Breast Cancer Risk From Modifiable and Nonmodifiable Risk Factors Among White Women in the United States

被引：243

作者：

Maas, Paige ^{[1
]}

Barrdahl, Myrto ^{[2
]}

Joshi, Amit D. ^{[3
]}

Auer, Paul L. ^{[4
,5
]}

Gaudet, Mia M. ^{[6
]}

Milne, Roger L. ^{[7
,8
]}

Schumacher, Fredrick R. ^{[9
]}

Anderson, William F. ^{[1
]}

Check, David ^{[1
]}

Chattopadhyay, Subham ^{[1
]}

Baglietto, Laura ^{[7
,8
]}

Berg, Christine D. ^{[10
]}

Chanock, Stephen J. ^{[1
]}

Cox, David G. ^{[11
,12
]}

Figueroa, Jonine D. ^{[1
]}

Gail, Mitchell H. ^{[1
]}

Graubard, Barry I. ^{[1
]}

Haiman, Christopher A. ^{[9
]}

Hankinson, Susan E. ^{[13
,14
,15
]}

Hoover, Robert N. ^{[1
]}

Isaacs, Claudine ^{[16
]}

Kolonel, Laurence N. ^{[17
]}

Le Marchand, Loic ^{[18
]}

Lee, I-Min ^{[15
,19
]}

Lindstrom, Sara ^{[3
]}

Overvad, Kim ^{[20
]}

Romieu, Isabelle ^{[21
]}

Sanchez, Maria-Jose ^{[22
,23
]}

Southey, Melissa C. ^{[24
]}

Stram, Daniel O. ^{[9
]}

Tumino, Rosario ^{[25
]}

VanderWeele, Tyler J. ^{[26
,27
]}

Willett, Walter C. ^{[28
]}

Zhang, Shumin ^{[15
,19
]}

Buring, Julie E. ^{[15
,19
]}

Canzian, Federico ^{[29
]}

Gapstur, Susan M. ^{[6
]}

Henderson, Brian E. ^{[9
]}

Hunter, David J. ^{[3
]}

Giles, Graham G. ^{[7
,8
,30
]}

Prentice, Ross L. ^{[4
,31
]}

Ziegler, Regina G. ^{[1
]}

Kraft, Peter ^{[3
]}

Garcia-Closas, Montse ^{[1
,32
]}

Chatterjee, Nilanjan ^{[1
,33
,34
]}

机构：

[1] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA

[2] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany

[3] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA USA

[4] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA

[5] Univ Wisconsin, Sch Publ Hlth, Milwaukee, WI 53201 USA

[6] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA

[7] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia

[8] Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia

[9] Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA

[10] NCI, Canc Prevent Div, Bethesda, MD 20892 USA

[11] Ctr Leon Berard, INSERM, U1052, Canc Res Ctr Lyon, Lyon, France

[12] Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England

[13] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Dept Biostat & Epidemiol, Amherst, MA 01003 USA

[14] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA

[15] Harvard Med Sch, Boston, MA USA

[16] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA

[17] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA

[18] Univ Hawaii, Ctr Canc, Honolulu, HI 96822 USA

[19] Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA

[20] Aarhus Univ, Dept Publ Hlth, Aarhus, Denmark

[21] Int Agcy Res Canc, Nutr & Metab Sect, Lyon, France

[22] Univ Granada, Hosp Univ Granada, Inst Invest Biosanitaria Ibs GRANADA, Escuela Andaluza Salud Publ, Granada, Spain

[23] CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain

[24] Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Melbourne, Vic, Australia

[25] Civ MP Arezzo Hosp, ASP Ragusa, Canc Registry & Histopathol Unit, Ragusa, Italy

[26] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA

[27] Harvard TH Chan Sch Publ Hlth, Dept Biostat, Boston, MA USA

[28] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA

[29] German Canc Res Ctr, Heidelberg, Germany

[30] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic, Australia

[31] Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA

[32] Inst Canc Res, Breakthrough Breast Canc Res Ctr, Div Genet & Epidemiol, London, England

[33] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, 615 N Wolfe St, Baltimore, MD 21205 USA

[34] Johns Hopkins Univ, Sch Med, Dept Oncol, 615 N Wolfe St, Baltimore, MD 21205 USA

来源：

JAMA ONCOLOGY | 2016年 / 2卷 / 10期

基金：

美国国家卫生研究院;

关键词：

GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISMS; GENE-ENVIRONMENT INTERACTIONS; SUSCEPTIBILITY LOCI; COHORT CONSORTIUM; MODELS; PREDICTION; INDIVIDUALS; INFORMATION; VARIANTS;

D O I：

10.1001/jamaoncol.2016.1025

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

IMPORTANCE An improved model for risk stratification can be useful for guiding public health strategies of breast cancer prevention. OBJECTIVE To evaluate combined risk stratification utility of common low penetrant single nucleotide polymorphisms (SNPs) and epidemiologic risk factors. DESIGN, SETTING, AND PARTICIPANTS Using a total of 17 171 cases and 19 862 controls sampled from the Breast and Prostate Cancer Cohort Consortium (BPC3) and 5879 women participating in the 2010 National Health Interview Survey, a model for predicting absolute risk of breast cancer was developed combining information on individual level data on epidemiologic risk factors and 24 genotyped SNPs from prospective cohort studies, published estimate of odds ratios for 68 additional SNPs, population incidence rate from the National Cancer Institute-Surveillance, Epidemiology, and End Results Program cancer registry and data on risk factor distribution from nationally representative health survey. The model is used to project the distribution of absolute risk for the population of white women in the United States after adjustment for competing cause of mortality. EXPOSURES Single nucleotide polymorphisms, family history, anthropometric factors, menstrual and/ or reproductive factors, and lifestyle factors. MAIN OUTCOMES AND MEASURES Degree of stratification of absolute risk owing to nonmodifiable (SNPs, family history, height, and some components of menstrual and/ or reproductive history) and modifiable factors (body mass index [BMI; calculated as weight in kilograms divided by height in meters squared], menopausal hormone therapy [MHT], alcohol, and smoking). RESULTS The average absolute risk for a 30-year-old white woman in the United States developing invasive breast cancer by age 80 years is 11.3%. A model that includes all risk factors provided a range of average absolute risk from 4.4% to 23.5% for women in the bottom and top deciles of the risk distribution, respectively. For women who were at the lowest and highest deciles of nonmodifiable risks, the 5th and 95th percentile range of the risk distribution associated with 4 modifiable factors was 2.9% to 5.0% and 15.5% to 25.0%, respectively. For women in the highest decile of risk owing to nonmodifiable factors, those who had low BMI, did not drink or smoke, and did not use MHT had risks comparable to an average woman in the general population. CONCLUSIONS AND RELEVANCE This model for absolute risk of breast cancer including SNPs can provide stratification for the population of white women in the United States. The model can also identify subsets of the population at an elevated risk that would benefit most from risk-reduction strategies based on altering modifiable factors. The effectiveness of this model for individual risk communication needs further investigation.

引用

页码：1295 / 1302

页数：8

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