Environmental and heritable causes of cancer among 9.6 million individuals in the Swedish family-cancer database

Environmental and heritable causes of cancer among 9.6 million individuals in the Swedish family-cancer database
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DOI:
10.1002/ijc.10332
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发表时间:
2002-05-10
影响因子:
6.4
通讯作者:
Hemminki, K
Hemminki, K
中科院分区:
医学1区
文献类型:
--
作者:
Czene, K;Lichtenstein, P;Hemminki, K

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利用瑞典全国家庭癌症数据库估计了15种常见癌症的遗传和环境因素。四分相关性用于描述家庭成员之间癌症易感性的相似性。结构方程模型被用来估计遗传和环境影响的重要性。除白血病外,所有被研究的癌症都获得了由遗传效应引起的癌症易感性比例的统计显著估计。甲状腺癌的估计最高(53%),其次是内分泌腺(28%)、睾丸(25%)、乳腺(25%)、子宫颈(22%)、黑色素瘤(21%)、结肠(13%)、神经系统(12%)、直肠(12%)、非霍奇金淋巴瘤(10%)、肺(8%)、肾(8%)、膀胱(7%)、胃(1%)和白血病(1%)。共同环境影响的估计范围从0%(宫颈)到15%(胃)。儿童期共同环境影响在睾丸癌(17%)、胃癌(13%)和宫颈原位癌(13%)中最为重要。我们的研究结果表明,除甲状腺外,环境在所有研究部位的癌症中起主要的致病作用。另一方面,遗传性在某些部位对癌症的影响相对较大,这表明尽管在许多癌症部位已经描述了易感基因,但它们可能只能解释部分遗传效应。(C) 2002 Wiley-Liss, Inc。
The genetic and environmental components in 15 common cancers were estimated using the nationwide Swedish Family-Cancer Database. Tetrachoric correlations were used to describe similarity in cancer liability among family members. Structural equation modeling was used to derive estimates of the importance of genetic and environmental effects. Statistically significant estimates of proportion of cancer susceptibility, accounted for by genetic effects, were obtained for all studied cancers except for leukemia. The estimate was highest in thyroid cancer (53%), followed by tumors at endocrine glands (28%), testis (25%), breast (25%), cervix (22%), melanoma (21%), colon (13%), nervous system (12%), rectum (12%), non-Hodgkin lymphoma (10%), lung (8%), kidney (8%), urinary bladder (7%), stomach (1%) and leukemia (1%). The estimates of shared environmental effects ranged from 0% (cervix) to 15% (stomach). The childhood shared environmental effects were most Important in testicular cancer (17%), stomach cancer (13%) and cervix in situ (13%). Our results indicate that environment has a principal causative role in cancer at all studied sites except for thyroid. The relatively large effect of heritability in cancer at some sites, on the other hand, indicates that even though susceptibility genes have been described at many cancer sites, they are likely to explain only part of the genetic effects. (C) 2002 Wiley-Liss, Inc.