Associations of Breast Cancer Risk Factors With Tumor Subtypes: A Pooled Analysis From the Breast Cancer Association Consortium Studies

被引：521

作者：

Yang, Xiaohong R. ^{[1
]}

Chang-Claude, Jenny ^{[3
]}

Goode, Ellen L. ^{[4
]}

Couch, Fergus J. ^{[4
,5
]}

Nevanlinna, Heli ^{[6
]}

Milne, Roger L. ^{[10
]}

Gaudet, Mia ^{[12
]}

Schmidt, Marjanka K. ^{[13
]}

Broeks, Annegien ^{[13
]}

Cox, Angela ^{[14
]}

Fasching, Peter A. ^{[17
]}

Hein, Rebecca ^{[3
]}

Spurdle, Amanda B. ^{[20
]}

Blows, Fiona ^{[21
]}

Driver, Kristy ^{[21
]}

Flesch-Janys, Dieter ^{[22
]}

Heinz, Judith ^{[22
]}

Sinn, Peter ^{[23
]}

Vrieling, Alina ^{[3
]}

Heikkinen, Tuomas ^{[6
]}

Aittomaeki, Kristiina ^{[7
]}

Heikkilae, Paeivi ^{[8
,44
]}

Blomqvist, Carl ^{[9
]}

Lissowska, Jolanta

Peplonska, Beata ^{[26
]}

Chanock, Stephen ^{[15
]}

Figueroa, Jonine

Brinton, Louise

Hall, Per ^{[27
]}

Czene, Kamila ^{[27
]}

Humphreys, Keith ^{[27
]}

Darabi, Hatef ^{[27
]}

Liu, Jianjun ^{[24
,25
,28
]}

Van 't Veer, Laura J. ^{[13
]}

Van Leeuwen, Flora E. ^{[13
]}

Andrulis, Irene L. ^{[29
,30
,31
]}

Glendon, Gord ^{[29
]}

Knight, Julia A. ^{[32
]}

Mulligan, Anna Marie ^{[33
]}

O'Malley, Frances P. ^{[34
]}

Weerasooriya, Nayana ^{[29
]}

John, Esther M. ^{[35
,36
,37
]}

Beckmann, Matthias W. ^{[18
]}

Hartmann, Arndt ^{[19
]}

Weihbrecht, Sebastian B. ^{[18
]}

Wachter, David L. ^{[19
]}

Jud, Sebastian M. S. ^{[18
]}

Loehberg, Christian R. ^{[18
]}

Baglietto, Laura ^{[38
,39
]}

English, Dallas R. ^{[38
,39
]}

机构：

[1] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Sci, Rockville, MD 20852 USA

[2] Inst Canc Res, Sect Epidemiol & Genet, Sutton, Surrey, England

[3] German Canc Res Ctr, Div Canc Epidemiol, D-6900 Heidelberg, Germany

[4] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA

[5] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA

[6] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland

[7] Univ Helsinki, Cent Hosp, Dept Clin Genet, FIN-00290 Helsinki, Finland

[8] Univ Helsinki, Cent Hosp, Dept Pathol, FIN-00290 Helsinki, Finland

[9] Univ Helsinki, Cent Hosp, Dept Oncol, FIN-00290 Helsinki, Finland

[10] Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain

[11] Spanish Natl Canc Res Ctr CNIO, Human Canc Genet Grp, Madrid, Spain

[12] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA

[13] Netherlands Canc Inst, Amsterdam Breast Canc Study, Amsterdam, Netherlands

[14] Univ Sheffield, Sch Med, Dept Oncol, Inst Canc Studies, Sheffield, S Yorkshire, England

[15] Univ Sheffield, Sch Med, Acad Unit Pathol, Sheffield, S Yorkshire, England

[16] Univ Sheffield, Sch Med, Acad Unit Surg Oncol, Dept Oncol, Sheffield, S Yorkshire, England

[17] Univ Calif Los Angeles, David Geffen Sch Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA

[18] Univ Hosp Erlangen, Univ Breast Ctr, Univ Breast Ctr Franconia, Dept Gynecol & Obstet, Erlangen, Germany

[19] Univ Hosp Erlangen, Univ Breast Ctr, Univ Breast Ctr Franconia, Inst Pathol, Erlangen, Germany

[20] Univ Queensland, Royal Brisbane Hosp, Queensland Inst Med Res Post Off, Herston, Qld, Australia

[21] Univ Cambridge, Dept Oncol, Cambridge, England

[22] Univ Med Ctr Hamburg Eppendorf, Dept Med Biometr & Epidemiol, Hamburg, Germany

