In vitro and in vivo activity of ATP-based kinase inhibitors AP23464 and AP23848 against activation-loop mutants of Kit

Blood

Volumn 106, Issue 1, 2005, Pages 227-234

  Corbin, Amie S ^b   Demehri, Shadmehr ^b   Griswold, Ian J ^b   Wang, Yihan ^b   Metcalf III, Chester A ^b   Sundaramoorthi, Raji ^b   Shakespeare, William C ^b   Snodgrass, Joseph ^b   Wardwell, Scott ^b   Dalgarno, David ^b   Iuliucci, John ^b   Sawyer, Tomi K ^b   Heinrich, Michael C ^b   Druker, Brian J ^b   Deininger, Michael W N ^a  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; AP 23848; COMPLEMENTARY DNA; PROTEIN TYROSINE KINASE INHIBITOR; STAT3 PROTEIN; STEM CELL FACTOR; UNCLASSIFIED DRUG; [4 [2 CYCLOPENTYL 9 (3 HYDROXYPHENETHYL)PURIN 6 YLAMINO]PHENYL]DIMETHYLPHOSPHINE OXIDE;

ACUTE GRANULOCYTIC LEUKEMIA; ANIMAL CELL; APOPTOSIS; ARTICLE; CELL CYCLE; CELL LINE; CELL PROLIFERATION; CHEMICAL STRUCTURE; ENZYME ASSAY; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; NONHUMAN; PRIORITY JOURNAL; SYSTEMIC MASTOCYTOSIS; TUMOR; TUMOR MODEL;

EID: 22044443112     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood-2004-12-4771     Document Type: Article

References (42)

