Impact of early dose intensity on cytogenetic and molecular responses in chronicphase CMLpatients receiving 600 mg/day of imatinib as initial therapy

Blood

Volumn 112, Issue 10, 2008, Pages 3965-3973

  Hughes, Timothy P ^a,b   Branford, Susan ^a,b   White, Deborah L ^a,b   Reynolds, John ^b   Koelmeyer, Rachel ^b   Seymour, John F ^b   Taylor, Kerry ^b   Arthur, Chris ^b   Schwarer, Anthony ^b   Morton, James ^b   Cooney, Julian ^b   Leahy, Michael F ^b   Rowlings, Philip ^b   Catalano, John ^b   Hertzberg, Mark ^b   Filshie, Robin ^b   Mills, Anthony K ^b   Fay, Keith ^b   Durrant, Simon ^b   Januszewicz, Henry ^b   Joske, David ^b   Underhill, Craig ^b   Dunkley, Scott ^b   Lynch, Kevin ^c   Grigg, Andrew ^b   more..

^a INSTITUTE OF MEDICAL AND VETERINARY SCIENCE   (Australia)

^b Australasian Leukaemia and Lymphoma Group   (Australia)

^c Novartis Pharmaceuticals Australia Ltd   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; CYTARABINE; IMATINIB; ANTINEOPLASTIC AGENT; PIPERAZINE DERIVATIVE; PYRIMIDINE DERIVATIVE;

ADULT; AGED; ANEMIA; ARTHRALGIA; ARTICLE; BLEEDING; CANCER COMBINATION CHEMOTHERAPY; CHRONIC MYELOID LEUKEMIA; COMPARATIVE STUDY; CYTOGENETICS; DIARRHEA; DISEASE SEVERITY; DOSE RESPONSE; DRUG DOSE ESCALATION; DRUG TOLERABILITY; DRUG WITHDRAWAL; EDEMA; FATIGUE; FEBRILE NEUTROPENIA; FEMALE; FLUID RETENTION; HUMAN; INCIDENCE; MAJOR CLINICAL STUDY; MALE; MULTIPLE CYCLE TREATMENT; MUSCLE CRAMP; MYALGIA; NAUSEA AND VOMITING; NEUTROPENIA; PATIENT MONITORING; PRIORITY JOURNAL; RASH; SIDE EFFECT; THROMBOCYTOPENIA; ADOLESCENT; CLINICAL TRIAL; METABOLISM; MIDDLE AGED; TIME;

ADOLESCENT; ADULT; AGED; ANTINEOPLASTIC AGENTS; DOSE-RESPONSE RELATIONSHIP, DRUG; FEMALE; FUSION PROTEINS, BCR-ABL; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MALE; MIDDLE AGED; PIPERAZINES; PYRIMIDINES; TIME FACTORS;

EID: 58149160055     PISSN: 00064971     EISSN: 15280020     Source Type: Journal    
DOI: 10.1182/blood-2008-06-161737     Document Type: Article

References (45)

