Mechanisms of resistance to BCR--ABL kinase inhibitors

被引：40

作者：

Diamond, Joana M. ^{[2
]}

Melo, Junia V. ^{[1
,3
]}

机构：

[1] Univ Adelaide, Dept Haematol, Ctr Canc Biol SA Pathol, Adelaide, SA 5000, Australia

[2] Inst Portugues Oncol Francisco Gentil, Mol Biol Unit, Hematooncol Lab, Lisbon, Portugal

[3] Univ London Imperial Coll Sci Technol & Med, Dept Haematol, London, England

来源：

LEUKEMIA & LYMPHOMA | 2011年 / 52卷

关键词：

CHRONIC MYELOID-LEUKEMIA; GENE-EXPRESSION SIGNATURE; PHILADELPHIA-POSITIVE PATIENTS; LOW OCT-1 ACTIVITY; IMATINIB MESYLATE; DOMAIN MUTATIONS; CML PATIENTS; CELL-LINES; DASATINIB BMS-354825; STEM-CELLS;

D O I：

10.3109/10428194.2010.546920

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Since the introduction of imatinib mesylate (IM) for the treatment of chronic myeloid leukemia (CML), impressive clinical responses have been observed in the majority of patients in chronic phase. However, not all patients experience an optimal response to IM or even to the more potent, second-generation tyrosine kinase inhibitors (TKIs). Furthermore, responses are not sustained in a number of patients, and it is yet unclear whether the inhibitors can be safely discontinued in patients who achieve long-term remission. The emergence of resistance to TKIs has become a significant problem that has led to extensive studies on the causal mechanisms. This review describes our current state of knowledge on why and how CML cells can develop resistance to TKIs.</.

引用

页码：12 / 22

页数：11

共 107 条

[1]

Part I: Mechanisms of resistance to imatinib in chronic myeloid leukaemia [J].

Apperley, Jane F. .

LANCET ONCOLOGY, 2007, 8 (11) :1018-1029

[2]

Imatinib resistance in multidrug-resistant K562 human leukemic cells [J].

Assef, Yanina ;

Rubio, Fernanda ;

Colo, Georgina ;

del Monaco, Silvana ;

Costas, Monica A. ;

Kotsias, Basilio A. .

LEUKEMIA RESEARCH, 2009, 33 (05) :710-716

[3]

Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet [J].

Baccarani, Michele ;

Saglio, Giuseppe ;

Goldman, John ;

Hochhaus, Andreas ;

Simonsson, Bengt ;

Appelbaum, Frederick ;

Apperley, Jane ;

Cervantes, Francisco ;

Cortes, Jorge ;

Deininger, Michael ;

Gratwohl, Alois ;

Guilhot, Frangois ;

Horowitz, Mary ;

Hughes, Timothy ;

Kantarjian, Hagop ;

Larson, Richard ;

Niederwieser, Dielger ;

Silver, Richard ;

Hehlmann, Rudiger .

BLOOD, 2006, 108 (06) :1809-1820

[4]

Chronic Myeloid Leukemia: An Update of Concepts and Management Recommendations of European LeukemiaNet [J].

Baccarani, Michele ;

Cortes, Jorge ;

Pane, Fabrizio ;

Niederwieser, Dietger ;

Saglio, Giuseppe ;

Apperley, Jane ;

Cervantes, Francisco ;

Deininger, Michael ;

Gratwohl, Alois ;

Guilhot, Francois ;

Hochhaus, Andreas ;

Horowitz, Mary ;

Hughes, Timothy ;

Kantarjian, Hagop ;

Larson, Richard ;

Radich, Jerald ;

Simonsson, Bengt ;

Silver, Richard T. ;

Goldman, John ;

Hehlmann, Rudiger .

JOURNAL OF CLINICAL ONCOLOGY, 2009, 27 (35) :6041-6051

[5]

Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia [J].

Barnes, DJ ;

Palaiologou, D ;

Panousopoulou, E ;

Schultheis, B ;

Yong, ASM ;

Wong, A ;

Pattacini, L ;

Goldman, JM ;

Melo, JV .

CANCER RESEARCH, 2005, 65 (19) :8912-8919

[6]

hOCT1 transcript levels and single nucleotide polymorphisms as predictive factors for response to imatinib in chronic myeloid leukemia [J].

Bazeos, A. ;

Marin, D. ;

Reid, A. G. ;

Gerrard, G. ;

Milojkovic, D. ;

May, P. C. ;

de Lavallade, H. ;

Garland, P. ;

Rezvani, K. ;

Apperley, J. F. ;

Goldman, J. M. ;

Foroni, L. ;

Khorashad, J. S. .

LEUKEMIA, 2010, 24 (06) :1243-1245

[7]

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 [J].

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 .

BLOOD, 2003, 102 (01) :276-283

[8]

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter? [J].

Branford, Susan ;

Melo, Junia V. ;

Hughes, Timothy P. .

BLOOD, 2009, 114 (27) :5426-5435

[9]

The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (gleevec): Implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients [J].

Breedveld, P ;

Pluim, D ;

Cipriani, G ;

Wielinga, P ;

van Tellingen, O ;

Schinkel, AH ;

Schellens, JHM .

CANCER RESEARCH, 2005, 65 (07) :2577-2582

[10]

Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps [J].

Burger, H ;

van Tol, H ;

Brok, M ;

Wiemer, EAC ;

de Bruijn, EA ;

Guetens, G ;

de Boeck, G ;

Sparreboom, A ;

Verweij, J ;

Nooter, K .

CANCER BIOLOGY & THERAPY, 2005, 4 (07) :747-752

← 1 2 3 4 5 6 7 8 9 10 →