zui近英國牛津大學科研人員進行的一項研究確認，遺傳因素和環(huán)境因素對乳腺癌發(fā)病風險的影響是相互獨立的，控制環(huán)境因素可有效降低乳腺癌的發(fā)病率。相關研究成果發(fā)表在zui近一期的《柳葉刀》雜志上。

乳腺癌的風險因素包括環(huán)境（生活方式和行為等）因素和遺傳因素兩大類，其中環(huán)境因素，如激素替代療法的使用、生育歷史、肥胖、飲酒等，是引發(fā)乳腺癌的主要原因。而遺傳因素是否會與環(huán)境因素相互作用，從而進一步增加患病風險，學界一直沒有明確。

牛津大學癌癥疫學所的研究人員對英國7160名乳腺癌患者和10196名健康婦女的基因和環(huán)境因素信息進行了研究。通過對12個和乳腺癌相關的常見基因變異與10個乳腺癌環(huán)境風險因素，包括生育次數、生育*胎時的年齡、是否母乳喂養(yǎng)、是否使用激素替代療法、肥胖、飲酒等，進行比較研究后確認，這兩類風險因素之間并不存在相互作用的情況，即使是激素替代療法也不會對遺傳因素產生影響。也就是說，基因變異與不良生活方式都會增加罹患乳腺癌的風險，但二者互不相干。

需要指出的是，12個變異基因中不包括罕見的乳腺癌易感基因BRCA1和BRCA2。這兩個基因攜帶者罹患乳腺癌的風險很高，但有此基因變異的人也很少。

研究人員指出，確認遺傳因素和環(huán)境因素這兩種風險因素間的關系可使醫(yī)生更好地理解它們對乳腺癌的影響。在罹患乳腺癌的婦女中，受遺傳因素影響發(fā)病的比例并不大，大多數婦女患病的原因要歸罪于環(huán)境因素，而這些因素是可以人為控制的。因此，通過對環(huán)境風險因素的控制，就可以在很大程度上降低乳腺癌的發(fā)病率。

上海勁馬生物（）推薦原文出處：

The Lancet doi:10.1016/S0140-6736（10）60636-8

Gene—environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study
Dr Ruth C Travis DPhil a , Gillian K Reeves PhD a, Jane Green MD a, Diana Bull a, Sarah J Tipper MSc a, Krys Baker a, Prof Valerie Beral FRS a, Prof Richard Peto FRS b, Prof John Bell FRS c, Diana Zelenika PhD d, Prof Mark Lathrop PhD d, for the Million Women

Background
Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors （reproductive, behavioural, and anthropometric risk factors for breast cancer）. To test for evidence of gene—environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study.
Methods
We tested gene—environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms （FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054） in relation to prospectively collected information about ten established environmental risk factors （age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption）.
Findings
After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene—environment interaction. By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease. Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers （mean height 162·4 cm [95% CI 162·1—162·7] vs 163·1 cm [162·9—163·2]; p=0·01 after allowance for multiple testing）.
Interpretation
Risks of breast cancer associated with low-penetrance susceptibility polymorphisms do not vary significantly with these ten established environmental risk factors.
Funding
Cancer Research UK and the UK Medical Research Council.