Acute lymphoblastic leukaemia: a model for the pharmacogenomics of cancer therapy

被引:164
作者
Cheok, MH
Evans, WE
机构
[1] St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA
[2] Univ Tennessee, Memphis, TN 38105 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/nrc1800
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The use of combination chemotherapy to cure acute lymphoblastic leukaemia (ALL) in children emerged in the 1980s as a paradigm for curing any disseminated cancer, and many of the therapeutic principles were subsequently applied to the treatment of other disseminated human cancers. Similarly, elucidation of the pharmacogenomics of ALL and its translation into new chemotherapeutic approaches might serve as a model for optimizing the treatment of other human cancers. Germline polymorphisms and gene-expression patterns in ALL cells have been linked to the toxicity and efficacy of chemotherapy for ALL and are beginning to emerge as useful clinical diagnostics.
引用
收藏
页码:117 / 129
页数:13
相关论文
共 118 条
[1]   With your genes? Take one of these, three times a day [J].
Abbott, A .
NATURE, 2003, 425 (6960) :760-762
[2]   Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy-induced leukemia [J].
Allan, JM ;
Wild, CP ;
Rollinson, S ;
Willett, EV ;
Moorman, AV ;
Dovey, GJ ;
Roddam, PL ;
Roman, E ;
Cartwright, RA ;
Morgan, GJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (20) :11592-11597
[3]   Polymorphisms within glutathione S-transferase genes and initial response to glucocorticoids in childhood acute lymphoblastic leukaemia [J].
Anderer, G ;
Schrappe, M ;
Brechlin, AM ;
Lauten, M ;
Muti, P ;
Welte, K ;
Stanulla, M .
PHARMACOGENETICS, 2000, 10 (08) :715-726
[4]   MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia [J].
Armstrong, SA ;
Staunton, JE ;
Silverman, LB ;
Pieters, R ;
de Boer, ML ;
Minden, MD ;
Sallan, SE ;
Lander, ES ;
Golub, TR ;
Korsmeyer, SJ .
NATURE GENETICS, 2002, 30 (01) :41-47
[5]  
BARREDO JC, 1994, BLOOD, V84, P564
[6]   Reduced folate carrier expression in acute lymphoblastic leukemia: A mechanism for ploidy but not lineage differences in methotrexate accumulation [J].
Belkov, VM ;
Krynetski, EY ;
Schuetz, JD ;
Yanishevski, Y ;
Masson, E ;
Mathew, S ;
Raimondi, S ;
Pui, CH ;
Relling, MV ;
Evans, WE .
BLOOD, 1999, 93 (05) :1643-1650
[7]   A polymorphism (80G->A) in the reduced folate carrier gene and its associations with folate status and homocysteinemia [J].
Chango, A ;
Emery-Fillon, N ;
de Courcy, GP ;
Lambert, D ;
Pfister, M ;
Rosenblatt, DS ;
Nicolas, JP .
MOLECULAR GENETICS AND METABOLISM, 2000, 70 (04) :310-315
[8]   Molecular determinants of resistance to antiandrogen therapy [J].
Chen, CD ;
Welsbie, DS ;
Tran, C ;
Baek, SH ;
Chen, R ;
Vessella, R ;
Rosenfeld, MG ;
Sawyers, CL .
NATURE MEDICINE, 2004, 10 (01) :33-39
[9]   Higher frequency of glutathione S-transferase deletions in black children with acute lymphoblastic leukemia [J].
Chen, CL ;
Liu, Q ;
Pui, CH ;
Rivera, GK ;
Sandlund, JT ;
Ribeiro, R ;
Evans, WE ;
Relling, MV .
BLOOD, 1997, 89 (05) :1701-1707
[10]   Karyotypic abnormalities create discordance of germline genotype and cancer cell phenotypes [J].
Cheng, Q ;
Yang, WJ ;
Raimondi, SC ;
Pui, CH ;
Relling, MV ;
Evans, WE .
NATURE GENETICS, 2005, 37 (08) :878-882