Recent advances about imatinib mesylate resistance;Résistance au Glivec®: Actualités

Hematologie

Volumn 13, Issue 1, 2007, Pages 43-53

  Roche Lestienne, Catherine ^a,b   Preudhomme, Claude ^a,b  

^a Institut de Recherche sur le Cancer de Lille   (France)

^b LILLE UNIVERSITY HOSPITAL   (France)

Author keywords

Chronic myeloid leukemia; Imatinib m sylate; Resistance

Indexed keywords

BCR ABL PROTEIN; IMATINIB; MESSENGER RNA;

CANCER REGRESSION; CANCER RELAPSE; CANCER RESISTANCE; CHRONIC MYELOID LEUKEMIA; DRUG MECHANISM; HUMAN; REVIEW; TREATMENT RESPONSE;

EID: 34047259319     PISSN: 12647527     EISSN: None     Source Type: Journal    
DOI: 10.1684/hma.2007.0087     Document Type: Review

References (55)

1. Baccarani M, Saglio G, Goldman J, Hochhaus A, Simonsson B, Appelbaum F, Apperley J, Cervantes F, Cortes J, Deininger M, Gratwohl A, Guilhot F, Horowitz M, Timothy Hughes T, Kantarjian H, Larson R, Niederwieser D, Silver R, Hehlmann R. Evolving concepts in the management of chronic myeloid leukaemia. Recommendations from an expert panel on behalf of the European Leukemianet. Blood 2006 ; (pré-publié on-line le 18 mai).
2. Gorre ME, Mohammed M, Ellwood K, Hsu N, Paquette R, Rao PN, Sawyers CL. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science 2001 ; 293 : 876-80.
3. Mahon FX, Deininger MW, Schultheis B, Chabrol J, Reiffers J, Goldman JM, Melo JV. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571 : diverse mechanisms of resistance. Blood 2000 ; 96 : 1070-9.
4. Roche-Lestienne C, Soenen-Cornu V, Grardel-Duflos N, Lai JL, Philippe N, Facon T, Fenaux P, Preudhomme C. Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment. Blood 2002 ; 100 : 1014-8.
5. Shah NP, Nicoll JM, Nagar B, Gorre ME, Paquette RL, Kuriyan J, Sawyers CL. 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 : 117-25.
6. Deininger M, Buchdunger E, Druker BJ. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood 2005 ; 105 : 2640-53.
7. Schindler T, Bornmann W, Pellicena P, Miller WT, Clarkson B, Kuriyan J. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000 ; 289 : 1938-42.
8. Nagar B, Bornmann WG, Pellicena P, Schindler T, Veach DR, Miller WT, Clarkson B, Kuriyan J. 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 : 4236-43.
9. Kantarjian HM, Talpaz M, O'Brien S, Giles F, Garcia-Manero G, Faderl S, Thomas D, Shan J, Rios MB, Cortes J. Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia. Blood 2003 ; 101 : 473-5.
10. Marin D, Goldman JM, Olavarria E, Apperley JF. Transient benefit only from increasing the imatinib dose in CML patients who do not achieve complete cytogenetic remissions on conventional doses. Blood 2003 ; 102 : 2702-3 ; (author reply 2703-4).
11. Cools J, DeAngelo DJ, Gotlib J, Stover EH, Legare RD, Cortes J, Kutok J, Clark J, Galinsky I, Griffin JD, Cross NC, Tefferi A, Malone J, Alam R, Schrier SL, Schmid J, Rose M, Vandenberghe P, Verhoef G, Boogaerts M, Wlodarska I, Kantarjian H, Marynen P, Coutre SE, Stone R, Gilliland DG. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 2003 ; 348 : 1201-14.
12. Corbin AS, La Rosee P, Stoffregen EP, Druker BJ, Deininger MW. Several Bcr-Abl kinase domain mutants associated with imatinib mésylate resistance remain sensitive to imatinib. Blood 2003 ; 101 : 4611-4.
13. Leguay T, Desplat V, Barthe C. Study of mutation in the ATP binding domain and the SH2/SH3 domain of BCR-ABL in 43 chronic myeloid leukaemia patients treated by imatinib mésylate (STI571). Blood 2003 ; 10 : 369 ; [abstract].
14. Azam M, Latek RR, Daley GQ. Mechanisms of autoinhibition and STI-571/Imatinib resistance revealed by mutagenesis of bcr-abl. Cell 2003 ; 112 : 831-43.
