Suppr超能文献

在T细胞急性淋巴细胞白血病中,Rhom-2表达并不总是与11号染色体p13带的异常相关。

Rhom-2 expression does not always correlate with abnormalities on chromosome 11 at band p13 in T-cell acute lymphoblastic leukemia.

作者信息

Fitzgerald T J, Neale G A, Raimondi S C, Goorha R M

机构信息

Department of Virology and Molecular Biology, St Jude Children's Research Hospital, Memphis, TN 38101.

出版信息

Blood. 1992 Dec 15;80(12):3189-97.

PMID:1281693
Abstract

A frequent site for nonrandom recombination in T-cell acute lymphoblastic leukemia (T-ALL) is chromosome 11 at p13. The molecular characterization of a (7;11)(q35;p13) translocation showed that the translocation breakpoint was 2 kb 5' to the T-ALLbcr locus resulting in the juxtaposition of the T-cell receptor (TCR) beta gene to the rhom-2 gene locus. Northern blot analysis did not detect expression of the rhom-2 gene in the leukemic blasts of the (7;11) translocation. However, using a sensitive polymerase chain reaction (PCR)-based assay, the (7;11) translocation showed a trace expression of rhom-2 at a level of 0.01% of TCR-beta message. Because rhom-2 is considered a proto-oncogene, the significance of the trace expression of rhom-2 in the (7;11) translocation was investigated by comparing the level of rhom-2 expression in 7 additional T-ALLs, normal thymocytes, and CEM (pre-T) and HPB (mature-T) cell lines using the PCR assay. The CEM cells, normal thymocytes, and one patient, whose blasts had no cytogenetic abnormality of chromosome 11, did not express rhom-2 indicating that rhom-2 is not normally expressed in T cells. The other six T-ALLs fell into three categories: (1) two T-ALLs overexpressed rhom-2 in the presence of a translocation; (2) two T-ALLs had trace expression in the presence of a translocation; and (3) two T-ALLs had trace expression with no observable abnormalities on chromosome 11 at p13. Therefore, the data indicate that not all translocations at the T-ALLbcr locus result in overexpression of rhom-2. To account for the sharp contrast in rhom-2 expression seen in these T-ALLs, a model is proposed with a negative regulatory element in the T-ALLbcr locus that is disrupted in some of the cases leading to overexpression of rhom-2.

摘要

T细胞急性淋巴细胞白血病(T-ALL)中一个常见的非随机重组位点是11号染色体的p13区域。对(7;11)(q35;p13)易位的分子特征分析表明,易位断点位于T-ALLbcr基因座5'端2 kb处,导致T细胞受体(TCR)β基因与rhom-2基因座并列。Northern印迹分析未在(7;11)易位的白血病母细胞中检测到rhom-2基因的表达。然而,使用基于聚合酶链反应(PCR)的灵敏检测方法,(7;11)易位显示rhom-2有微量表达,其水平为TCR-β信使的0.01%。由于rhom-2被认为是一种原癌基因,通过使用PCR检测方法比较另外7例T-ALL、正常胸腺细胞以及CEM(前T)和HPB(成熟T)细胞系中rhom-2的表达水平,研究了(7;11)易位中rhom-2微量表达的意义。CEM细胞、正常胸腺细胞以及一名其母细胞无11号染色体细胞遗传学异常的患者均未表达rhom-2,这表明rhom-2在T细胞中通常不表达。其他6例T-ALL分为三类:(1)2例T-ALL在存在易位的情况下rhom-2过表达;(2)2例T-ALL在存在易位的情况下有微量表达;(3)2例T-ALL有微量表达,而11号染色体p13区域未观察到明显异常。因此,数据表明并非所有T-ALLbcr基因座的易位都会导致rhom-2过表达。为了解释这些T-ALL中rhom-2表达的显著差异,提出了一个模型,即在T-ALLbcr基因座中存在一个负调控元件,在某些情况下该元件被破坏,导致rhom-2过表达。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验