Erratum: Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells (Journal of Clinical Investigation (2009) 119:5 (1109-1123) DOI: 10.1172/JCI35660);Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells

Journal of Clinical Investigation

Volumn 119, Issue 5, 2009, Pages 1109-1123

  Bellodi, Cristian ^a   Lidonnici, Maria Rosa ^b   Hamilton, Ashley ^c   Helgason, G Vignir ^c   Soliera, Angela Rachele ^b   Ronchetti, Mattia ^b   Galavotti, Sara ^a   Young, Kenneth W ^a   Selmi, Tommaso ^a   Yacobi, Rinat ^d   Van Etten, Richard A ^d   Donato, Nick ^e   Hunter, Ann ^f   Dinsdale, David ^a   Tirrò, Elena ^g   Vigneri, Paolo ^g   Nicotera, Pierluigi ^a   Dyer, Martin J ^a   Holyoake, Tessa ^c   Salomoni, Paolo ^a   Calabretta, Bruno ^b   more..

^a UNIVERSITY OF LEICESTER   (United Kingdom)

^b THOMAS JEFFERSON UNIVERSITY   (United States)

^c UNIVERSITY OF GLASGOW   (United Kingdom)

^d TUFTS MEDICAL CENTER   (United States)

^e UNIVERSITY OF MICHIGAN COMPREHENSIVE CANCER CENTER   (United States)

^f LEICESTER ROYAL INFIRMARY   (United Kingdom)

^g UNIVERSITY OF CATANIA   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; BOSUTINIB; CALCIUM; CHLOROQUINE; DASATINIB; IMATINIB; NILOTINIB; PROTEIN TYROSINE KINASE INHIBITOR; 4 METHYL N (3 (4 METHYLIMIDAZOL 1 YL) 5 (TRIFLUOROMETHYL)PHENYL) 3 ((4 PYRIDIN 3 YLPYRIMIDIN 2 YL)AMINO)BENZAMIDE; 4-METHYL-N-(3-(4-METHYLIMIDAZOL-1-YL)-5-(TRIFLUOROMETHYL)PHENYL)-3-((4-PYRIDIN-3-YLPYRIMIDIN-2-YL)AMINO)BENZAMIDE; ANTINEOPLASTIC AGENT; BAFILOMYCIN A1; DDIT3 PROTEIN, HUMAN; GROWTH ARREST AND DNA DAMAGE INDUCIBLE PROTEIN 153; LIGHT CHAIN 3, HUMAN; MACROLIDE; MICROTUBULE ASSOCIATED PROTEIN; PIPERAZINE DERIVATIVE; PROTEIN KINASE INHIBITOR; PROTEIN TYROSINE KINASE; PYRIMIDINE DERIVATIVE; THIAZOLE DERIVATIVE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; AUTOPHAGY; BLAST CELL CRISIS; CALCIUM CELL LEVEL; CALCIUM DEPLETION; CANCER STEM CELL; CELL DEATH; CELL LINE; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; DRUG POTENTIATION; ENDOPLASMIC RETICULUM STRESS; ENHANCER REGION; HUMAN; HUMAN CELL; MOUSE; MYELOID PROGENITOR CELL; NONHUMAN; PHENOTYPE; PHILADELPHIA CHROMOSOME POSITIVE CELL; PRIORITY JOURNAL; RNA INTERFERENCE; THERAPY EFFECT; ANIMAL; C3H MOUSE; CYTOLOGY; DRUG ANTAGONISM; DRUG EFFECT; DRUG SCREENING; ENDOPLASMIC RETICULUM; GENE EXPRESSION; GENETICS; METABOLISM; PATHOLOGY; PHYSIOLOGY; TUMOR CELL LINE;

ANIMALS; ANTINEOPLASTIC AGENTS; AUTOPHAGY; CALCIUM; CELL DEATH; CELL LINE, TUMOR; CHLOROQUINE; ENDOPLASMIC RETICULUM; FUSION PROTEINS, BCR-ABL; GENE EXPRESSION; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MACROLIDES; MICE; MICE, INBRED C3H; MICROTUBULE-ASSOCIATED PROTEINS; NEOPLASTIC STEM CELLS; PIPERAZINES; PROTEIN KINASE INHIBITORS; PROTEIN-TYROSINE KINASES; PYRIMIDINES; RNA INTERFERENCE; THIAZOLES; TRANSCRIPTION FACTOR CHOP; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 66449122303     PISSN: 00219738     EISSN: 15588238     Source Type: Journal    
DOI: 10.1172/JCI71197     Document Type: Erratum

