous leukemia. Proc Natl Acad Sci U S A. 2011; 108: 17468-73

63）Schmidt T, Kharabi Masouleh B, Loges S, et al. Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+)leukemia. Cancer Cell. 2011; 19: 740-53

64）Takeuchi M, Kimura S, Kuroda J, et al. Glyoxalase-I is a novel target against Bcr-Abl＋ leukemic cells acquiring stem-like characteristics in a hypoxic environment. Cell Death Differ. 2010; 17: 1211-20

65）Giuntoli S, Rovida E, Barbetti V, et al. Hypoxia suppresses BCR/Abl and selects imatinib-insensitive progenitors within clonal CML populations. Leukemia. 2006; 20: 1291-3

66）Tanturli M, Giuntoli S, Barbetti V, et al. Hypoxia selects bortezomib-resistant stem cells of chronic myeloid leukemia. PLoS One. 2011; 6: e17008

67）Desplat V, Faucher JL, Mahon FX, et al. Hypoxia modifies proliferation and differentiation of CD34(+)CML cells. Stem Cells. 2002; 20: 347-54

68）Corbin AS, Agarwal A, Loriaux M, et al. Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. J Clin Invest. 2011; 121: 396-409

69）Copland M, Hamilton A, Elrick LJ, et al. Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood. 2006; 107: 4532-9

70）Chomel JC, Bonnet ML, Sorel N, et al. Leukemic stem cell persistency in chronic myeloid leukemia patients with sustained undetectable molecular residual disease. Blood. 2011; 118: 3657-60

71）Zhao C, Blum J, Chen A, et al. Loss of beta-catenin impairs the renewal of normal and CML stem cells in vivo. Cancer Cell. 2007; 12: 528-41

72）Dierks C, Beigi R, Guo GR, et al. Expansion of Bcr-Abl-positive leukemic stem cells is dependent on Hedgehog pathway activation. Cancer Cell. 2008; 14: 238-49

73）Su W, Meng F, Huang L, et al. Sonic hedgehog maintains survival and growth of chronic myeloid leukemia progenitor cells through β-catenin signaling. Exp Hematol. 2012; 40: 418-27

74）Chen Y, Hu Y, Zhang H, et al. Loss of the Alox5 gene impairs leukemia stem cells and prevents chronic myeloid leukemia. Nat Genet. 2009; 41: 783-92

75）Ito K, Bernardi R, Morotti A, et al. PML targeting eradicates quiescent leukaemia-initiating cells. Nature. 2008; 453: 1072-8

76）Peng C, Chen Y, Yang Z, et al. PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice. Blood. 2010; 115: 626-35

77）Samanta AK, Chakraborty SN, Wang Y, et al. Jak2 inhibition deactivates Lyn kinase through the SET-PP2A-SHP1 pathway, causing apoptosis in drug-resistant cells from chronic myelogenous leukemia patients. Oncogene. 2009; 28: 1669-81

78）Neviani P, Santhanam R, Trotta R, et al. The tumor suppressor PP2A is functionally inacti-vated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein. Cancer Cell. 2005; 8: 355-68

79）White DL, Dang P, Engler J, et al. Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. J Clin Oncol. 2010; 28: 2761-7

80）Engler JR, Frede A, Saunders VA, et al. Chronic myeloid leukemia CD34＋ cells have reduced uptake of imatinib due to low OCT-1 activity. Leukemia. 2010; 24: 765-70

81）Bunting KD. ABC transporters as phenotypic markers and functional regulators of stem cells. Stem Cells. 2002; 20: 11-20

82）Engler JR, Frede A, Saunders V, et al. The poor response to imatinib observed in CML patients with low OCT-1 activity is not attributable to lower uptake of imatinib into their CD34＋ cells. Blood. 2010; 116: 2776-8

83）Minami Y, Abe A, Minami M, et al. Retention of CD34(+)CML stem/progenitor cells during imatinib treatment and rapid decline after treatment with second-generation BCR-ABL inhibitors. Leukemia. 2012; 26: 2142-3

84）Yuan H, Wang Z, Li L, Zhang H, et al. Activation of stress response gene SIRT1 by BCR-ABL promotes leukemogenesis. Blood. 2012; 119: 1904-14

85）Wang Z, Yuan H, Roth M, et al. SIRT1 deacetyl-ase promotes acquisition of genetic mutations for drug resistance in CML cells. Oncogene. 2012, in print

86）Esposito N, Colavita I, Quintarelli C, et al. SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemia. Blood. 2011; 118: 3634-44

87）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: 3409-20

88）Quentmeier H, Eberth S, Romani J, et al. BCR-ABL1-independent PI3 kinase activation causing imatinib-resistance. J Hematol Oncol. 2011; 4: 6-15

89）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: 2211-21

90）Wu J, Meng F, Lu H, et al. Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells. Blood. 2008; 111: 3821-9

91）Dai Y, Rahmani M, Corey SJ, et al. A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2. J Biol Chem. 2004; 279: 34227-39

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