15. Mahon FX, Belloc F, Lagarde V, Chollet C, Moreau-Gaudry F, Reiffers J, Goldman JM, Melo JV. MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood 2003 ; 101 : 2368-73.
16. Ferrao PT, Frost MJ, Siah SP, Ashman LK. Overexpression of P-glycoprotein in K562 cells does not confer resistance to the growth inhibitory effects of imatinib (STI571) in vitro. Blood 2003 ; 102 : 4499-503.
17. Thomas J, Wang L, Clark RE, Pirmohamed M. Active transport of imatinib into and out of cells : implications for drug resistance. Blood 2004 ; 104 : 3739-45.
18. Crossman LC, Druker BJ, Deininger MW, Pirmohamed M, Wang L, Clark RE. hOCT 1 and resistance to imatinib. Blood 2005 ; 106 : 1133-4.
19. Mahon FX, Picard S, Titier K, Nicolini F, Ducint D, Moore N, Marit G. Quantification of imatinib in human plasma with high performance liquid chromatography-tandem mass spectrometry : application to therapeutic drug monitoring of patients with chronic myelogeneous leukaemia. [abstract. Blood 2005 ; 106 : 1995.
20. Deutsch E, Dugray A, AbdulKarim B, Marangoni E, Maggiorella L, Vaganay S, M'Kacher R, Rasy SD, Eschwege F, Vainchenker W, Turhan AG, Bourhis J. BCR-ABL down-regulates the DNA repair protein DNA-PKcs. Blood 2001 ; 97 : 2084-90.
21. Deutsch E, Jarrousse S, Buet D, Dugray A, Bonnet ML, Vozenin-Brotons MC, Guilhot F, Turhan AG, Feunteun J, Bourhis J. Down-regulation of BRCA1 in BCR-ABL-expressing hematopoietic cells. Blood 2003 ; 10 : 4583-8.
22. Campbell LJ, Fidler C, Eagleton H, Peniket A, Kusec R, Gal S, Littlewood TJ, Wainscoat JS, Boultwood J. hTERT, the catalytic component of telomerase, is downregulated in the haematopoietic stem cells of patients with chronic myeloid leukaemia. Leukemia 2006 ; 20 : 671-9.
23. Donato NJ, Wu JY, Stapley J, Gallick G, Lin H, Arlinghaus R, Talpaz M. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571 . Blood 2003 ; 101 : 690-8.
24. Ptasznik A, Nakata Y, Kalota A, Emerson SG, Gewirtz AM. Short interfering RNA (siRNA) targeting the Lyn kinase induces apoptosis in primary, and drug-resistant, BCR-ABL1(+) leukemia cells. Nat Med 2004 ; 10 : 1187-9.
25. Guerzoni C, Bardini M, Mariani SA, Ferrari-Amorotti G, Neviani P, Panno ML, Zhang Y, Martinez R, Perrotti D, Calabretta B. Inducible activation of CEBPB, a gene negatively regulated by BCR/ABL, inhibits proliferation and promotes differentiation of BCR/ABL-expressing cells. Blood 2006 ; 107 : 4080-9.
26. Ferrari-Amorotti G, Keeshan K, Zattoni M, Guerzoni C, Iotti G, Cattelani S, Donato NJ, Calabretta B. Leukemogenesis induced by wild-type and STI571-resistant BCR/ABL is potently suppressed by C/EBPalpha. Blood 2006 ; 108 : 1353-62.
27. Wendel HG, de Stanchino E, Cepero E, Ray S, Emig M, Fridman JS, Veach DR, Bornmann WG, Clarkson B, Mc Combie WR, Kogan SC, Hochhaus A, Lowe SW. Loss of p53 impedes the antileukemic response to BCR-ABL inhibition. Proc Natl Acad Sci USA 2006 ; 103 : 7444-9.
28. Crossman LC, Mori M, Hsieh YC, Lange T, Paschka P, Harrington CA, Krohn K, Niederwieser DW, Hehlmann R, Hochhaus A, Druker BJ, Deininger MW. In chronic myeloid leukemia white cells from cytogenetic responders and non-responders to imatinib have very similar gene expression signatures. Haematologica 2005 ; 90 : 459-64.
29. Crossman LC, Loriaux M, Vartanian K. Gene expression profiling of CML CD34+ cells prior to imatinib therapy reveals differences between patients with and without subsequent complete cytogenetic response. Blood 2005 ; 103 : 2794 ; [abstract].
