Chronic myeloid leukaemia as a model of disease evolution in human cancer

被引:454
作者
Melo, Junia V. [1 ]
Barnes, David J. [1 ]
机构
[1] Hammersmith Hosp, Imperial Coll London, Dept Haematol, London W12 0NN, England
关键词
D O I
10.1038/nrc2147
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Chronic myeloid leukaemia (CML) can be considered as a paradigm for neoplasias that evolve through a multi-step process. CML is also one of the best examples of a disease that can be targeted by molecular therapy; however, the success of new 'designer drugs' is largely restricted to the chronic phase of the disease. If not cured at this stage, CML invariably progresses and transforms into an acute-type leukaemia undergoing a 'blast crisis'. The causes of this transformation are still poorly understood. What mechanisms underlie this progression, and are they shared by other common cancers?
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页码:441 / 453
页数:13
相关论文
共 152 条
[1]   MAMMALIAN DNA NUCLEOTIDE EXCISION-REPAIR RECONSTITUTED WITH PURIFIED PROTEIN-COMPONENTS [J].
ABOUSSEKHRA, A ;
BIGGERSTAFF, M ;
SHIVJI, MKK ;
VILPO, JA ;
MONCOLLIN, V ;
PODUST, VN ;
PROTIC, M ;
HUBSCHER, U ;
EGLY, JM ;
WOOD, RD .
CELL, 1995, 80 (06) :859-868
[2]   ALTERATIONS IN THE P53 GENE AND THE CLONAL EVOLUTION OF THE BLAST CRISIS OF CHRONIC MYELOCYTIC-LEUKEMIA [J].
AHUJA, H ;
BARELI, M ;
ADVANI, SH ;
BENCHIMOL, S ;
CLINE, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (17) :6783-6787
[3]  
AHUJA HG, 1991, BLOOD, V78, P3259
[4]  
Ahuja HG, 2001, GENE CHROMOSOME CANC, V30, P410, DOI 10.1002/1098-2264(2001)9999:9999<::AID-GCC1108>3.0.CO
[5]  
2-9
[6]   Bcr-Abl exerts its antiapoptotic effect against diverse apoptotic stimuli through blockage of mitochondrial release of cytochrome c and activation of caspase-3 [J].
Amarante-Mendes, GP ;
Kim, CN ;
Liu, L ;
Huang, Y ;
Perkins, CL ;
Green, DR ;
Bhalla, K .
BLOOD, 1998, 91 (05) :1700-1705
[7]  
Apperley Jane F, 2006, Hematology Am Soc Hematol Educ Program, P226
[8]   A critical role for telomeres in suppressing and facilitating carcinogenesis [J].
Artandi, SE ;
DePinho, RA .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2000, 10 (01) :39-46
[9]   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
[10]   Dose-dependent effects of Bcr-Abl in cell line models of different stages of chronic myeloid leukemia [J].
Barnes, DJ ;
Schultheis, B ;
Adedeji, S ;
Melo, JV .
ONCOGENE, 2005, 24 (42) :6432-6440