References (75)

1. Kantarjian, H.M., et al. 1987. Chronic myelogenous leukemia in blast crisis. Analysis of 242 patients. Am. J. Med. 83:445-454.
2. Savage, D.G., Szydlo, R.M., and Goldman, J.M. 1997. Clinical features at diagnosis in 430 patients with chronic myeloid leukaemia seen at a referral centre over a 16-year period. Br. J. Haematol. 96:111-116.
3. Spiers, A.S. 1995. Clinical manifestations of chronic granulocytic leukemia. Semin. Oncol. 22:380-395.
4. Ben-Neriah, Y., Daley, G.Q., Mes-Masson, A.M., Witte, O.N., and Baltimore, D. 1986. The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene. Science. 233:212-214.
5. Cortez, D., Kadlec, L., and Pendergast, A.M. 1995. Structural and signaling requirements for BCRABL-mediated transformation and inhibition of apoptosis. Mol. Cell. Biol. 15:5531-5541.
6. Gordon, M.Y. 1999. Biological consequences of the BCR/ABL fusion gene in humans and mice. J. Clin. Pathol. 52:719-722.
7. Goga, A., McLaughlin, J., Afar, D.E., Saffran, D.C., and Witte, O.N. 1995. Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene. Cell. 82:981-988.
8. Skorski, T., et al. 1995. Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells. Blood. 86:726-736.
9. Vivanco, I., and Sawyers, C.L. 2002. The phosphatidylinositol 3-Kinase AKT pathway in human cancer. Nat. Rev. Cancer. 2:489-501.
10. Sebolt-Leopold, J.S., and Herrera, R. 2004. Targeting the mitogen-activated protein kinase cascade to treat cancer. Nat. Rev. Cancer. 4:937-947.
11. Van Etten, R.A. 2007. Oncogenic signaling: new insights and controversies from chronic myeloid leukemia. J. Exp. Med. 204:461-465.
12. Ottmann, O.G., et al. 2002. A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. Blood. 100:1965-1971.
13. Sawyers, C.L., et al. 2002. Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. Blood. 99:3530-3539.
14. Hofmann, W.K., et al. 2002. Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation. Blood. 99:1860-1862.
15. Branford, S., et al. 2003. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphatebinding loop (P-loop) are associated with a poor prognosis. Blood. 102:276-283.
16. Nardi, V., Azam, M., and Daley, G.Q. 2004. Mechanisms and implications of imatinib resistance mutations in BCR-ABL. Curr. Opin. Hematol. 11:35-43.
17. Deininger, M., Buchdunger, E., and Druker, B.J. 2005. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood. 105:2640-2653.
18. Soverini, S., et al. 2005. ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. J. Clin. Oncol. 23:4100-4109.
19. Graham, S.M., et al. 2002. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood. 99:319-325.
20. Shah, N.P., et al. 2004. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science. 305:399-401.
21. Weisberg, E., et al. 2005. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell. 7:129-141.
22. O'Hare, T., Eide, C.A., and Deininger, M.W. 2007. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood. 110:2242-2249.
23. Jiang, X., et al. 2007. Chronic myeloid leukemia stem cells possess multiple unique features of resistance to BCR-ABL targeted therapies. Leukemia. 21:926-935.
24. Copland, M., et al. 2006. Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood. 107:4532-4539.
25. Jorgensen, H.G., Allan, E.K., Jordanides, N.E., Mountford, J.C., and Holyoake, T.L. 2007. Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells. Blood. 109:4016-4019.
26. Konig, H., et al. 2008. Enhanced BCR-ABL kinase inhibition does not result in increased inhibition of downstream signaling pathways or increased growth suppression in CML progenitors. Leukemia. 22:748-755.
27. Konig, H., Holyoake, T.L., and Bhatia, R. 2008. Effective and selective inhibition of chronic myeloid leukemia primitive hematopoietic progenitors by the dual Src/Abl kinase inhibitor SKI-606. Blood. 111:2329-2338.
