Savas Sevtap, Schmidt Steffen, Jarjanazi Hamdi, Ozcelik Hilmi
Fred A. Litwin Centre for Cancer Genetics, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, M5G 1X5, Canada.
Hum Genomics. 2006 Mar;2(5):287-96. doi: 10.1186/1479-7364-2-5-287.
Although highly penetrant alleles of BRCA1 and BRCA2 have been shown to predispose to breast cancer, the majority of breast cancer cases are assumed to result from the presence of low-moderate penetrant alleles and environmental carcinogens. Non-synonymous single nucleotide polymorphisms (nsSNPs) are hypothesised to contribute to disease susceptibility and approximately 30 per cent of them are predicted to have a biological significance. In this study, we have applied a bioinformatics-based strategy to identify breast cancer-related nsSNPs from 981 carcinogenesis-related genes expressed in breast tissue. Our results revealed a total of 367 validated nsSNPs, 109 (29.7 per cent) of which are predicted to affect the protein function (functional nsSNPs), suggesting that these nsSNPs are likely to influence the development and homeostasis of breast tissue and hence contribute to breast cancer susceptibility. Sixty-seven of the functional nsSNPs presented as commonly occurring nsSNPs (minor allele frequencies > or =5 per cent), representing excellent candidates for breast cancer susceptibility. Additionally, a non-uniform distribution of the common functional nsSNPs among different human populations was observed: 15 nsSNPs were reported to be present in all populations analysed, whereas another set of 15 nsSNPs was specific to particular population(s). We propose that the nsSNPs analysed in this study constitute a unique resource of potential genetic factors for breast cancer susceptibility. Furthermore, the variations in functional nsSNP allele frequencies across major population backgrounds may point to the potential variability of the molecular basis of breast cancer predisposition and treatment response among different human populations.
虽然已证明BRCA1和BRCA2的高 penetrant 等位基因易患乳腺癌,但大多数乳腺癌病例被认为是由低 - 中度 penetrant 等位基因和环境致癌物的存在所致。非同义单核苷酸多态性(nsSNPs)被假设与疾病易感性有关,其中约30%预计具有生物学意义。在本研究中,我们应用了一种基于生物信息学的策略,从乳腺组织中表达的981个致癌相关基因中鉴定与乳腺癌相关的nsSNPs。我们的结果共揭示了367个经过验证的nsSNPs,其中109个(29.7%)预计会影响蛋白质功能(功能性nsSNPs),这表明这些nsSNPs可能会影响乳腺组织的发育和内稳态,从而导致乳腺癌易感性。67个功能性nsSNPs表现为常见的nsSNPs(次要等位基因频率≥5%),是乳腺癌易感性的极佳候选者。此外,观察到常见功能性nsSNPs在不同人群中的分布不均匀:据报道,15个nsSNPs在所有分析的人群中都存在,而另一组15个nsSNPs则特定于特定人群。我们认为,本研究中分析的nsSNPs构成了乳腺癌易感性潜在遗传因素的独特资源。此外,主要人群背景中功能性nsSNP等位基因频率的变化可能表明不同人群中乳腺癌易感性和治疗反应的分子基础存在潜在变异性。