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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).

为了调查日本肺癌迅速增加的原因，我们分析了基因变化和致癌吸入物，包括吸烟和石棉。我们检查了原发肺癌(20世纪50年代9例，70年代52例，90年代60例)肺内石棉沉积情况。S在20世纪50年代、70年代和1990年的石棉体平均浓度(每克肺(干)石棉数)分别为559、1804和563。与90年代相比，20世纪70年代的集中度在统计上显著上升(p&lt；0.005)。由于日本的肺癌发病率从1950年到1990年一直在上升，接触石棉并不被认为是肺癌增加的主要原因。此外，我们还比较了1970年代原发和转移性肺腺癌患者肺中石棉的浓度。此外，我们还检测了90年代肺腺癌的分化程度、LOH频率(以FAL值表示)和P53突变，根据石棉体浓度(AB，数目/干g)将其细分为3组：零AB组(AB=0，n=21)，低AB组(0&lt；AB&lt；1000，n=14)和高AB组(1000=&lt；AB，n=L1)。20世纪70年代男性原发癌AB为2050，显著高于转移性癌症AB 703，但女性差异不显著。在三组中，良好/中等。/较差。FAL值分别为6/11/4、6/8/0、4/7/0，FAL值分别为0.17、0.07、0.13，P53基因突变率分别为3/19、4/14、5/11。有趣的是，高AB组的P53突变频率显著高于零AB组(p=0.006)。