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The development of imatinib as a therapeutic agent for chronic myeloid leukemia.伊马替尼作为慢性髓性白血病治疗药物的研发。
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4
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7
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通过强制表达SCL（TAL1）和GATA-1抑制全反式维甲酸诱导的WEHI-3B D+细胞的粒细胞分化。

Inhibition of all-trans retinoic acid-induced granulocytic differentiation of WEHI-3B D+ cells by forced expression of SCL (TAL1) and GATA-1.

作者信息

Ishiguro Kimiko, Rice Anna M, Rice Kevin P, Sartorelli Alan C

机构信息

Department of Pharmacology and Developmental Therapeutics Program, Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

Leuk Res. 2009 Sep;33(9):1249-54. doi: 10.1016/j.leukres.2009.01.022. Epub 2009 Feb 20.

DOI:10.1016/j.leukres.2009.01.022
PMID:19230972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2780339/
Abstract

All-trans retinoic acid (ATRA) induces granulocytic maturation of WEHI-3B D+ leukemia cells and LiCl enhances this maturation, while WEHI-3B D- cells are non-responsive to ATRA. Transfection of SCL, expressed in D- but absent in D+ cells, into D+ cells, caused resistance to ATRA, while transfection of GATA-1 into D+ cells produced resistance to the combination of ATRA and LiCl. SCL expression in D+ cells did not induce the expression of c-Kit, a putative target gene for SCL. LiCl, known to inhibit some kinases by displacing Mg2+, did not affect tyrosine kinase activity of the cytoplasmic domain of c-Kit.

摘要

全反式维甲酸（ATRA）可诱导WEHI-3B D+白血病细胞的粒细胞成熟，而氯化锂可增强这种成熟，而WEHI-3B D-细胞对ATRA无反应。将在D-细胞中表达但在D+细胞中不存在的SCL转染到D+细胞中，会导致对ATRA产生抗性，而将GATA-1转染到D+细胞中则会产生对ATRA和氯化锂组合的抗性。D+细胞中SCL的表达并未诱导c-Kit（一种推测的SCL靶基因）的表达。已知氯化锂通过置换Mg2+来抑制某些激酶，但它并不影响c-Kit胞质结构域的酪氨酸激酶活性。