唾液腺黏液表皮样癌中p16INK4a肿瘤抑制基因的改变。
Alterations of p16INK4a tumour suppressor gene in mucoepidermoid carcinoma of the salivary glands.
作者信息
Guo X-L, Sun S-Z, Wang W-X, Wei F-C, Yu H-B, Ma B-L
机构信息
Department of Oral and Maxillofacial Surgery, School of Stomatology, Shandong University, 44-1 Wenhua West Road, Jinan 250012, China.
出版信息
Int J Oral Maxillofac Surg. 2007 Apr;36(4):350-3. doi: 10.1016/j.ijom.2006.11.004. Epub 2007 Jan 16.
Mucoepidermoid carcinoma (MEC) is common in the salivary glands, but alterations of the p16(INK4a) tumour suppressor gene are largely unknown. The aim of this study was to analyse p16(INK4a) gene alterations in MEC, and evaluate their significance for carcinogenesis. Thirty-eight salivary glands with MEC and six normal salivary glands were studied for p16(INK4a) alterations. In the MEC-affected group, there were 23.7% (9/38) and 13.2% (5/38) cases of homozygous deletion, and 5.3% (2/38) and 2.6% (1/38) cases of point mutation in p16(INK4a) exon 1 and exon 2, respectively. Hypermethylation of the p16(INK4a) gene promoter was found in 13 cases (13/38, 34.2%). Alterations of the p16(INK4a) gene were not found in the normal salivary glands. These findings suggest that the main mechanisms of inactivation of the p16(INK4a) gene in MEC of the salivary glands are promoter hypermethylation and homozygous deletion.
黏液表皮样癌（MEC）在涎腺中较为常见，但p16（INK4a）肿瘤抑制基因的改变在很大程度上尚不清楚。本研究的目的是分析MEC中p16（INK4a）基因的改变，并评估其在致癌过程中的意义。对38例患有MEC的涎腺和6例正常涎腺进行了p16（INK4a）改变的研究。在MEC受累组中，p16（INK4a）外显子1和外显子2的纯合缺失病例分别为23.7%（9/38）和13.2%（5/38），点突变病例分别为5.3%（2/38）和2.6%（1/38）。在13例（13/38，34.2%）中发现了p16（INK4a）基因启动子的高甲基化。在正常涎腺中未发现p16（INK4a）基因的改变。这些发现表明，涎腺MEC中p16（INK4a）基因失活的主要机制是启动子高甲基化和纯合缺失。
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