Hibi Kenji, Koike Masahiko, Nakayama Hiroshi, Fujitake Shinichi, Kasai Yasushi, Ito Katsuki, Akiyama Seiji, Nakao Akimasa
Second Department of Surgery, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Clin Cancer Res. 2003 Mar;9(3):1053-6.
To date, the presence of p16 gene promoter methylation associated with loss of protein expression has been demonstrated frequently in digestive tract cancers. In this study, we tested for the methylation status of p16 promoter in normal tissue specimens using the methylation-specific PCR technique to examine whether p16 methylation already existed in the background of tumors.
Aberrant promoter methylation of p16 gene was detected in 1 of 40 esophageal and 1 of 69 gastric and no colorectal epithelium specimens, and these 2 specimens were derived from the same patient. We also found the same methylation change in both tumor and blood cell DNA.
These results suggested that the p16 gene was inactivated by methylation in normal background cells of this patient and that other additional factors may promote tumor development in his esophageal and gastric tissues.
迄今为止，与蛋白表达缺失相关的p16基因启动子甲基化在消化道肿瘤中已被频繁证实。在本研究中，我们使用甲基化特异性PCR技术检测正常组织标本中p16启动子的甲基化状态，以检查p16甲基化是否在肿瘤背景中已然存在。
在40份食管上皮标本中的1份、69份胃上皮标本中的1份以及所有结直肠上皮标本中均未检测到p16基因启动子异常甲基化，这2份异常标本来自同一名患者。我们还在肿瘤和血细胞DNA中发现了相同的甲基化变化。
这些结果表明，该患者正常背景细胞中的p16基因因甲基化而失活，其他额外因素可能促使其食管和胃组织发生肿瘤。
