Janus Kinase Deregulation in Leukemia and Lymphoma

被引：118

作者：

Chen, Edwin ^{[2
]}

Staudt, Louis M. ^{[1
]}

Green, Anthony R. ^{[2
,3
]}

机构：

[1] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA

[2] Univ Cambridge, Cambridge Inst Med Res, Cambridge CB2 0XY, England

[3] Addenbrookes Hosp, Dept Haematol, Cambridge CB2 0XY, England

来源：

IMMUNITY | 2012年 / 36卷 / 04期

基金：

美国国家卫生研究院;

关键词：

ACUTE LYMPHOBLASTIC-LEUKEMIA; B-CELL LYMPHOMA; JAK2 V617F MUTATION; ACUTE MEGAKARYOBLASTIC LEUKEMIA; HEMATOPOIETIC STEM-CELL; CHRONIC MYELOPROLIFERATIVE DISORDERS; JUVENILE MYELOMONOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; OF-FUNCTION MUTATIONS; POLYCYTHEMIA-VERA;

D O I：

10.1016/j.immuni.2012.03.017

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Genetic alterations affecting members of the Janus kinase (JAK) family have been discovered in a wide array of cancers and are particularly prominent in hematological malignancies. In this review, we focus on the role of such lesions in both myeloid and lymphoid tumors. Oncogenic JAK molecules can activate a myriad of canonical downstream signaling pathways as well as directly interact with chromatin in noncanonical processes, the interplay of which results in a plethora of diverse biological consequences. Deciphering these complexities is shedding unexpected light on fundamental cellular mechanisms and will also be important for improved diagnosis, identification of new therapeutic targets, and the development of stratified approaches to therapy.

引用

页码：529 / 541

页数：13

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