1. Ashman LK. The biology of stem cell factor and its receptor C-kit. Int J Biochem Cell Biol. 1999; 31:1037-1051.
2. Linnekin D. Early signaling pathways activated by c-Kit in hematopoietic cells. Int J Biochem Cell Biol. 1999;31:1053-1074.
3. Heinrich MC, Blanke CD, Druker BJ, Corless CL. Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignancies. J Clin Oncol. 2002;20:1692-1703.
4. Kemmer K, Corless CL, Fletcher JA, et al. KIT mutations are common in testicular seminomas. Am J Pathol. 2004;164:305-313.
5. Mol CD, Dougan DR, Schneider TR, et al. Structural basis for the autoinhibition and STI-57 inhibition of c-Kit tyrosine kinase. J Biol Chem. 2004; 279:31655-31663.
6. Piao X, Paulson R, van der Geer P, Pawson T, Bernstein A. Oncogenic mutation in the Kit receptor tyrosine kinase alters substrate specificity and induces degradation of the protein tyrosine phosphatase SHP-1. Proc Natl Acad Sci U S A. 1996; 93:14665-14669.
7. Moriyama Y, Tsujimura T, Hashimoto K, et al. Role of aspartic acid 814 in the function and expression of c-kit receptor tyrosine kinase. J Biol Chem. 1996;271:3347-3350.
8. Chian R, Young S, Danilkovitch-Miagkova A, et al. Phosphatidylinositol 3 kinase contributes to the transformation of hematopoietic cells by the D816V c-Kit mutant. Blood. 2001;98:1365-1373.
9. Ning ZQ, Li J, Arceci RJ. Signal transducer and activator of transcription 3 activation is required for Asp(816) mutant c-Kit-mediated cytokine-independent survival and proliferation in human leukemia cells. Blood. 2001;97:3559-3567.
10. Ning ZQ, Li J, McGuinness M, Arceci RJ. STAT3 activation is required for Asp816 mutant c-Kit induced tumorigenicity. Oncogene. 2001;20:4528-4536.
11. Longley BJ Jr, Metcalfe DD, Tharp M, et al. Activating and dominant inactivating c-KIT catalytic domain mutations in distinct clinical forms of human mastocytosis. Proc Natl Acad Sci U S A. 1999;96:1609-1614.
12. Pullarkat VA, Pullarkat ST, Calverley DC, Brynes RK. Mast cell disease associated with acute myeloid leukemia: detection of a new c-kit mutation Asp816His. Am J Hematol. 2000;65:307-309.
13. Care RS, Valk PJ, Goodeve AC, et al. Incidence and prognosis of c-KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias. Br J Haematol. 2003;121:775-777.
14. Beghini A, Peterlongo P, Ripamonti CB, et al. C-kit mutations in core binding factor leukemias. Blood. 2000;95:726-727.
15. Casassus P, Caillat-Vigneron N, Martin A, et al. Treatment of adult systemic mastocytosis with interferon-alpha: results of a multicentre phase II trial on 20 patients. Br J Haematol. 2002;119:1090-1097.
16. Kluin-Nelemans HC, Oldhoff JM, Van Doormaal JJ, et al. Cladribine therapy for systemic mastocytosis. Blood. 2003;102:4270-4276.
17. Sawyers CL. Finding the next Gleevec: FLT3 targeted kinase inhibitor therapy for acute myeloid leukemia. Cancer Cell. 2002;1:413-415.
18. Buchdunger E, Cioffi CL, Law N, et al. Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors. J Pharmacol Exp Ther. 2000;295:139-145.
19. Frost MJ, Ferrao PT, Hughes TP, Ashman LK. Juxtamembrane mutant V560GKit is more sensitive to imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant. Mol Cancer Ther. 2002;1:1115-1124.
20. Demetri GD, von Mehren M, Blanke CD, et al. Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. N Engl J Med. 2002;347:472-480.
21. Ma Y, Zeng S, Metcalfe DD, et al. The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors: kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations. Blood. 2002;99:1741-1744.
22. Zermati Y, De Sepulveda P, Feger F, et al. Effect of tyrosine kinase inhibitor STI571 on the kinase activity of wild-type and various mutated c-kit receptors found in mast cell neoplasms. Oncogene. 2003;22:660-664.
23. Pardanani A, Elliott M, Reeder T, et al. Imatinib for systemic mast-cell disease. Lancet. 2003;362: 535-536.
24. Kelly LM, Yu JC, Boulton CL, et al. CT53518, a novel selective FLT3 antagonist for the treatment of acute myelogenous leukemia (AML). Cancer Cell. 2002;1:421-432.
25. DeAngelo DJ, Stone RM, Bruner RJ, et al. Phase I clinical results with MLN518, a novel Flt3 antagonist: tolerability, pharmacokinetics and pharmacodynamics [abstract 219]. Blood. 2003;102:65.
26. Fiedler W, Mesters R, Tinnefeld H, et al. A phase 2 clinical study of SU5416 in patients with refractory acute myeloid leukemia. Blood. 2003;102:2753-2767.
27. Liao AT, Chien MB, Shenoy N, et al. Inhibition of constitutively active forms of mutant kit by multi-targeted indolinone tyrosine kinase inhibitors. Blood. 2002;100:585-593.
28. Corbin AS, Griswold U, La Rosee P, et al. Sensitivity of oncogenic KIT mutants to the kinase inhibitors MLN518 and PD180970. Blood. 2004; 104:3754-3757.
29. O'Hare T, Pollock R, Stoffregen EP, et al. Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML. Blood. 2004;104: 2532-2539.
30. La Rosee P, Corbin AS, Stoffregen EP, Deininger MW, Druker BJ. Activity of the Bcr-Abl kinase inhibtor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571). Cancer Res. 2002;62:7149-7153.
31. Griswold IJ, Shen LJ, LaRosee P, et al. Effects of MLN518, a dual FLT3 and KIT inhibitor, on normal and malignant hematopoiesis. Blood. 2004;104: 2912-2918.
32. Heinrich MC, Griffith DJ, Druker BJ, Wait CL, On KA, Zigler AJ. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000;96:925-932.
33. Shivakrupa R, Bernstein A, Watring N, Linnekin D. Phosphatidylinositol 3′-kinase is required for growth of mast cells expressing the kit catalytic domain mutant. Cancer Res. 2003;63:4412-4419.
34. Casteran N, De Sepulveda P, Beslu N, et al. Signal transduction by several KIT juxtamembrane domain mutations. Oncogens. 2003;22:4710-4722.
35. Duensing A, Medeiros F, McConarty B, et al. Mechanisms of oncogenic KIT signal transduction in primary gastrointestinal stromal tumors (GISTs). Oncogene. 2004;23:3999-4006.
36. Gotoh A, Takahira H, Mantel C, Litz-Jackson S, Boswell HS, Broxmeyer HE. Steel factor induces serine phosphorylation of Stat3 in human growth factor-dependent myeloid cell lines. Blood. 1996;88:138-145.
37. Kamate C, Baloul S, Grootenboer S, et al. Inflammation and cancer, the mastocytoma P815 tumor model revisited: triggering of macrophage activation in vivo with pro-tumorigenic consequences. Int J Cancer. 2002;100:571-579.
38. Lam LP, Chow RY, Berger SA. A transforming mutation enhances the activity of the c-Kit soluble tyrosine kinase domain. Biochem J. 1999;338(Pt 1):131-138.
39. le Coutre P, Mologni L, Cleris L, et al. In vivo eradication of human BCR/ABL-positive leukemia cells with an ABL kinase inhibitor. J Natl Cancer Inst. 1999;91:163-168.
40. Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science. 2004;304:1497-1500.
41. Dancey JE. Predictive factors for epidermal growth factor receptor inhibitors: the bull's-eye hits the arrow. Cancer Cell. 2004;5:411-415.
42. Noble ME, Endicott JA, Johnson LN. Protein kinase inhibitors: insights into drug design from structure. Science. 2004;303:1800-1805.