为成功治疗 T 细胞 ALL 而努力。
"Root"ing for successful T-ALL treatment.
机构信息
University of Connecticut Health Center.
University of Arizona.
出版信息
Blood. 2021 May 6;137(18):2422-2423. doi: 10.1182/blood.2020009748.
Abstract
In this issue of , Anand et al provide compelling evidence that resistance to Notch inhibitor therapy in early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) occurs as a result of an activated phosphatidylinositol 3-kinase (PI3K) pathway. To further decipher the resistance mechanism, the investigators performed single-cell RNA sequencing analysis on the bone marrow of 5 patients treated with the γ-secretase inhibitor (GSI) BMS-906024 and found 13 different cell clusters, of which 6 were specific to leukemia patients.
摘要
在本期《》中，Anand 等人提供了令人信服的证据，表明早期 T 细胞前体急性淋巴细胞白血病（ETP-ALL）对 Notch 抑制剂治疗的耐药性是由于磷酸肌醇 3-激酶（PI3K）途径的激活所致。为了进一步解析耐药机制，研究人员对 5 例接受 γ-分泌酶抑制剂（GSI）BMS-906024 治疗的患者的骨髓进行了单细胞 RNA 测序分析，发现了 13 个不同的细胞簇，其中 6 个是白血病患者所特有的。
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本文引用的文献
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