Нилотиниб — новый этап успеха в терапии хронического миелолейкоза

хронический миелолейкоз, нилотиниб, иматиниб, ингибиторы тирозинкиназы

1. Druker B.J., Guilhot F, O'Brien S.G. et al.; IRIS Investigators. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med 2006;355(23):2408—17.

2. Matsuo E., Miyazaki Y, Tsutsumi C. et al. Imatinib provides durable molecular and cytogenetic responses in a practical setting for both newly diagnosed and previously treated chronic myelogenous leukemia: a study in nagasaki prefecture, Japan. Int J Hematol 2007;85(2):132—9.

3. Зарицкий А.Ю., Ломайа Э.Г, Виноградова О.Ю. и др. Результаты многоцентрового исследования терапии гливеком больных хроническим миелолейкозом в хронической фазе. Гематол и трансфу-зиол 2007;(2):13—7.

4. Xu Y, Wahner A.E., Nguyen PL. Progression of chronic myeloid leukemia to blast crisis during treatment with ima-tinib mesylate. Arch Pathol Lab Med 2004;128(9):980—5.

5. Lahaye T, Riehm B., Berger U. et al. Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up. Cancer 2005;103(8):1659—69.

6. Alimena G., Breccia M., Latagliata R. et al Sudden blast crisis in patients with Philadelphia chromosome-positive chronic myeloid leukemia who achieved complete cytogenetic remission after imatinib therapy Cancer 2006;107(5):1008—13.

7. O'Brien S.G., Guilhot F, Larson R.A. et al. IRIS nvestigators. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med 2003;348(11): 994—1004.

8. Kantarjian H., Sawyers C., Hochhaus A. et al.; International STI571 CML Study Group. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. N Engl J Med 2002;346(9):645—52.

9. Hochhaus A., La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia 2004;18(8):1321—31.

10. Hochhaus A., Kreil S., Corbin A.S. et al Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy Leukemia 2002;16(11):2190—6.

11. Branford S., Hughes T. Detection of BCR-ABL mutations and resistance to ima-tinib mesylate. Methods Mol Med 2006;125:93—106.

12. Jiang X., Zhao Y., Smith C. et al. Chronic myeloid leukemia stem cells possess multiple unique features of resistance to BCR-ABL targeted therapies. Leukemia 2007;21:926—35.

13. Soverini S., Martinelli G., Rosti G. et al. 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 2005;23(18):4100—9.

14. Nagar B., Bornmann W.G., Pellicena P et al. Crystal structures of the kinase domain of c-abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571). Cancer Res 2002;62(15):4236—43.

15. Weisberg E., Manley P.W., Breitenstein W et al. Characterization of AMN107, a selective inhibitors of wild-type and mutant BCR-ABL. Cancer Cell 2005;7:129—41.

16. O'Hare T., Walters D.K., Stoffregen E.P et al. In vitro activity of BCR-ABL inhibitors AMN-107 and BMS-354825 against clinically relevant imatinib-resistant ABL kinase domain mutants. Cancer Res 2005;65(11):4500—5.

17. Golemovich M., Verstovsek S., Giles F. et al. AMN107, a novel aminopyrimidine inhibitor of BCR-ABL, has an in vitro activity against imatinib-resistant chronic myeloid leukemia. Clin Cancer Res 2005;11(13):4941—7.

18. Stover E.H., Chen J., Lee B.H. et al. The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRp and FIP1L1-PDGFRa in vitro and in vivo. Blood 2005;106(9):3206—13.

19. von Bubnoff N., Gorantla S.H.P, Kancha R.K. et al. The systemic mastocytosis - specific activating c-kit mutation D816V can be inhibited by the tyrosine kinase inhibitor AMN107. Leukemia 2005;19(9):1670—1.

20. Kantarjian H., Giles F, Wunderle L. et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med 2006;354:2542—51.

21. Kantarjian H.M., Giles F., Gattermann N. et al. Nilotinib (formerly AMN107), a highly selective Bcr-Abl tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance. Blood 2007. Aug 22;[Epub ahead of print].