28. Kroemer, G., and Jaattela, M. 2005. Lysosomes and autophagy in cell death control. Nat. Rev. Cancer. 5:886-897.
29. Klionsky, D.J. 2007. Autophagy: from phenomenology to molecular understanding in less than a decade. Nat. Rev. Mol. Cell Biol. 8:931-937.
30. Baehrecke, E.H. 2005. Autophagy: dual roles in life and death? Nat. Rev. Mol. Cell Biol. 6:505-510.
31. Kondo, Y., Kanzawa, T., Sawaya, R., and Kondo, S. 2005. The role of autophagy in cancer development and response to therapy. Nat. Rev. Cancer. 5:726-734.
32. Maiuri, M.C., Zalckvar, E., Kimchi, A., and Kroemer, G. 2007. Self-eating and self-killing: crosstalk between autophagy and apoptosis. Nat. Rev. Mol. Cell Biol. 8:741-752.
33. Lum, J.J., et al. 2005. Growth factor regulation of autophagy and cell survival in the absence of apoptosis. Cell. 120:237-248.
34. Maclean, K.H., Dorsey, F.C., Cleveland, J.L., and Kastan, M.B. 2008. Targeting lysosomal degradation induces p53-dependent cell death and prevents cancer in mouse models of lymphomagenesis. J. Clin. Invest. 118:79-88.
35. Lum, J.J., DeBerardinis, R.J., and Thompson, C.B. 2005. Autophagy in metazoans: cell survival in the land of plenty. Nat. Rev. Mol. Cell Biol. 6:439-448.
36. Degenhardt, K., et al. 2006. Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Cancer Cell. 10:51-64.
37. Amaravadi, R.K., et al. 2007. Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma. J. Clin. Invest. 117:326-336.
38. Paglin, S., et al. 2001. A novel response of cancer cells to radiation involves autophagy and formation of acidic vesicles. Cancer Res. 61:439-444.
39. Ito, H., Daido, S., Kanzawa, T., Kondo, S., and Kondo, Y. 2005. Radiation-induced autophagy is associated with LC3 and its inhibition sensitizes malignant glioma cells. Int. J. Oncol. 26:1401-1410.
40. Abedin, M.J., Wang, D., McDonnell, M.A., Lehmann, U., and Kelekar, A. 2007. Autophagy delays apoptotic death in breast cancer cells following DNA damage. Cell Death Differ. 14:500-510.
41. Kanzawa, T., et al. 2004. Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells. Cell Death Differ. 11:448-457.
42. Kanzawa, T., Kondo, Y., Ito, H., Kondo, S., and Ger mano, I. 2003. Induction of autophagic cell death in malignant glioma cells by arsenic trioxide. Cancer Res. 63:2103-2108.
43. Berger, Z., et al. 2006. Rapamycin alleviates toxicity of different aggregate-prone proteins. Hum. Mol. Genet. 15:433-442.
44. Colell, A., et al. 2007. GAPDH and autophagy preserve survival after apoptotic cytochrome c release in the absence of caspase activation. Cell. 129:983-997.
45. Calabretta, B., and Perrotti, D. 2004. The biology of CML blast crisis. Blood. 103:4010-4022.
46. Sharma, S.V., et al. 2006. A common signaling cascade may underlie "addiction" to the Src, BCRABL, and EGF receptor oncogenes. Cancer Cell. 10:425-435.
47. Kabeya, Y., et al. 2004. LC3, GABARAP and GATE16 localize to autophagosomal membrane depending on form-II formation. J. Cell Sci. 117:2805-2812.
48. Kuma, A., Matsui, M., and Mizushima, N. 2007. LC3, an autophagosome marker, can be incorporated into protein aggregates independent of autophagy: caution in the interpretation of LC3 localization. Autophagy. 3:323-328.
49. Fader, C.M., Sanchez, D., Furlan, M., and Colombo, M.I. 2008. Induction of autophagy promotes fusion of multivesicular bodies with autophagic vacuoles in K562 cells. Traffic. 9:230-250.
50. Kerkela, R., et al. 2006. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat. Med. 12:908-916.
51. Tirasophon, W., Welihinda, A.A., and Kaufman, R.J. 1998. A stress response pathway from the endoplasmic reticulum to the nucleus requires a novel bifunctional protein kinase/endoribonuclease (Ire1p) in mammalian cells. Genes Dev. 12:1812-1824.
52. Hoyer-Hansen, M., et al. 2007. Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2. Mol. Cell. 25:193-205.
