Suppr超能文献

MYC在T细胞急性淋巴细胞白血病中的作用:功能影响及靶向治疗策略

MYC in T-cell acute lymphoblastic leukemia: functional implications and targeted strategies.

作者信息

Li Qilong, Pan Sa, Xie Ting, Liu Hudan

机构信息

Department of Hematology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, Wuhan 430071, China.

出版信息

Blood Sci. 2021 Jun 7;3(3):65-70. doi: 10.1097/BS9.0000000000000073. eCollection 2021 Jul.

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological cancer that frequently occurs in children and adolescents, which results from the transformation of immature T-cell progenitors. Aberrant cell growth and proliferation of T-ALL lymphoblasts are sustained by activation of strong oncogenic drivers. Mounting evidence highlights the critical role of the NOTCH1-MYC highway toward the initiation and progression of T-ALL. MYC has been emphasized as a primary NOTCH1 transcriptional target impinging in leukemia-initiating cell activity particularly responsible for disease onset and relapse. These findings lay a foundation of T-ALL as an ideal disease model for studying MYC-mediated cancer. The biology of MYC deregulation in T-ALL supports innovative strategies for therapeutic targeting of MYC. To summarize the relevant literature and data in recent years, we here provide a comprehensive overview of the functional importance of MYC in T-ALL development, and the molecular mechanisms underlying MYC deregulation in T-ALL. Finally, we illustrate the innovative MYC-targeted approaches that have been evaluated in pre-clinical models and shown significant efficacy. Given the complexity of T-ALL molecular pathogenesis, we propose that a combination of anti-MYC strategies with conventional chemotherapies or other targeted/immunotherapies may provide the most durable response, especially for those patients with relapsed and refractory T-ALL.

摘要

T细胞急性淋巴细胞白血病(T-ALL)是一种侵袭性血液癌症,常见于儿童和青少年,由未成熟T细胞祖细胞转化而来。T-ALL淋巴母细胞异常的细胞生长和增殖通过强大致癌驱动因子的激活得以维持。越来越多的证据突显了NOTCH1-MYC通路在T-ALL起始和进展中的关键作用。MYC被强调为NOTCH1的主要转录靶点,影响白血病起始细胞活性,尤其与疾病的发生和复发有关。这些发现奠定了T-ALL作为研究MYC介导癌症的理想疾病模型的基础。T-ALL中MYC失调的生物学特性支持针对MYC的创新治疗策略。为总结近年来的相关文献和数据,我们在此全面概述MYC在T-ALL发展中的功能重要性,以及T-ALL中MYC失调的分子机制。最后,我们阐述了在临床前模型中评估并显示出显著疗效的创新型MYC靶向方法。鉴于T-ALL分子发病机制的复杂性,我们提出将抗MYC策略与传统化疗或其他靶向/免疫疗法联合使用可能会产生最持久的反应,特别是对于那些复发和难治性T-ALL患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc5/8974894/81a12f715dce/bls-3-065-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验