Nilotinib as frontline and second-line therapy in chronic myeloid leukemia: Open questions

Critical Reviews in Oncology/Hematology

Volumn 82, Issue 3, 2012, Pages 370-377

  Valent, Peter ^a,b   Gastl, Günther ^c,d   Geissler, Klaus ^e   Greil, Richard ^f   Hantschel, Oliver ^g   Lang, Alois ^a   Linkesch, Werner ^h   Lion, Thomas ^i,j   Petzer, Andreas L ^k   Pittermann, Elisabeth ^l   Pleyer, Lisa ^f   Thaler, Josef ^m   Wolf, Dominik ^c,d  

^a MEDICAL UNIVERSITY OF VIENNA   (Austria)

^b LUDWIG BOLTZMANN INSTITUTE FOR LUNG VASCULAR RESEARCH   (Austria)

^c INNSBRUCK MEDICAL UNIVERSITY   (Austria)

^d TYROLEAN CANCER RESEARCH INSTITUTE   (Austria)

^e Hietzing Hospital   (Austria)

^f PARACELSUS MEDICAL UNIVERSITY   (Austria)

^g ERICH SCHMID INSTITUTE OF MATERIALS SCIENCE   (Austria)

^h MEDICAL UNIVERSITY OF GRAZ   (Austria)

ⁱ Labdia Labordiagnostik   (Austria)

^j CHILDREN'S CANCER RESEARCH INSTITUTE   (Austria)

^k Internal Medicine I: Hematology and Medical Oncology   (Austria)

^l HANUSCH HOSPITAL   (Austria)

^m Hospital Wels Grieskirchen   (Austria)

more..

Author keywords

Adverse events; Arterial occlusive disease; BCR ABL1; Nilotinib

Indexed keywords

BOSUTINIB; DASATINIB; IMATINIB; NILOTINIB;

BILIRUBIN BLOOD LEVEL; CANCER SURVIVAL; CHRONIC MYELOID LEUKEMIA; COMORBIDITY; CYTOPENIA; DRUG APPROVAL; DRUG CONTRAINDICATION; DRUG EFFICACY; DRUG ERUPTION; DRUG MECHANISM; DRUG SAFETY; DRUG TARGETING; GLUCOSE BLOOD LEVEL; HUMAN; INFECTION; PHARMACOLOGICAL BLOCKING; PLEURA EFFUSION; REVIEW; RISK FACTOR; SIDE EFFECT; SURVIVAL RATE; TREATMENT DURATION; TREATMENT RESPONSE; VIRUS REACTIVATION;

ANTINEOPLASTIC AGENTS; CEREBROVASCULAR DISORDERS; CLINICAL TRIALS AS TOPIC; COMORBIDITY; DIABETES MELLITUS; DRUG ADMINISTRATION SCHEDULE; FUSION PROTEINS, BCR-ABL; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; PATIENT SELECTION; PIPERAZINES; PRACTICE GUIDELINES AS TOPIC; PROTEIN KINASE INHIBITORS; PROTEIN-TYROSINE KINASES; PYRIMIDINES; TREATMENT OUTCOME;

EID: 84861194234     PISSN: 10408428     EISSN: 18790461     Source Type: Journal    
DOI: 10.1016/j.critrevonc.2011.08.002     Document Type: Review

References (45)

