Effective and selective inhibition of chronic myeloid leukemia primitive hematopoietic progenitors by the dual Src/Abl kinase inhibitor SKI-606

Blood

Volumn 111, Issue 4, 2008, Pages 2329-2338

  Konig, Heiko ^a   Holyoake, Tessa L ^b   Bhatia, Ravi ^a  

^a CITY OF HOPE NATIONAL MEDICAL CENTER   (United States)

^b UNIVERSITY OF GLASGOW   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; BOSUTINIB; IMATINIB; PROTEIN TYROSINE KINASE;

APOPTOSIS; ARTICLE; CELL ASSAY; CELL GROWTH; CELL PROLIFERATION; CHRONIC MYELOID LEUKEMIA; ENZYME ACTIVITY; ENZYME INHIBITION; HEMATOPOIETIC STEM CELL; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

EID: 41349083561     PISSN: 00064971     EISSN: 00064971     Source Type: Journal    
DOI: 10.1182/blood-2007-05-092056     Document Type: Article

References (29)

1. Druker BJ, Guilhot F, O'Brien SG, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med. 2006;355:2408-2417.
2. Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001;293:876-880.
3. Thomas J, Wang L, Clark RE, Pirmohamed M. Active transport of imatinib into and out of cells: implications for drug resistance. Blood. 2004;104:3739-3745.
4. Dai Y, Rahmani M, Corey SJ, Dent P, Grant S. 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;279:34227-34239.
5. Donato NJ, Wu JY, Stapley J, et al. Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia. Cancer Res. 2004;64:672-677.
6. Wodarz D. Targeted cancer treatment: resisting arrest. Nat Med. 2006;12:1125-1126.
7. Michor F, Hughes TP, Iwasa Y, et al. Dynamics of chronic myeloid leukaemia. Nature. 2005;435:1267-1270.
8. Bhatia R, Holtz M, Niu N, et al. Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. Blood. 2003;101:4701-4707.
9. Cortes J, O'Brien S, Kantarjian H. Discontinuation of imatinib therapy after achieving a molecular response. Blood. 2004;104:2204-2205.
10. Higashi T, Tsukada J, Kato C, et al. Imatinib mesylate-sensitive blast crisis immediately after discontinuation of imatinib mesylate therapy in chronic myelogenous leukemia: report of two cases. Am J Hematol. 2004;76:275-278.
11. Holtz MS, Slovak ML, Zhang F, Sawyers CL, Forman SJ, Bhatia R. Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation. Blood. 2002;99:3792-3800.
12. Graham SM, Jorgensen HG, Allan E, et al. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood. 2002;99:319-325.
13. Deininger M, Buchdunger E, Druker BJ. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood. 2005;105:2640-2653.
14. Hochhaus A, La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia. 2004;18:1321-1331.
15. Chaturvedi P, Reddy MV, Reddy EP. Src kinases and not JAKs activate STATs during IL-3 induced myeloid cell proliferation. Oncogene. 1998;16:1749-1758.
16. Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S. Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice. Proc Natl Acad Sci U S A. 2006;103:16870-16875.
17. Talpaz M, Shah NP, Kantarjian H, et al. Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med. 2006;354:2531-2541.
18. Manley PW, Cowan-Jacob SW, Mestan J. Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia. Biochim Biophys Acta. 2005;1754:3-13.
19. Boschelli DH, Wu B, Barrios Sosa AC, et al. Identification of 7-phenylaminothieno- [3,2-b]pyridine-6-carbonitriles as a new class of Src kinase inhibitors. J Med Chem. 2004;47:6666-6668.
20. Cortes J, Kantarjian H. New targeted approaches in chronic myeloid leukemia. J Clin Oncol. 2005;23:6316-6324.
21. Martinelli G, Soverini S, Rosti G, Baccarani M. Dual tyrosine kinase inhibitors in chronic myeloid leukemia. Leukemia. 2005;19:1872-1879.
22. Cortes J, Baccarani M, Brummendorf TH, et al. A Phase 1/2 study of SKI-606, a dual inhibitor of Src and Abl kinases, in adult patients with Philadelphia chromosome positive (Ph+) chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) relapsed, refractory or intolerant of imatinib [Abstract]. Blood. 2006;108:168a.
23. Bhatia R, Munthe HA, Williams AD, Zhang F, Forman SJ, Slovak ML. Chronic myelogenous leukemia primitive hematopoietic progenitors demonstrate increased sensitivity to growth factor-induced proliferation and maturation. Exp Hematol. 2000;28:1401-1412.
24. Chu S, Holtz M, Gupta M, Bhatia R. BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells. Blood. 2004;103:3167-3174.
25. Konig H, Modi H, Manley P, Holyoake TH, Forman SJ, Bhatia R. Niltonib inhibits Bcr-Abl kinase activity in CML progenitor cells more effectively than imatinib but is equipotent in inducing growth inhibition [Abstract]. Blood. 2006;108:223a.
26. Owens DM, Keyse SM. Differential regulation of MAP kinase signalling by dual-specificity protein phosphatases. Oncogene. 2007;26:3203-3213.
27. 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;107:4532-4539.
28. Guzman ML, Rossi RM, Karnischky L, et al. The sesquiterpene lactone parthenolide induces apoptosis of human acute myelogenous leukemia stem and progenitor cells. Blood. 2005;105:4163-4169.
29. Copland M, Hamilton A, Allan EK, Melo JV, Holyoake TL. BMS-214662 eliminates CML stem cells and is active against blast crisis CML and cells expressing Bcr-Abl kinase mutations. Blood. 2006;108:739.