30. Kronenwett R, Diaz-Bianco E, Graef T, Steidl U, Kliszewski S, Bruns I, Neumann F, Bork S, Butterweck U, Roes N, Brors B, Eils R, Kobbe G, Gattermann N. Molecular phenotype of malignant CD34+ hematopoietic Stem and progenitor cells in chronic myelogeneous leukemia. Blood 2005 ; 106 : 2863 ; [abstract].
31. Zheng C, Li L, Haak M, Brors B, Frank O, Giehl M, Fabarius A, Schatz M, Weisser A, Lorentz C, Gretz N, Hehlmann R, Hochhaus A, Seifarth W. Gene expression profiling of CD34+ cells identifies a molecular signature of chronic myeloid leukemia blast crisis. Leukemia 2006 ; 20 : 1028-34.
32. Branford S, Rudzki Z, Lynch K, Hughes T. Pre-imatinib factors can be used to define the risk of BCR-ABL mutations for patients with CML in chronic phase and identify a minority who should have regular mutation screening. Blood 2005 ; 106 : 1079 ; [abstract].
33. Deininger MW, Willis S, Lange T, McWeeney S, Otto S, Druker BJ. Detection of imatinib-resistant BCR-ABL mutants in drug-naïve patients : correlation with disease phase and clonal evolution but not with response to treatment. Blood 2005 ; 106 : 273 ; [abstract].
34. Soverini S, Martinelli G, Rosti G, Bassi S, Amabile M, Poerio A, Giannini B, Trabacchi E, Castagnetti F, Testoni N, Luatti S, de Vivo A, Cilloni D, Izzo B, Fava M, Abruzzese E, Alberti D, Pane F, Saglio G, Baccarani M. 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 a shorter survival : a study of the GIMEMA Working Party on Chronic Myeloid leukemia. J Clin Oncol 2005 ; 23 : 4100-9.
35. Branford S, Rudzki Z, Walsh S, Parkinson I, Grigg A, Szer J, Taylor K, Herrmann R, Seymour JF, Arthur C, Joske D, Lynch K, Hughes T. 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 : 276-83.
36. Nicolini FE, Corm S, Le QH, Sorel N, Hayette S, Bories D, Leguay T, Roy L, Giraudier S, Tulliez M, Facon T, Mahon FX, Cayuela JM, Rousselot P, Michallet M, Preudhomme C, Guilhot F, Roche-Lestienne C. Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients : a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP). Leukemia 2006 ; 20 : 1061-6.
37. Soverini S, Martinelli G, Rosti G, Bassi S, Amabile M, Poerio A, Giannini B, Trabacchi E, Castagnetti F, Testoni N, Luatti S, de Vivo A, Cilloni D, Izzo B, Fava M, Abruzzese E, Alberti D, Pane F, Saglio G, Baccarani M. 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 : 4100-9.
38. Roumiantsev S, Shah NP, Gorre ME, Nicoll J, Brasher BB, Sawyers CL, Van Etten RA. Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. Proc Natl Acad Sci USA 2002 ; 99 : 10700-5.
39. Roche-Lestienne C, Laï JL, Darré S, Facon T, Preudhomme C. A mutation conferring resistance to Imatinib at the time of diagnosis of chronic myelogenous leukemia. N Engl J Med 2003 ; 348-22 : 2265-6.
40. Khorashad JS, Anand M, Marin D, Saunders S, Al-Jabary T, Iqbal A, Margerison S, Melo JV, Goldman JM, Apperley JF, Kaeda J. The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia 2006 ; 20 : 658-63.
41. Sherbenou DW, Wong MJ, Humayun A, Mc Greevey L, Yang R, Heinrich MC, Press RD, Druker BJ, Deininger MW. In chronic myeloid leukemia patients with a complete cytogenetic response to imatinib, bcr-abl kinase domain mutations are rarely and not consistently associated with subsequent relapse. [abstract. Blood 2005 ; 106 : 434.
42. Lange T, Gunther C, Kohler T, Krahl R, Musiol S, Leiblein S, Al-Ali HK, van Hoomissen I, Niederwieser D, Deininger MW. High levels of BAX, low levels of MRP-1, and high platelets are independent predictors of response to imatinib in myeloid blast crisis of CML. Blood 2003 ; 101 : 2152-5.