[23] Univ Hosp, Dept Pathol, Heidelberg, Germany

[24] Ctr Canc, Dept Canc Epidemiol & Prevent, Warsaw, Poland

[25] M Sklodowska Curie Inst Oncol, Warsaw, Poland

[26] Nofer Inst Occupat Med, Dept Occupat & Environm Epidemiol, Lodz, Poland

[27] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden

[28] Genome Inst Singapore, Singapore, Singapore

[29] Canc Care Ontario, Ontario Canc Genet Network OCGN, Toronto, ON, Canada

[30] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada

[31] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada

[32] Univ Toronto, Mt Sinai Hosp, Dalla Lana Sch Publ Hlth, Prosserman Ctr Hlth Res,Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada

[33] Univ Toronto, St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Ctr, Toronto, ON M5B 1W8, Canada

[34] Univ Toronto, Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada

[35] Canada No Calif Canc Ctr, Fremont, CA USA

[36] Stanford Univ, Sch Med, Dept Hlth Res & Policy, Stanford, CA 94305 USA

[37] Stanford Canc Ctr, Stanford, CA 94305 USA

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

[39] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia

[40] Katholieke Univ Leuven, Vesalius Res Ctr, Leuven, Belgium

[41] VIB, Leuven, Belgium

[42] Alfred Hosp, Melbourne, Vic, Australia

[43] Univ Hosp, Dept Radiotherapy, Leuven, Belgium

[44] Hannover Med Sch, Dept Obstet & Gynaecol, Hannover, Germany

[45] Hannover Med Sch, Dept Radiat Oncol, Hannover, Germany

[46] Hosp Monte Naranco, Serv Cirugia Gen, Oviedo, Spain

[47] Hosp Monte Naranco, Serv Anat Patol, Oviedo, Spain

[48] Hosp La Paz, Med Oncol Serv, Madrid, Spain

[49] CIBERER, Madrid, Spain

[50] Johanniter Krankenhaus, Evangel Kliniken Bonn gGmbH, Dept Internal Med, Bonn, Germany

来源：

JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE | 2011年 / 103卷 / 03期

基金：

芬兰科学院; 澳大利亚国家健康与医学研究理事会; 英国医学研究理事会; 美国国家卫生研究院;

关键词：

SINGLE-NUCLEOTIDE POLYMORPHISMS; DIFFERENT HISTOPATHOLOGIC TYPES; EPITHELIAL OVARIAN-CANCER; BASAL-LIKE SUBTYPE; PROGESTERONE-RECEPTOR; HORMONE-RECEPTOR; REPAIR GENES; ESTROGEN; MUTATIONS; PATTERNS;

D O I：

10.1093/jnci/djq526

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Background Previous studies have suggested that breast cancer risk factors are associated with estrogen receptor (ER) and progesterone receptor (PR) expression status of the tumors. Methods We pooled tumor marker and epidemiological risk factor data from 35 568 invasive breast cancer case patients from 34 studies participating in the Breast Cancer Association Consortium. Logistic regression models were used in case-case analyses to estimate associations between epidemiological risk factors and tumor subtypes, and case-control analyses to estimate associations between epidemiological risk factors and the risk of developing specific tumor subtypes in 12 population-based studies. All statistical tests were two-sided. Results In case-case analyses, of the epidemiological risk factors examined, early age at menarche (<= 12 years) was less frequent in case patients with PR- than PR+ tumors (P = .001). Nulliparity (P = 3 x 10(-6)) and increasing age at first birth (P = 2 x 10(-9)) were less frequent in ER- than in ER+ tumors. Obesity (body mass index [BMI] >= 30 kg/m(2)) in younger women (<= 50 years) was more frequent in ER /PR than in ER+/PR+ tumors (P = 1 x 10(-7)), whereas obesity in older women (>50 years) was less frequent in PR- than in PR+ tumors (P = 6 x 10(-4)). The triple-negative (ER-/PR-/HER2-) or core basal phenotype (CBP; triple-negative and cytokeratins [CK]5/6(+) and/ or epidermal growth factor receptor [EGFR] 1) accounted for much of the heterogeneity in parity-related variables and BMI in younger women. Case-control analyses showed that nulliparity, increasing age at first birth, and obesity in younger women showed the expected associations with the risk of ER+ or PR+ tumors but not triple-negative (nulliparity vs parity, odds ratio [OR] = 0.94, 95% confidence interval [CI] = 0.75 to 1.19, P = .61; 5-year increase in age at first full-term birth, OR = 0.95, 95% CI = 0.86 to 1.05, P = .34; obesity in younger women, OR = 1.36, 95% CI = 0.95 to 1.94, P = .09) or CBP tumors. Conclusions This study shows that reproductive factors and BMI are most clearly associated with hormone receptor-positive tumors and suggest that triple-negative or CBP tumors may have distinct etiology.

引用

页码：250 / 263

页数：14

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