生物
同源盒
染色体易位
白血病
髓系白血病
癌症研究
Hox基因
谱系(遗传)
DNMT3B型
造血
髓样
基因
干细胞
遗传学
转录因子
DNA甲基化
基因表达
作者
Andrew G. Muntean,Jay L. Hess
出处
期刊:Annual Review of Pathology-mechanisms of Disease
[Annual Reviews]
日期:2012-02-28
卷期号:7 (1): 283-301
被引量:291
标识
DOI:10.1146/annurev-pathol-011811-132434
摘要
Aggressive leukemias arise in both children and adults as a result of rearrangements to the mixed-lineage leukemia gene (MLL) located on chromosome 11q23. MLL encodes a large histone methyltransferase that directly binds DNA and positively regulates gene transcription, including homeobox (HOX) genes. MLL is involved in chromosomal translocations, partial tandem duplications, and amplifications, all of which result in hematopoietic malignancies due to sustained HOX expression and stalled differentiation. MLL lesions are associated with both acute myeloid leukemia and acute lymphoid leukemia and are usually associated with a relatively poor prognosis despite improved treatment options such as allogeneic hematopoietic stem cell transplantation, which underscores the need for new treatment regimens. Recent advances have begun to reveal the molecular mechanisms that drive MLL-associated leukemias, which, in turn, have provided opportunities for therapeutic development. Here, we discuss the etiology of MLL leukemias and potential directions for future therapy.
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