22. Jabbour E., Cortes J. et al. Preliminary activity of nilotinib, a novel selective potent oral BCR-ABL tyrosine kinase inhibitor, in newly diagnosed philadelphia chromosome (Ph)-positive chronic phase chronic myelogenous leukemia (CML-CP). Blood 2006;108(11):abstr 2172.

23. Kantarjian H., O'Brien S., Talpaz M. et al. Outcome of patients with philadelphia positive chronic myelogenous leukemia post-imatinib mesylate failure. Cancer 2007;109:1556—60.

24. Giles F., le Coutre P et al. A phase II study of nilotinib, a novel tyrosine kinase inhibitor administered to patients with ima-tinib resistant or intolerant chronic myelogenous leukemia (CML) in chronic phase (CP), accelerated phase (AP) and blast crisis (BC) who have also failed dasatinib therapy Blood 2006;108(11):abstr 2170.

25. Jabbour E., Jones D. et al. Dynamics of BCR-ABL kinase domain mutations in patients with one, two or three tirosine kinase inhibitors (TKI). Blood 2006;108(11):abstr 750.

26. Quintas-Cardama A., Kantarjian H. et al. Pleural effusion in patients with chronic myelogenous leukemia (CML) treated with dasatinib after imatinibe failure. Blood 2006;108(11):abstr 2164.

27. Quintas-Cardama A., Kantarjian H. et al. Cytopenias in patients (pts) with chronic myelogenous leukemia (CML) treated with dasatinib(sprycel): clinical features and management, including outcome after hematopoietic growth factor therapy Blood 2006;108(11):abstr 2163.

28. Rix U., Hantschel O., Durnberger G. et al. Chemical proteonomic profile of the BCR-ABL inhibitors imatinib, nilotinib and dasatinib revealed novel kinase and nonkinase targets. Blood 2007. Aug 24;[Epub ahead of print].

29. Ray A., Cowan-Jacob S.W., Manley PW. et al. Identification of BCR-ABL point mutations conferring resistance to the abl kinase inhibitor AMN107(Nilotinib) by a random mutagenesis study. Blood 2007;109(11):5011—5.

30. Burges M.R., Skaggs B.J., Shah N.P et al. Comparative analysis of two clinically active BCR-ABLkinase inhibitors reveals the role of conformation-specific binding in resistance. Proc Natl Acad Sci USA 2005;102(9):3395—400.

31. Way Y, Cai D., Brendel C. et al. Adaptive secretion of granulocyte -macrophage colony-stimolating factor (GM-CSF) mediates imatinib and nolotinib resistance in BCR-ABL+ progenitors via Jak-2/STAT-5 pathway activation. Blood 2007:109(5):2147—55.

32. Prenen H., Guetens G., de Boeck G. et al. Cellular uptake of the tyrosine kinase inhibitors imatinib and AMN107 in gastrointestinal stromal tumor cell lines. Pharmacology 2006:77(1):11—6.

33. White D.L., Saunders VA., Dang P et al. OCT-1 mediated influx is a key determinant of the intracellular uptake of ima-tinib but not nilotinib(AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. Blood 2006;196(2):697—704.

34. Weisberg E., Catley L., Wright R.D. et al. Beneficial effects of combining nilo-tinib and imatinib in preclinical models of BCR-ABL+ leukemias. Blood 2007;109(5):2112—20.

35. White D.L., Saunders V.A., Quinn S.R. et al. Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs. Blood 2007;109(8):3609—10.

36. Jordarides N.E., Jorgensen H.G., Holyoake T.L., Mountford J.C. Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate. Blood 2006;108:1370—3.

37. FiskusW., Pranpat M., Bali M. et al. Combined effects of novel tyrosine kinase inhibitor AMN107 and hisotne deacety-lase inhibitor LBH589 against BCR-ABL-expressing human leukemia cells. Blood 2006;108(2):645—52.