1. Druker BJ, Lydon NB. Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia. J Clin Invest. 2000;105:3-7.
2. Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996;2:561-566.
3. Druker BJ, Sawyers CL, Kantarjian H, et al. Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. N Engl J Med. 2001; 344:1038-1042.
4. Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med. 2001;344:1031-1037.
5. Buchdunger E, Matter A, Druker BJ. Bcr-Abl inhibition as a modality of CML therapeutics. Biochim Biophys Acta. 2001;1551:M11-M18.
6. Druker BJ. Imatinib and chronic myeloid leukemia: validating the promise of molecularly targeted therapy. Eur J Cancer. 2002;38[suppl 5]:S70-S76.
7. Kantarjian HM, Cortes J, O'Brien S, et al. Imatinib mesylate (STI571) therapy for Philadelphia chromosome- positive chronic myelogenous leukemia in blast phase. Blood. 2002;99:3547-3553.
8. Kantarjian H, Sawyers C, Hochhaus A, et al. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. N Engl J Med. 2002;346:645-652.
9. Talpaz M, Silver RT, Druker BJ, et al. Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. Blood. 2002;99:1928-1937.
10. Sawyers CL, Hochhaus A, Feldman E, et al. Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. Blood. 2002;99:3530- 3539.
11. Kantarjian HM, Cortes JE, O'Brien S, et al. Longterm survival benefit and improved complete cytogenetic and molecular response rates with imatinib mesylate in Philadelphia chromosomepositive chronic-phase chronic myeloid leukemia after failure of interferon-α. Blood. 2004;104: 1979-1988.
12. O'Brien SG, Guilhot F, Larson RA, 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.
13. 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.
14. Hughes TP, Kaeda J, Branford S, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003;349:1423-1432.
15. Kantarjian HM, Cortes JE, O'Brien S, et al. Imatinib mesylate therapy in newly diagnosed patients with Philadelphia chromosome-positive chronic myelogenous leukemia: high incidence of early complete and major cytogenetic responses. Blood. 2003;101:97-100.
16. Cortes J, Giles F, O'Brien S, et al. Result of highdose imatinib mesylate in patients with Philadelphia chromosome-positive chronic myeloid leukemia after failure of interferon-α. Blood. 2003;102: 83-86.
17. Kantarjian HM, Talpaz M, O'Brien S, et al. Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia. Blood. 2003; 101:473-475.
18. Kantarjian H, Talpaz M, O'Brien S, et al. Highdose imatinib mesylate therapy in newly diagnosed Philadelphia chromosome-positive chronic phase chronic myeloid leukemia. Blood. 2004; 103:2873-2878.
19. Deenik W, van der Holt B, Verhoef GE, et al. Dose finding study of imatinib in combination with intravenous cytarabine: feasibility in newly diagnosed patients with chronic myeloid leukemia. Blood. 2008;111:2581-2588.
20. Hochhaus A, Hughes T. Clinical resistance to imatinib: mechanisms and implications. Hematol Oncol Clin North Am. 2004;18:641-656.
21. Hui CH, Hughes TP. Strategies for the treatment of imatinib-resistant chronic myeloid leukemia. Clin Adv Hematol Oncol. 2003;1:538-545.
22. Kantarjian HM, Talpaz M, Cortes J, et al. Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571; gleevec) in chronic-phase chronic myelogenous leukemia. Clin Cancer Res. 2003;9: 160-166.
23. Branford S, Hughes TP, Rudzki Z. Monitoring chronic myeloid leukaemia therapy by real-time quantitative PCR in blood is a reliable alternative to bone marrow cytogenetics. Br J Haematol. 1999;107:587-599.
24. Hochhaus A, Kreil S, Corbin A, et al. Roots of clinical resistance to STI-571 cancer therapy. Science. 2001;293:2163.
25. Merx K, Muller MC, Kreil S, et al. Early reduction of BCR-ABL mRNA transcript levels predicts cytogenetic response in chronic phase CML patients treated with imatinib after failure of interferon alpha. Leukemia. 2002;16:1579-1583.
26. Hochhaus A, Kreil S, Corbin AS, et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia. 2002;16: 2190-2196.
27. Branford S, Rudzki Z, Walsh S, et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood. 2003; 102:276-283.
28. Branford S, Rudzki Z, Walsh S, et al. High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. Blood. 2002;99:3472-3475.
29. Hughes T, Branford S. Molecular monitoring of chronic myeloid leukemia. Semin Hematol. 2003; 40:62-68.
30. Gorre ME, Ellwood-Yen K, Chiosis G, Rosen N, Sawyers CL. BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90. Blood. 2002;100:3041- 3044.
31. Shah NP, Nicoll JM, Nagar B, et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell. 2002;2:117-125.
32. Branford S, Rudzki Z, Miller B, et al. Mutations in the catalytic core (P-loop) of the BCR-ABL kinase domain of imatinib-treated chronic myeloid leukemia patients in chronic phase are strongly associated with imminent progression to blast crisis. Blood. 2003;102:71a.
33. Branford S, Rudzki Z, Parkinson I, et al. Realtime quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations. Blood. 2004;104:2926- 2932.
34. Hochhaus A, La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia. 2004; 18:1321-1331.
35. Thiesing JT, Ohno-Jones S, Kolibaba KS, Druker BJ. Efficacy of STI571, an abl tyrosine kinase inhibitor, in conjunction with other antileukemic agents against bcr-abl-positive cells. Blood. 2000;96:3195-3199.
36. Fang G, Kim CN, Perkins CL, et al. CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs. Blood. 2000;96:2246-2253.
37. Hughes T, Deininger M, Hochhaus A, et al. Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. Blood. 2006;108:28-37.
38. Ross DM, Branford S, Moore S, Hughes TP. Limited clinical value of regular bone marrow cytogenetic analysis in imatinib-treated chronic phase CML patients monitored by RQ-PCR for BCRABL. Leukemia. 2006;20:664-670.
39. Branford S, Hughes T. Detection of BCR-ABL mutations and resistance to imatinib mesylate. In: Illand H, Hertzgerg M, Marlton P, eds. Myeloid Leukemia: Methods and Protocols, Methods in Molecular Medicine. Vol. 125. Totawa, NJ: Humana Press; 2006:93-106.
40. Picard S, Titier K, Etienne G, et al. Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standarddose imatinib in chronic myeloid leukemia. Blood. 2007;109:3496-3499.
41. Ross DM, Hughes TP. Cancer treatment with kinase inhibitors: what have we learnt from imatinib? Br J Cancer. 2004;90:12-19.
42. Garcia-Manero G, Faderl S, O'Brien S, Cortes J, Talpaz M, Kantarjian HM. Chronic myelogenous leukemia: a review and update of therapeutic strategies. Cancer. 2003;98:437-457.
43. O'Hare T, Eide CA, Deininger MW. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood. 2007;110:2242-2249.
44. Goldman JM. How I treat chronic myeloid leukemia in the imatinib era. Blood. 2007;110:2828-2837.
45. White DL, Saunders VA, Dang P, et al. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood. 2007;110 4064-4072.