1. Faderl S., Tapaz M., Estrov Z. The biology of chronic myelogenous leukemia. N Eng J Med 1999, 341:164-172.
2. Sattler M., Griffin J.D. Molecular mechanisms of transformation by the BCR-ABL oncogene. Semin Hematol 2003, 40:4-10.
3. Druker B.J. Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML. Oncogene 2002, 21:8541-8546.
4. O'Brien S.G., Guilhot F., Larson R.A., et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med 2003, 348:994-1004.
5. Gorre M.E., 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.
6. Druker B.J., Guilhot F., O'Brien S.G., et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med 2006, 355:2408-2417.
7. Martinelli G., Soverini S., Rosti G., Cilloni D., Baccarani M. New tyrosine kinase inhibitors in chronic myeloid leukemia. Haematologica 2005, 90:534-541.
8. Deininger M.W. Optimizing therapy of chronic myeloid leukemia. Exp Hematol 2007, 35:144-154.
9. Valent P. Emerging stem cell concepts for imatinib-resistant CML: implications for the biology, management, and therapy of the disease. Br J Haematol 2008, 36:1244-1253.
10. Goldman J.M. How I treat chronic myeloid leukemia in the imatinib era. Blood 2007, 110(8):2828-2837.
11. Saglio G., Ulisciani S., Bosa M., Cilloni D., Rege-Cambrin G. New therapeutic approaches and prognostic factors in chronic myeloid leukemia. Leuk Lymphoma 2008, 49:625-628.
12. Cortes J., Kantarjian H. Beyond dose escalation: clinical options for relapse or resistance in chronic myelogenous leukemia. J Natl Compr Canc Netw 2008, 6:S22-S30.
13. Weisberg E., Manley P.W., Breitenstein W., et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell 2005, 7:129-141.
14. O'Hare T., Walters D.K., Deininger M.W., Druker B.J. AMN107: tightening the grip of imatinib. Cancer Cell 2005, 7:117-119.
15. Kantarjian H., Giles F., Wunderle L., et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med 2006, 354:2542-2551.
16. Rosti G., Castagnetti F., Gugliotta G., Palandri F., Martinelli G., Baccarani M. Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'. Leuk Lymphoma 2010, 51:583-591.
17. Rosti G., Palandri F., Castagnetti F., et al. Nilotinib for the frontline treatment of Ph(+) chronic myeloid leukemia. Blood 2009, 114:4933-4938.
18. Saglio G., Kim D.W., Issaragrisil S., et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med 2010, 362:2251-2259.
19. Giles F.J., Rosti G., Beris P., et al. Nilotinib is superior to imatinib as first-line therapy of chronic myeloid leukemia: the ENESTnd study. Expert Rev Hematol 2010, 3:665-673.
20. Rosti G, Castagnetti F, Gugliotta G, Palandri F, Baccarani M. Second-generation BCR-ABL inhibitors for frontline treatment of chronic myeloid leukemia in chronic phase. Crit Rev Oncol Hematol; in press, doi:10.1016/j.critrevonc.2011.04.002.
21. Rix U., Hantschel O., Dürnberger G., et al. Chemical proteomic profiling of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal different interaction networks and novel kinase and non-kinase targets. Blood 2007, 110:4055-4063.
22. Manley P.W., Drueckes P., Fendrich G., et al. Extended kinase profile and properties of the protein kinase inhibitor nilotinib. Biochim Biophys Acta 2010, 1804(3):445-453.
23. Breccia M., Muscaritoli M., Gentilini F., et al. Impaired fasting glucose level as metabolic side effect of nilotinib in non-diabetic chronic myeloid leukemia patients resistant to imatinib. Leuk Res 2007, 31:1770-1772.
24. Aichberger K.J., Herndlhofer S., Schernthaner G.H., et al. Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML. Am J Hematol 2011, 86:533-539.
25. le Coutre P, Rea D, Abruzzese E, et al. Severe peripheral arterial disease during nilotinib therapy. J Natl Cancer Inst; in press.
26. 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, 23:679-685.
27. Pittoni P., Piconese S., Tripodo C., Colombo M.P. Tumor-intrinsic and -extrinsic roles of c-Kit: mast cells as the primary off-target of tyrosine kinase inhibitors. Oncogene 2010, 30:757-769.
28. Sillaber C., Baghestanian M., Bevec D., et al. The mast cell as site of tissue-type plasminogen activator expression and fibrinolysis. J Immunol 1999, 162(2):1032-1041.
29. Valent P., Baghestanian M., Bankl H.C., et al. New aspects in thrombosis research: possible role of mast cells as profibrinolytic and antithrombotic cells. Thromb Haemost 2002, 87(5):786-790.
30. Day E., Waters B., Spiegel K., et al. Inhibition of collagen-induced discoidin domain receptor 1 and 2 activation by imatinib, nilotinib and dasatinib. Eur J Pharmacol 2008, 599(1-3):44-53.
31. DDR1 distribution profile in various cell systems and cell types available at: http://biogps.gnf.org/.
32. Ferri N., Carragher N.O., Raines E.W. Role of discoidin domain receptors 1 and 2 in human smooth muscle cell-mediated collagen remodeling: potential implications in atherosclerosis and lymphangioleiomyomatosis. Am J Pathol 2004, 164(5):1575-1585.
33. Franco C., Hou G., Ahmad P.J., et al. Discoidin domain receptor 1 (ddr1) deletion decreases atherosclerosis by accelerating matrix accumulation and reducing inflammation in low-density lipoprotein receptor-deficient mice. Circ Res 2008, 102(10):1202-1211.
34. Franco C., Britto K., Wong E., et al. Discoidin domain receptor 1 on bone marrow-derived cells promotes macrophage accumulation during atherogenesis. Circ Res 2009, 105(11):1141-1148.
35. Franco C., Ahmad P.J., Hou G., Wong E., Bendeck M.P. Increased cell and matrix accumulation during atherogenesis in mice with vessel wall-specific deletion of discoidin domain receptor 1. Circ Res 2010, 106(11):1775-1783.
36. Hughes T.P., Hochhaus A., Saglio G., et al. ENESTnd Update: continued superiority of nilotinib versus imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP). Blood 2010, 116:94-95.
37. Baccarani M., Saglio G., Goldman J., et al. European LeukemiaNet. Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet. Blood 2006, 108(6):1809-1820.
38. Baccarani M., Cortes J., Pane F., et al. European LeukemiaNet. Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet. J Clin Oncol 2009, 27(35):6041-6051.
39. Stein B., Smith B.D. Treatment options for patients with chronic myeloid leukemia who are resistant to or unable to tolerate imatinib. Clin Ther 2010, 32(5):804-820.
40. Lassila M., Allen T.J., Cao Z., et al. Imatinib attenuates diabetes-associated atherosclerosis. Arterioscler Thromb Vasc Biol 2004, 24(5):935-942.
41. Breccia M., Alimena G. The significance of early, major and stable molecular responses in chronic myeloid leukemia in the imatinib era. Crit Rev Oncol Hematol 2011, 79(2):135-143.
42. Barnes D.J., Melo J.V. Primitive, quiescent and difficult to kill: the role of non-proliferating stem cells in chronic myeloid leukemia. Cell Cycle 2006, 5(24):2862-2866.
43. 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(5):926-935.
44. Rousselot P., Huguet F., Rea D., et al. Imatinib mesylate discontinuation in patients with chronic myelogenous leukemia in complete molecular remission for more than 2 years. Blood 2007, 109(1):58-60.
45. Mahon F.X., Réa D., Guilhot J., et al. Intergroupe Français des Leucémies Myéloïdes 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(11):1029-1035.