Division of Cancer Medicine, Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, TX, 77030, USA.
Blood Cancer J. 2021 Mar 22;11(3):64. doi: 10.1038/s41408-021-00457-9.
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.
嗜同性病毒整合位点 1(Evi1)于 1988 年被发现,是嗜同性病毒整合的常见靶点,导致小鼠发生髓系恶性肿瘤。EVI1 是一种致癌性锌指转录因子,其过度表达有助于疾病进展和侵袭性表型,与髓系恶性肿瘤的不良临床结局相关。尽管在理解 EVI1 失调的生物学方面取得了进展,但在治疗结果方面仍未取得显著改善。在这里,我们重点介绍了对 EVI1 生物学的理解进展,并讨论了这些新知识如何为新型治疗干预措施的发展提供信息。EVI1 的过表达与某些上皮癌的不良预后相关。然而,本篇综述的重点是表达 EVI1 的髓系恶性肿瘤的遗传病变、生物学和当前治疗方法。