细胞周期蛋白D1
生物
互补DNA
非翻译区
套细胞淋巴瘤
编码区
分子生物学
南方斑点
基因
癌症研究
北方斑点
细胞周期蛋白D
基因重排
淋巴瘤
遗传学
信使核糖核酸
细胞周期
免疫学
作者
Ruth Rimokh,F Berger,Christian Bastard,Benjamin Y. Klein,Martine French,E Archimbaud,JP Rouault,B Santa Lucia,Laurent Duret,M Vuillaume
出处
期刊:Blood
[American Society of Hematology]
日期:1994-06-15
卷期号:83 (12): 3689-3696
被引量:131
标识
DOI:10.1182/blood.v83.12.3689.3689
摘要
Abstract Rearrangement and overexpression of CCND1 (BCL1/PRAD1), a member of the cyclin G1 gene family, are consistent features of t(11q13)-bearing B- lymphoid tumors (particularly mantle-cell lymphoma [MCL]). Its deregulation is thought to perturb the G1-S transition of the cell cycle and thereby to contribute to tumor development. As suggested by previously published studies, rearrangement of the 3′ untranslated region (3′ UTR) of CCND1 may contribute to its activation in some lymphoid tumors. To define further the prevalence of such rearrangements, we report here the result of the molecular study of 34 MCL and six t(11q13)-associated leukemias using a set of probes specific to the different parts of the CCND1 transcript. We also sequenced the entire cDNA of the overexpressed CCND1 transcripts in a t(11q13)-associated leukemia. DNA from four of these 40 patients showed rearrangement of the 3′ UTR of CCND1 coexisting with major translocation cluster (MTC) rearrangement. Southern blot and sequence analyses showed that, as a result of these rearrangements, the 3′ AU- rich region containing sequences involved in mRNA stability and in translational control is eliminated. Moreover, the finding that the CCND1 mRNA half-life was greater than 3 hours (normal tissues, 0.5 hours) in three t(11q13)-associated cell lines stresses the importance of posttranscriptional derangement in the activation of CCND1. Finally, we did not observe any mutation in the coding frame of the CCND1 cDNA analyzed.
科研通智能强力驱动
Strongly Powered by AbleSci AI