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Familial risk of breast cancer by dynamic, accumulative, and static definitions of family history.

动态、累积和静态家族史定义的乳腺癌家族性风险。

  • 影响因子:4.78
  • DOI:10.1002/cncr.32815
  • 作者列表:"Mukama T","Kharazmi E","Sundquist K","Sundquist J","Brenner H","Fallah M
  • 发表时间:2020-06-15
Abstract

BACKGROUND:Familial breast cancer risk studies usually overlook the dynamic nature of family history. METHODS:The authors assessed the effect of incorporating the timing of cancer diagnosis events into the assessment of familial risks of breast cancer in first-degree and second-degree relatives in a nationwide cohort study of 5,099,172 women (follow-up was between 1958-2015). Family history was assessed using 3 approaches: 1) as a static variable (ever having a relative with breast cancer); 2) as accumulative history; and 3) as a dynamic variable (time-dependent variable). RESULTS:For women aged <50 years, familial risk was mostly higher when family history was assessed as a dynamic variable compared with using a static or accumulative family history. For example, the cumulative risk of receiving a breast cancer diagnosis until age 50 years for women with a history of breast cancer in 1 first-degree relative was 2.6% (95% CI, 2.5%-2.7%) using the static method, 2.4% (95% CI, 2.3%-2.4%) using the accumulative method, and 3.1% (95% CI, 3.0%-3.2%) using the dynamic method. Relative risk in women aged <50 years with a breast cancer diagnosis in a sister was 1.40-fold (95% CI, 1.31-fold to 1.48-fold) using the static method, 1.66-fold (95% CI, 1.57-fold to 1.76-fold) using the accumulative method, and 2.28-fold (95% CI, 2.07-fold to 2.51-fold) using the dynamic method. CONCLUSIONS:The results of the current study demonstrated that assessing family history as static, accumulative, or dynamic results in different familial risk estimates. The answer as to which method to use for family history assessment depends on the implications of the study, with the dynamic method appearing to be better suited for risk stratification studies, the accumulative method being the most convenient in practice and the least favored for risk prediction, and the static method being suitable for etiological impact and risk attribution studies.

摘要

背景: 家族性乳腺癌风险研究通常忽视家族史的动态性质。 方法: 作者在一项 5,099,172 名女性的全国性队列研究中评估了将癌症诊断事件的时间纳入一级和二级亲属乳腺癌家族风险评估的效果 (随访在 1958-2015 之间)。使用 3 种方法评估家族史: 1) 作为静态变量 (曾经患有乳腺癌的亲属); 2) 作为累积病史; 3) 作为动态变量 (随时间变化的变量)。 结果: 对于 <50 岁的女性,与使用静态或累积家族史相比,将家族史评估为动态变量时,家族风险大多较高。例如,1 位一级亲属有乳腺癌病史的女性在 50 岁之前接受乳腺癌诊断的累积风险为 2.6% (95% CI,2.5%-2.7%) 使用静态方法,使用累积方法的 2.4% (95% CI,2.3%-2.4%) 和 3.1% (95% CI,3.0%-3.2%) 采用动态法。使用静态方法,年龄 <50 岁的女性中诊断为乳腺癌的姐妹的相对风险为 1.40 倍 (95% CI,1.31 倍至 1.48 倍),使用累积法的 1.66 倍 (95% CI,1.57 倍到 1.76 倍) 和 2.28 倍 (95% CI,2.07 倍到 2.51 倍) 使用动态方法。 结论: 目前的研究结果表明,在不同的家族风险估计中,评估家族史为静态、累积或动态结果。使用哪种方法进行家族史评估的答案取决于研究的意义,动态方法似乎更适合风险分层研究,累积法是实践中最方便、最不受欢迎的风险预测方法,静态方法适用于病因影响和风险归因研究。

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影响因子:2.87
发表时间:2020-01-31
来源期刊:Bioscience reports
DOI:10.1042/BSR20192546
作者列表:["Chen X","Theobard R","Zhang J","Dai X"]

METHODS::RAD50 is commonly depleted in basal-like breast cancer with concomitant absence of INPP4B and several tumor suppressors such as BRCA1 and TP53. Our previous study revealed that INPP4B and RAD50 interact and such an interaction is associated with breast cancer survival at the transcriptional, translational and genomic levels. In the present study, we explored single nucleotide polymorphisms (SNPs) of these two genes that have synergistic effects on breast cancer survival to decipher mechanisms driving their interactions at the genetic level. The Cox's proportional hazards model was used to test whether SNPs of these two genes are interactively associated with breast cancer survival, following expression quantitative trait loci (eQTL) analysis and functional investigations. Our study revealed two disease-associating blocks, each encompassing five and two non-linkage disequilibrium linked SNPs of INPP4B and RAD50, respectively. Concomitant presence of any rare homozygote from each disease-associating block is synergistically prognostic of poor breast cancer survival. Such synergy is mediated via bypassing pathways controlling cell proliferation and DNA damage repair, which are represented by INPP4B and RAD50. Our study provided genetic evidence of interactions between INPP4B and RAD50, and deepened our understandings on the orchestrated genetic machinery governing tumor progression.

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发表时间:2020-01-31
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DOI:10.1186/s12885-020-6534-z
作者列表:["Soliman H","Shah V","Srkalovic G","Mahtani R","Levine E","Mavromatis B","Srinivasiah J","Kassar M","Gabordi R","Qamar R","Untch S","Kling HM","Treece T","Audeh W"]

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