M L Gulley, Q Zhang, R D Gascoyne, B R DuPont, P M Banks, C G Cho, J M Huang, E A Montalvo
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引用次数: 0
摘要
我们最近克隆了一个基因,其蛋白产物与eb病毒BZLF1基因启动子结合。同样的基因之前已经被另一个小组克隆,他们将其命名为S mu bp-2,因为它的蛋白产物与免疫球蛋白重链基因的S mu基序结合,在那里它被假定在免疫球蛋白类转换中起作用。在目前的研究中,我们证实S mu bp-2基因位于染色体11q13上,该位点已知在50-70%的套细胞淋巴瘤中因易位而改变。我们使用Southern blot分析来确定在25个套细胞淋巴瘤中是否有S mu bp-2基因在结构上重排。我们在这些淋巴瘤中没有发现重排的证据,包括18个通过细胞遗传学分析被证明含有t(11;14)的淋巴瘤。这些数据表明,S mu bp-2基因的结构改变并不是套细胞淋巴瘤发生的潜在机制。
Translocations of 11q13 in mantle cell lymphoma fail to disrupt the S mu bp-2 gene.
We recently cloned a gene whose protein product binds to the Epstein-Barr virus BZLF1 gene promoter. The same gene has been previously cloned by another group who named it S mu bp-2 because its protein product binds to the S mu motif of the immunoglobulin heavy chain gene where it is postulated to function in immunoglobulin class switching. In the current study, we confirm that the S mu bp-2 gene is located on chromosome 11q13, a locus known to be altered by translocation in 50-70% of mantle cell lymphomas. We used Southern blot analysis to determine whether the S mu bp-2 gene was structurally rearranged in any of 25 mantle cell lymphomas. We found no evidence of rearrangement in any of these lymphomas including 18 that were proven to contain t(11;14) by cytogenetic analysis. These data suggest that structural alteration of the S mu bp-2 gene is not an underlying mechanism of tumorigenesis in mantle cell lymphomas.