Genomic profiling of high-risk acute lymphoblastic leukemia

被引：39

作者：

Collins-Underwood, J. R. ^{[1
]}

Mullighan, C. G. ^{[1
]}

机构：

[1] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA

来源：

LEUKEMIA | 2010年 / 24卷 / 10期

基金：

美国国家卫生研究院;

关键词：

acute lymphoblastic leukemia; IKAROS; relapse; CRLF2; JAK; THYMIC STROMAL LYMPHOPOIETIN; ONCOGENIC IKAROS ISOFORMS; TYROSINE KINASE JAK2; B-CELL DEVELOPMENT; DOWN-SYNDROME; TRANSCRIPTION FACTOR; ACTIVATING MUTATION; GENETIC ALTERATIONS; PEDIATRIC-PATIENTS; POOR-PROGNOSIS;

D O I：

10.1038/leu.2010.177

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Acute lymphoblastic leukemia (ALL) is a heterogeneous disease comprising multiple subtypes with different genetic alterations and responses to therapy. Recent genome-wide profiling studies of ALL have identified a number of novel genetic alterations that target key cellular pathways in lymphoid growth and differentiation and are associated with treatment outcome. Notably, genetic alteration of the lymphoid transcription factor gene IKZF1 is a hallmark of multiple subtypes of ALL with poor prognosis, including BCR-ABL1-positive lymphoid leukemia and a subset of 'BCR-ABL1-like' ALL cases that, in addition to IKZF1 alteration, harbor genetic mutations resulting in aberrant lymphoid cytokine receptor signaling, including activating mutations of Janus kinases and rearrangement of cytokine receptor-like factor 2 (CRLF2). Recent insights from genome-wide profiling studies of B-progenitor ALL and the potential for new therapeutic approaches in high-risk disease are discussed. Leukemia (2010) 24, 1676-1685; doi:10.1038/leu.2010.177; published online 26 August 2010

引用

页码：1676 / 1685

页数：10

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