Signal transduction therapy in haematological malignancies: identification and targeting of tyrosine kinases

被引:11
作者
Chase, Andrew
Cross, Nicholas C. P. [1 ]
机构
[1] Wessex Reg Genet Lab, Salisbury SP2 8BJ, Wilts, England
[2] Univ Southampton, Salisbury Dist Hosp, Div Human Genet, Salisbury SP2 8BJ, Wilts, England
关键词
BCR-ABL; haematological malignancy; imatinib; leukaemia; signalling inhibitor; tyrosine kinase;
D O I
10.1042/CS20060035
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Tyrosine kinases play key roles in cell proliferation, survival and differentiation. Their aberrant activation, caused either by the formation of fusion genes by chromosome translocation or by intragenic changes, such as point mutations or internal duplications, is of major importance in the development of many haematological malignancies. An understanding of the mechanisms by which BCR-ABL contributes to the pathogenesis of chronic myeloid leukaemia led to the development of imatinib, the first of several tyrosine kinase inhibitors to enter clinical trials. Although the development of resistance has been problematic, particularly in aggressive disease, the development of novel inhibitors and combination with other forms of therapy shows promise.
引用
收藏
页码:233 / 249
页数:17
相关论文
共 246 条
[1]   Fusion of the platelet-derived growth factor receptor beta to a novel gene CEV14 in acute myelogenous leukemia after clonal evolution [J].
Abe, A ;
Emi, N ;
Tanimoto, M ;
Terasaki, H ;
Marunouchi, T ;
Saito, H .
BLOOD, 1997, 90 (11) :4271-4277
[2]   Identification of novel FLT-3 Asp835 mutations in adult acute myeloid leukaemia [J].
Abu-Duhier, FM ;
Goodeve, AC ;
Wilson, GA ;
Care, RS ;
Peake, IR ;
Reilly, JT .
BRITISH JOURNAL OF HAEMATOLOGY, 2001, 113 (04) :983-988
[3]   A t(8;9) translocation with PCM1-JAK2 fusion in a patient with T-cell lymphoma [J].
Adélaïde, J ;
Pérot, C ;
Gelsi-Boyer, V ;
Pautas, C ;
Murati, A ;
Copie-Bergman, C ;
Imbert, M ;
Chaffanet, M ;
Birnbaum, D ;
Mozziconacci, MJ .
LEUKEMIA, 2006, 20 (03) :536-537
[4]   Allosteric inhibitors of Bcr-abl-dependent cell proliferation [J].
Adrián, FJ ;
Ding, Q ;
Sim, TB ;
Velentza, A ;
Sloan, C ;
Liu, Y ;
Zhang, GB ;
Hur, W ;
Ding, S ;
Manley, P ;
Mestan, J ;
Fabbro, D ;
Gray, NS .
NATURE CHEMICAL BIOLOGY, 2006, 2 (02) :95-102
[5]   A novel form of mastocytosis associated with a transmembrane c-kit mutation and response to imatinib [J].
Akin, C ;
Fumo, G ;
Yavuz, AS ;
Lipsky, PE ;
Neckers, L ;
Metcalfe, DD .
BLOOD, 2004, 103 (08) :3222-3225
[6]   Clonality and molecular pathogenesis of mastocytosis [J].
Akin, C .
ACTA HAEMATOLOGICA, 2005, 114 (01) :61-69
[7]  
ANAFI M, 1993, BLOOD, V82, P3524
[8]  
ANAFI M, 1992, J BIOL CHEM, V267, P4518
[9]  
ANDREJAUSKASBUCHDUNGER E, 1992, CANCER RES, V52, P5353
[10]   Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta [J].
Apperley, JF ;
Gardembas, M ;
Melo, JV ;
Russell-Jones, R ;
Bain, BJ ;
Baxter, J ;
Chase, A ;
Chessells, JM ;
Colombat, M ;
Dearden, CE ;
Dimitrijevic, S ;
Mahon, FX ;
Marin, D ;
Nikolova, Z ;
Olavarria, E ;
Silberman, S ;
Schultheis, B ;
Cross, NCP ;
Goldman, JM .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (07) :481-487