43. Villuendas R, Steegmann JL, Pollan M, Tracey L, Granda A, Fernandez-Ruiz E, Casado LF, Martinez J, Martinez P, Lombardia L, Villalon L, Odriozola J, Piris MA. Identification of genes involved in imatinib resistance in CML : a gene-expression profiling approach. Leukemia 2006 ; 20 : 1047-54.
44. Huntly BJ, Reid AG, Bench AJ, Campbell LJ, Telford N, Shepherd P, Szer J, Prince HM, Turner P, Grace C, Nacheva EP, Green AR. Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia. Blood 2001 ; 98 : 1732-8.
45. Kovitz C, Kantarjian H, Garcia-Manero G, Abruzzo LV, Cortes J. Myelodysplastic syndromes and acute leukemia developing after imatinib mesylate therapy for chronic myeloid leukemia. Blood 2006 ; (online publication Jun 29).
46. Fabarius A, Giehl M, Frank O, Duesberg P, Hochhaus A, Hehlmann R, Seifarth W. Induction of centrosome and chromosome aberrations by imatinib in vitro. Leukemia 2005 ; 19 : 1573-8.
47. Terre C, Eclache V, Rousselot P, Imbert M, Charrin C, Gervais C, Mozziconacci MJ, Maarek O, Mossafa H, Auger N, Dastugue N, Talmant P, Van den Akker J, Leonard C, Khac FN, Mugneret F, Viguie F, Lafage-Pochitaloff M, Bastie JN, Roux GL, Nicolini F, Maloisel F, Vey N, Laurent G, Recher C, Vigier M, Yacouben Y, Giraudier S, Vernant JP, Salles B, et al. France Intergroupe pour la Leucemie Myeloide Chronique. Report of 34 patients with clonal chromosomal abnormalities in Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia. Leukemia 2004 ; 18 : 1340-6.
48. Talpaz M, Shah NP, Kantarjian H, Donato N, Nicoll J, Paquette R, Cortes J, O'Brien S, Nicaise C, Bleickardt E, Blackwood-Chirchir MA, Iyer V, Chen TT, Huang F, Decillis AP, Sawyers CL. Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med 2006 ; 354 : 2531-41.
49. Kantarjian H, Giles F, Wunderle L, Bhalla K, O'Brien S, Wassmann B, Tanaka C, Manley P, Rae P, Mietlowski W, Bochinski K, Hochhaus A, Griffin JD, Hoelzer D, Albitar M, Dugan M, Cortes J, Alland L, Ottmann OG. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med 2006 ; 354 : 2542-51.
50. Jabbour E, Cortes J, Talpaz M, Jones D, O'Bien S, Nicaise C, Kantarjian H. Correlation of clinical response to dasatinib (BMS-354825) with BCR-ABL mutation status in imatinib-resistant patients with chronic myelogeneous leukemia treated at the MD Anderson Cancer Center. [abstract. Blood 2005 ; 106 : 1091.
51. Weisberg E, Manley PW, Breitenstein W, Bruggen J, Cowan-Jacob SW, Ray A, Huntly B, Fabbro D, Fendrich G, Hall-Meyers E, Kung AL, Mestan J, Daley GQ, Callahan L, Catley L, Cavazza C, Azam M, Neuberg D, Wright RD, Gilliland DG, Griffin JD. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell 2005 ; 7 : 129-41.
52. Tokarski JS, Newitt JA, Chang CY, Cheng JD, Wittekind M, Kiefer SE, Kish K, Lee FY, Borzillerri R, Lombardo LJ, Xie D, Zhang Y, Klei HE. The structure of dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Cancer Res 2006 ; 66 : 5790-7.
53. Clark JB, Xiao A, Griffiths M, Falcon S, Pollard J, Freedman SJ, Giles F. MK-0457, a novel multikinase inhibitor, inhibits BCR-ABL activity in patients with chronic myeloid leukaemia and acute lymphocytic leukaemia with the T315I BCR-ABL mutation. [abstract. Blood 2006 ; 108 : 637.
54. Rousselot P, Huguet F, Rea D, Legros L, Cayuela JM, Maarek O, Blanchet O, Marit G, Gluckman E, Reiffers J, Gardembas M, Mahon FX. Imatinib mesylate discontinuation in patients with chronic myelogenous leukemia in complete molecular remission for more than two years. Blood 2006 ; (Sep 14 [online]).
55. Copland M, Hamilton A, Elrick LJ, Baird JW, Allan EK, Jordanides N, Barow M, Mountford JC, Holyoake TL. Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood 2006 ; 107 : 4532-9.