53. Hoyer-Hansen, M., and Jaattela, M. 2007. Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium. Cell Death Differ. 14:1576-1582.
54. Deming, P.B., et al. 2004. Bcr-Abl-mediated protection from apoptosis downstream of mitochondrial cytochrome c release. Mol. Cell. Biol. 24:10289-10299.
55. Cirinna, M., et al. 2000. Bcl-2 expression restores the leukemogenic potential of a BCR/ABL mutant defective in transformation. Blood. 96:3915-3921.
56. Pattingre, S., and Levine, B. 2006. Bcl-2 inhibition of autophagy: a new route to cancer? Cancer Res. 66:2885-2888.
57. Puttini, M., et al. 2006. In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells. Cancer Res. 66:11314-11322.
58. Wang, Y., et al. 2007. Adaptive secretion of granulocyte-macrophage colony stimulating factor (GMCSF) mediates imatinib and nilotinib resistance in BCR/ABL+ progenitors via JAK-2/STAT-5 pathway activation. Blood. 109:2147-2155.
59. Gorre, M.E., et al. 2001. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 293:876-880.
60. Maekawa, T., Ashihara, E., and Kimura, S. 2007. The Bcr-Abl tyrosine kinase inhibitor imatinib and promising new agents against Philadelphia chromosome-positive leukemias. Int. J. Clin. Oncol. 12:327-340.
61. Donato, N.J., et al. 2003. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood. 101:690-698.
62. Dai, Y., Rahmani, M., Corey, S.J., Dent, P., and Grant, S. 2004. A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2. J. Biol. Chem. 279:34227-34239.
63. Ptasznik, A., Nakata, Y., Kalota, A., Emerson, S.G., and Gewirtz, A.M. 2004. Short interfering RNA (siRNA) targeting the Lyn kinase induces apoptosis in primary, and drug-resistant, BCR-ABL1(+) leukemia cells. Nat. Med. 10:1187-1189.
64. Tokarski, J.S., et al. 2006. The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Cancer Res. 66:5790-5797.
65. Soverini, S., et al. 2007. Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL. Lancet Oncol. 8:273-274.
66. Shah, N.P., et al. 2007. Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency. J. Clin. Invest. 117:2562-2569.
67. Piwocka, K., Vejda, S., Cotter, T.G., O'Sullivan, G.C., and McKenna, S.L. 2006. Bcr-Abl reduces endoplasmic reticulum releasable calcium levels by a Bcl-2-independent mechanism and inhibits calcium-dependent apoptotic signaling. Blood. 107:4003-4010.
68. Law, J.C., Ritke, M.K., Yalowich, J.C., Leder, G.H., and Ferrell, R.E. 1993. Mutational inactivation of the p53 gene in the human erythroid leukemic K562 cell line. Leuk. Res. 17:1045-1050.
69. Ahuja, H., Bar-Eli, M., Advani, S.H., Benchimol, S., and Cline, M.J. 1989. Alterations in the p53 gene and the clonal evolution of the blast crisis of chronic myelocytic leukemia. Proc. Natl. Acad. Sci. U. S. A. 86:6783-6787.
70. Feinstein, E., et al. 1991. p53 in chronic myelogenous leukemia in acute phase. Proc. Natl. Acad. Sci. U. S. A. 88:6293-6297.
71. Carew, J.S., et al. 2007. Targeting autophagy augments the anticancer activity of the histone deacetylase inhibitor SAHA to overcome Bcr-Abl-mediated drug resistance. Blood. 110:313-322.
72. Cain, K., Brown, D.G., Langlais, C., and Cohen, G.M. 1999. Caspase activation involves the formation of the aposome, a large (approximately 700 kDa) caspase-activating complex. J. Biol. Chem. 274:22686-22692.
73. Ferrari-Amorotti, G., et al. 2006. Leukemogenesis induced by wild-type and STI571-resistant BCR/ ABL is potently suppressed by C/EBPalpha. Blood. 108:1353-1362.
74. Bellodi, C., et al. 2006. Cytoplasmic function of mutant promyelocytic leukemia (PML) and PML-retinoic acid receptor-alpha. J. Biol. Chem. 281:14465-14473.
75. Inoue, S., et al. 2004. Histone deacetylase inhibitors potentiate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in lymphoid malignancies. Cell Death Differ. 11(Suppl. 2):S193-S206.