Roles of transbronchial factors including cigarette smoke and asbestos for rapidly increasing lungcancer

香烟烟雾和石棉等经支气管因素对肺癌迅速增加的作用

基本信息

批准号：
11470052
负责人：
ISHIKAWA Yuichi
金额：
$ 4.16万
依托单位：
Japanese Foundation for Cancer Research
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

项目摘要

To investigate the causes of rapidly increasing lung cancer in Japan, we analysed both genetic changes and carcinogenic inhalants including smoking and asbestos. We examined primary lung cancers (9 in 1950s, 52 in 1970s and 60 1990s) in terms of asbestos deposition in the lung. Mean asbestos body concentrations (numbers per g of lung (dry)) were 559, 1804 and 563 in 1950s, 1970s and 1990 s, respectively. Statistically significant elevation in the concentration of 1970s was noted as compared to that of 1990s (p<0.005). Since the lung cancer incidence in Japan has been rising from 1950 to 1990, asbestos exposure is not thought to be a main cause of lung cancer increase. Further, we compared asbestos concentrations in the lung between primary and metastatic lung adenocarcinomas in 1970s. Also, we examined differentiation grades, LOH frequency (presented by FAL values) and p53 mutations in lung adenocarcinomas in 1990s, subclassified to 3 groups by asbestos body concentration (AB, numbers/dry g) : zero AB group (AB=0, n=21), low AB group (0<AB<1000, n=14 and high AB group (1000=<AB, n=l1). AB in primary cancers in 1970s was 2050 in males, significantly higher than that of metastatic cancers, 703, although the difference was not significant in females. In the three groups, well/moderate./poor. were 6/11/4, 6/8/0, 4/7/0 ; FAL values were 0.17, 0.07, 0.13 ; and p53 mutation frequencies were 3/19, 4/14, 5/11. Regardless of asbestos levels, well and moderatelydifferentiated carcinomas were predominant and FAL values were smaller than that for smokers (0.21, n=66). Interestingly, p53 mutation frequency was significantly more frequent in high AB group than in zero AB group (p =0.006).

为了研究日本迅速增加肺癌的原因，我们分析了包括吸烟和石棉在内的遗传变化和致癌吸入剂。我们在肺中的石棉沉积方面检查了原发性肺癌（1950年代的9例，1970年代52和60 1990年代）。在1950年代，1970年代和1990年代，平均石棉体浓度分别为559、1804和563。与1990年代相比，1970年代浓度的统计显着升高（p <0.005）。由于日本的肺癌发病率从1950年到1990年升高，因此，石棉暴露并不是肺癌增加的主要原因。此外，我们比较了1970年代原发性肺腺癌和转移性肺腺癌之间肺中的石棉浓度。另外，我们检查了1990年代肺腺癌中的差异等级，LOH频率（由FAL值提出）和p53突变，通过石棉体浓度（AB，数量/干g）来分类为3组：零AB组（AB = 0，n = 0，n = 21），低AB组（0 <ab <ab <1000，N = 14 = 14 = 14 = 1000 = 1000 = 1000 = 1000 = 1000 = 1000 = 1000 = < 1970年代的男性高于转移性癌症，尽管女性在三组中的差异不大。良好和中等分化的癌主要是吸烟者的癌症（0.21，n = 66）。