Röijer E, Dahlenfors R, Mark J, Stenman G
Department of Pathology, Göteborg University, Sahlgrenska University Hospital, Sweden.
Virchows Arch. 1997 Apr;430(4):339-42. doi: 10.1007/BF01092758.
We report on an adenoid cystic-carcinoma (ACC) with a clonal deletion of 17p as the only karyotypic abnormality. Using different chromosome 17-derived probes we showed by FISH that the deletion encompassed the p53 tumour suppressor gene. Immunohistochemical analysis revealed overexpression of p53 protein in a subpopulation of cells, suggesting a mutation in the remaining p53 allele in these cells. Our findings provide novel information about possible progressional pathways in ACC, and demonstrate the value of combining conventional cytogenetic analysis with-molecular cytogenetic and immunohistochemical methods. This approach is particularly useful in cases with minor cytogenetic abnormalities at the border of visibility.
我们报告了一例腺样囊性癌（ACC），其唯一的核型异常为17号染色体短臂的克隆性缺失。使用不同的源自17号染色体的探针，我们通过荧光原位杂交（FISH）显示该缺失包含p53肿瘤抑制基因。免疫组织化学分析显示在一部分细胞中p53蛋白过表达，提示这些细胞中剩余的p53等位基因发生了突变。我们的研究结果提供了关于腺样囊性癌可能的进展途径的新信息，并证明了将传统细胞遗传学分析与分子细胞遗传学和免疫组织化学方法相结合的价值。这种方法在可见度边界处存在微小细胞遗传学异常的病例中特别有用。
