TP53-Mutated Myelodysplastic Syndrome and Acute Myeloid Leukemia: Biology, Current Therapy, and Future Directions.
TP53-Mutated Myelodysplastic Syndrome and Acute Myeloid Leukemia: Biology, Current Therapy, and Future Directions.
复制标题
DOI：
10.1158/2159-8290.cd-22-0332
复制
发表时间：
2022-11-02
期刊：
影响因子：
28.2
通讯作者：
Kantarjian, Hagop M.
中科院分区：
文献类型：
--
作者：
Daver, Naval G.;Maiti, Abhishek;Kadia, Tapan M.;Vyas, Paresh;Majeti, Ravindra;Wei, Andrew H.;Garcia-Manero, Guillermo;Craddock, Charles;Sallman, David A.;Kantarjian, Hagop M.
TP 53突变的骨髓增生异常综合征（MDS）和急性髓性白血病（AML）形成了一组不同的骨髓疾病，结局令人沮丧。与非TP 53突变的MDS和AML相比，TP 53突变的MDS和AML对诱导化疗、基于低甲基化剂的方案或基于维奈托克的治疗的应答率较低，中位OS为5-10个月。最近的进展已经确定了TP 53突变的髓系恶性肿瘤的新的致病机制，这有可能改善这一独特的临床亚组的治疗策略。在这篇综述中，我们讨论了TP 53突变的MDS/AML的生物学，目前的治疗和新兴的治疗方法，包括免疫和非免疫为基础的方法，这个实体的最新见解。
TP53-mutated myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) form a distinct group of myeloid disorders with dismal outcomes. TP53-mutated MDS and AML have lower response rates to either induction chemotherapy, hypomethylating agent-based regimens, or venetoclax-based therapies compared with non-TP53-mutated counterparts, and poor median OS of 5–10 months. Recent advances have identified novel pathogenic mechanisms in TP53-mutated myeloid malignancies, which have the potential to improve treatment strategies in this distinct clinical subgroup. In this review we discuss recent insights into the biology of TP53-mutated MDS/AML, current treatments and emerging therapies including immunotherapeutic and non-immune-based approaches for this entity.