文章：

EVI1失调：对髓系恶性肿瘤生物学和治疗的影响

EVI1 dysregulation: impact on biology and therapy of myeloid malignancies

原文发布日期：2021-03-22

DOI: 10.1038/s41408-021-00457-9

类型: Review Article

开放获取: 是

英文摘要：

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.
 

摘要翻译： 

嗜酸性病毒整合位点1（Evi1）于1988年被发现，是小鼠髓系恶性肿瘤中嗜酸性病毒整合的常见位点。EVI1是一种致癌锌指转录因子，其过度表达会促进疾病进展和侵袭性表型，并与髓系恶性肿瘤的不良临床结局相关。尽管对EVI1失调生物学机制的认识有所进展，但治疗结局的显著改善仍难以实现。本文重点阐述EVI1生物学机制的研究进展，并探讨这些新知识如何指导新型治疗干预策略的开发。EVI1过度表达与某些上皮癌的不良预后相关。然而，本综述主要关注过度表达EVI1的髓系恶性肿瘤的遗传学改变、生物学特性及当前治疗策略。

原文链接：

EVI1 dysregulation: impact on biology and therapy of myeloid malignancies