Egashira Akinori, Morita Masaru, Kakeji Yoshihiro, Sadanaga Noriaki, Oki Eiji, Honbo Takuya, Ohta Mitsuhiko, Maehara Yoshihiko
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Cancer Sci. 2007 Aug;98(8):1152-6. doi: 10.1111/j.1349-7006.2007.00524.x. Epub 2007 Jun 15.
Esophageal squamous cell carcinoma is a form of cancer that has varying incidence rates among different countries, distinct geographic areas and different ethnic groups. According to previous reports, p53 gene mutations have been identified in 20-80% of these tumors, and these mutations have occurred at an early stage. These findings suggest that such mutations play an important role in esophageal carcinogenesis, and highlight the importance of mutagens, which cause sequence alterations in the p53 gene. In order to clarify the environmental factors and the molecular mechanisms that may be responsible for the occurrence and prevention of a specific mutation in the process of esophageal carcinogenesis, we analyzed p53 gene mutations in 95 samples of esophageal squamous cell carcinoma. We further reviewed published reports investigating the frequency of p53 gene mutations in esophageal cancer from high-risk areas to normal-risk areas and compared these findings to our results in Japan. The frequency of p53 gene mutations in Japanese esophageal cancer is 47.4% and there are three prominent features: (1) a predominance of transversions, in particular the G:C to T:A transversion; (2) a relatively low frequency of transitions; and (3) a relatively high percentage of frameshift mutations. These results indicate the possible importance of the benzo[a]pyrene metabolite and oxidative DNA damage in esophageal carcinogenesis and scarcely correlate with DNA replication errors or alkylation in comparison to other gastrointestinal cancers. In addition, we observed a peculiar sequence of frameshift mutations. Taken together, these data suggest that this tumor suppressor gene plays a critical role in the multistep carcinogenesis process for esophageal squamous cell cancer.
食管鳞状细胞癌是一种在不同国家、不同地理区域和不同种族群体中发病率各异的癌症形式。根据先前的报道,在20%至80%的此类肿瘤中已鉴定出p53基因突变,且这些突变发生在早期阶段。这些发现表明此类突变在食管癌发生过程中起重要作用,并凸显了诱变剂的重要性,诱变剂会导致p53基因序列改变。为了阐明可能导致食管癌发生过程中特定突变的环境因素和分子机制,我们分析了95例食管鳞状细胞癌样本中的p53基因突变情况。我们还进一步回顾了已发表的关于从高危地区到低危地区食管癌中p53基因突变频率的报告,并将这些发现与我们在日本的研究结果进行了比较。日本食管癌中p53基因突变频率为47.4%,且有三个显著特征:(1)颠换占优势,尤其是G:C到T:A的颠换;(2)转换频率相对较低;(3)移码突变百分比相对较高。这些结果表明苯并[a]芘代谢产物和氧化性DNA损伤在食管癌发生过程中可能具有重要意义,与其他胃肠道癌症相比,与DNA复制错误或烷基化几乎没有关联。此外,我们观察到了一种特殊的移码突变序列。综上所述,这些数据表明该肿瘤抑制基因在食管鳞状细胞癌的多步骤致癌过程中起关键作用。