EVI1 dysregulation: impact on biology and therapy of myeloid malignancies

被引：41

作者：

Birdwell, Christine ^{[1
]}

Fiskus, Warren ^{[1
]}

Kadia, Tapan M. ^{[1
]}

DiNardo, Courtney D. ^{[1
]}

Mill, Christopher P. ^{[1
]}

Bhalla, Kapil N. ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Div Canc Med, Houston, TX 77030 USA

来源：

BLOOD CANCER JOURNAL | 2021年 / 11卷 / 03期

关键词：

D O I：

10.1038/s41408-021-00457-9

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Ecotropic viral integration site 1 (Evi1) was discovered in 1988 as a common site of ecotropic viral integration resulting in myeloid malignancies in mice. EVI1 is an oncogenic zinc-finger transcription factor whose overexpression contributes to disease progression and an aggressive phenotype, correlating with poor clinical outcome in myeloid malignancies. Despite progress in understanding the biology of EVI1 dysregulation, significant improvements in therapeutic outcome remain elusive. Here, we highlight advances in understanding EVI1 biology and discuss how this new knowledge informs development of novel therapeutic interventions. EVI1 is overexpression is correlated with poor outcome in some epithelial cancers. However, the focus of this review is the genetic lesions, biology, and current therapeutics of myeloid malignancies overexpressing EVI1.

引用

页数：14

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