Role of TET2 Mutations in Myeloproliferative Neoplasms

被引：24
|
作者：
Pronier, Elodie [2 ,3 ]
Delhommeau, Francois [1 ]
机构：
[1] Univ Paris 06, Hematol Lab, Hop St Antoine, F-75012 Paris, France
[2] Univ Paris 11, Inst Gustave Roussy, UMR 1009, INSERM, Villejuif, France
[3] Univ Paris 07, Paris, France
来源：
CURRENT HEMATOLOGIC MALIGNANCY REPORTS | 2012年 / 7卷 / 01期
关键词：
TET2; Mutations; 5-hydroxymethylcytosine; Myeloproliferative neoplasms; Myeloid malignancies; Hematopoietic stem cells; Epigenetics; Pathogenesis; ACUTE MYELOID-LEUKEMIA; HEMATOPOIETIC STEM-CELLS; ACTIVE DNA DEMETHYLATION; TYROSINE KINASE JAK2; POLYCYTHEMIA-VERA; ESSENTIAL THROMBOCYTHEMIA; ACTIVATING MUTATION; CLONAL ANALYSIS; SELF-RENEWAL; 5-HYDROXYMETHYLCYTOSINE;
D O I：
10.1007/s11899-011-0108-8
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Recently, 5-hydroxymethylcytosine (5-hmC), the 6th base of DNA, was discovered as the product of the hydroxylation of 5-methylcytosine (5-mC) by the ten-eleven translocation (TET) oncogene family members. One of them, TET oncogene family member 2 (TET2), is mutated in a variety of myeloid malignancies, including in 15% of myeloproliferative neoplasms (MPNs). Recent studies tried to go further into the biological and epigenetic function of TET2 protein and 5-hmC marks in the pathogenesis of myeloid malignancies. Although its precise function remains partially unknown, TET2 appears to be an important regulator of hematopoietic stem cell biology. In both mouse and human cells, its inactivation leads to a dramatic deregulation of hematopoiesis that ultimately triggers blood malignancies. Understanding this leukemogenic process will provide tools to develop new epigenetic therapies against blood cancers.
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收藏
页码：57 / 64
页数：8
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