The heterogeneity of pediatric MLL-rearranged acute myeloid leukemia

被引:103
作者
Balgobind, B. V. [1 ]
Zwaan, C. M. [1 ]
Pieters, R. [1 ]
Van den Heuvel-Eibrink, M. M. [1 ]
机构
[1] Sophia Childrens Univ Hosp, Erasmus MC, Dept Pediat Oncol Hematol, NL-3000 CB Rotterdam, Netherlands
关键词
MLL; pediatric AML; heterogeneity; ACUTE MYELOGENOUS LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOBLASTIC-LEUKEMIA; GENE-EXPRESSION SIGNATURES; PARTIAL TANDEM DUPLICATION; TYROSINE KINASE INHIBITOR; FUSION PARTNER; CHROMOSOMAL-ABNORMALITIES; PROGNOSTIC IMPACT; ADULT PATIENTS;
D O I
10.1038/leu.2011.90
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Translocations involving the mixed-lineage leukemia (MLL) gene, localized at 11q23, comprise 15 to 20% of all pediatric acute myeloid leukemia (AML) cases. This review summarizes current knowledge about the etiology, biology, clinical characteristics and differences in outcome in MLL-rearranged pediatric AML. Furthermore, we discuss the role of cooperating events in MLL-rearranged pediatric AML, and future therapeutic strategies to improve outcome. We conclude that MLL-rearranged pediatric AML is a heterogeneous disease, and prognosis depends on various factors, for example, translocation partner, age, WBC and additional cytogenetic aberrations. The relationship of outcome with specific translocation partners requires that they be searched for in the diagnostic work-up of AML. To achieve further improvements in outcome, unraveling the biology of MLL-rearranged pediatric AML is warranted. Leukemia (2011) 25, 1239-1248; doi:10.1038/leu.2011.90; published online 13 May 2011
引用
收藏
页码:1239 / 1248
页数:10
相关论文
共 130 条
[1]  
Alexander FE, 2001, CANCER RES, V61, P2542
[2]  
Andersen MK, 1998, HAEMATOLOGICA, V83, P483
[3]   Chromosomal translocations involving the MLL gene:: Molecular mechanisms [J].
Aplan, Peter D. .
DNA REPAIR, 2006, 5 (9-10) :1265-1272
[4]   Inhibition of FLT3 in MLL: Validation of a therapeutic target identified by gene expression based classification [J].
Armstrong, SA ;
Kung, AL ;
Mabon, ME ;
Silverman, LB ;
Stam, RW ;
Den Boer, ML ;
Pieters, R ;
Kersey, JH ;
Sallan, SE ;
Fletcher, JA ;
Golub, TR ;
Griffin, JD ;
Korsmeyer, SJ .
CANCER CELL, 2003, 3 (02) :173-183
[5]   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
[6]   Binding to nonmethylated CpG DNA is essential for target recognition, transactivation, and myeloid transformation by an MLL oncoprotein [J].
Ayton, PM ;
Chen, EH ;
Cleary, ML .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (23) :10470-10478
[7]   Transformation of myeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9 [J].
Ayton, PM ;
Cleary, ML .
GENES & DEVELOPMENT, 2003, 17 (18) :2298-2307
[8]   Molecular pathology of mixed-lineage leukemia [J].
Bach, Christian ;
Slany, Robert K. .
FUTURE ONCOLOGY, 2009, 5 (08) :1271-1281
[9]  
Bacher U, 2005, HAEMATOLOGICA, V90, P1502
[10]   High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome [J].
Balgobind, B. V. ;
Zwaan, C. M. ;
Reinhardt, D. ;
Arentsen-Peters, T. J. C. M. ;
Hollink, I. H. I. M. ;
de Haas, V. ;
Kaspers, G. J. L. ;
de Bont, E. S. J. M. ;
Baruchel, A. ;
Stary, J. ;
Meyer, C. ;
Marschalek, R. ;
Creutzig, U. ;
den Boer, M. L. ;
Pieters, R. ;
van den Heuvel-Eibrink, M. M. .
LEUKEMIA, 2010, 24 (12) :2048-2055