表观遗传学
罗咪酯肽
淋巴瘤
切碎
外周T细胞淋巴瘤
医学
表观遗传疗法
肿瘤科
生物信息学
疾病
DNA甲基化
癌症研究
免疫学
内科学
生物
T细胞
遗传学
组蛋白脱乙酰基酶
组蛋白
基因
基因表达
免疫系统
作者
Suheil Albert Atallah‐Yunes,Michael J. Robertson,Utpal P. Davé
标识
DOI:10.1016/j.clml.2022.04.015
摘要
Peripheral T cell lymphomas (PTCL) comprise a diverse group of aggressive T-cell and NK-cell lymphomas with many subtypes sharing same treatment algorithms despite having different pathobiology and responses to treatment. The molecular advances made in discovery of genetic mutations that disrupt epigenetic modulation in some subtypes of PTCL such as angioimmunoblastic T cell lymphoma and PTCL-not otherwise specified (NOS) may explain the poor outcomes and unsatisfactory responses to frontline line CHOP and CHOP-like therapy seen in this group of lymphomas. In this article, we address the main genetic mutations such as IDH2, TET2 and DNMT3A seen in PTCL and that disrupt the epigenetic modulation pathways, focusing on acetylation, deacetylation and methylation. Since therapeutic agents that target the disrupted epigenetic modulation pathways in PTCL may change treatment landscape in the near future, we will highlight the ones approved for treatment of refractory and/or relapsed PTCL and also the pivotal regimens being evaluated in clinical trials for treatment of frontline and refractory relapsed disease. We stress the importance of determining whether there is an association between the discussed genetic mutations and responses to the highlighted therapeutic agents such that treatments could be better tailored in patients with this kind of lymphoma with unmet needs.
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