Enlund Fredrik, Persson Fredrik, Stenman Göran
Lundberg Laboratory for Cancer Research, Department of Pathology, Göteborg University, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden.
Eur J Oral Sci. 2004 Dec;112(6):545-7. doi: 10.1111/j.1600-0722.2004.00174.x.
Deletions affecting the long arm of chromosome 6 are a characteristic feature of all major subtypes of malignant salivary gland tumors. Moreover, a subgroup of adenoid cystic carcinomas have t(6;9)(q23-25;p21-24) translocations with breakpoints located within the commonly deleted region. Here we have examined the possible involvement of the candidate tumor suppressor gene, PLAGL1, in these deletions and translocations. Northern blot and fluorescence in situ hybridization (FISH) analyses of a series of 27 salivary gland tumors revealed no significant changes in the gene expression or rearrangements of PLAGL1. FISH analysis also demonstrated that the 6q translocation breakpoint in adenoid cystic carcinomas with t(6;9) is proximal to the PLAGL1 locus. Collectively, these results indicate that PLAGL1 is not likely to be the major target gene of the 6q rearrangements in salivary gland tumors.
影响6号染色体长臂的缺失是恶性涎腺肿瘤所有主要亚型的特征性表现。此外,一部分腺样囊性癌存在t(6;9)(q23 - 25;p21 - 24)易位,其断点位于常见的缺失区域内。在此,我们研究了候选抑癌基因PLAGL1在这些缺失和易位中可能发挥的作用。对一系列27例涎腺肿瘤进行的Northern印迹和荧光原位杂交(FISH)分析显示,PLAGL1的基因表达或重排没有显著变化。FISH分析还表明,发生t(6;9)的腺样囊性癌中6q易位断点位于PLAGL1基因座近端。总体而言,这些结果表明PLAGL1不太可能是涎腺肿瘤6q重排的主要靶基因。