New pieces of a puzzle: The current biological picture of MPN

被引:8
|
作者
Kleppe, Maria [1 ]
Levine, Ross L. [1 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA
来源
关键词
MPN; JAK2; Signaling; Epigenetics; STAT3; Leukemia; ENDOTHELIAL GROWTH-FACTOR; PHASE MYELOPROLIFERATIVE NEOPLASMS; CHRONIC MYELOMONOCYTIC LEUKEMIA; HEALTH-ORGANIZATION CRITERIA; METHYLTRANSFERASE GENE EZH2; TYROSINE KINASE JAK2; BONE-MARROW STROMA; POLYCYTHEMIA-VERA; ESSENTIAL THROMBOCYTHEMIA; MYELODYSPLASTIC SYNDROMES;
D O I
10.1016/j.bbcan.2012.07.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Over the last years, we have witnessed significant improvement in our ability to elucidate the genetic events, which contribute to the pathogenesis of acute and chronic leukemias, and also in patients with myeloproliferative neoplasms (MPN). However, despite significant insight into the role of specific mutations, including the JAK2V617F mutation, in MPN pathogenesis, the precise mechanisms by which specific disease alleles contribute to leukemic transformation in MPN remain elusive. Here we review recent studies aimed at understanding the role of downstream signaling pathways in MPN initiation and phenotype, and discuss how these studies have begun to lead to novel insights with biologic, clinical, and therapeutic relevance. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:415 / 422
页数:8
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