Evidence for Etiologic Subtypes of Breast Cancer in the Carolina Breast Cancer Study.
Journal
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
ISSN: 1538-7755
Titre abrégé: Cancer Epidemiol Biomarkers Prev
Pays: United States
ID NLM: 9200608
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
received:
02
04
2019
revised:
12
06
2019
accepted:
01
08
2019
pubmed:
10
8
2019
medline:
26
8
2020
entrez:
10
8
2019
Statut:
ppublish
Résumé
Distinctions in the etiology of triple-negative versus luminal breast cancer have become well established using immunohistochemical surrogates [notably estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2)]. However, it is unclear whether established immunohistochemical subtypes are the sole or definitive means of etiologically subdividing breast cancers. We evaluated clinical biomarkers and tumor suppressor p53 with risk factor data from cases and controls in the Carolina Breast Cancer Study, a population-based study of incident breast cancers. For each individual marker and combinations of markers, we calculated an aggregate measure to distinguish the etiologic heterogeneity of different classification schema. To compare schema, we estimated subtype-specific case-control odds ratios for individual risk factors and fit age-at-incidence curves with two-component mixture models. We also evaluated subtype concordance of metachronous contralateral breast tumors in the California Cancer Registry. ER was the biomarker that individually explained the greatest variability in risk factor profiles. However, further subdivision by p53 significantly increased the degree of etiologic heterogeneity. Age at diagnosis, nulliparity, and race were heterogeneously associated with ER/p53 subtypes. The ER Clinical marker-based intrinsic subtypes have established value, yet other schema may also yield important etiologic insights. Novel environmental or genetic risk factors may be identifiable by considering different etiologic schema, including cross-classification based on ER/p53.
Sections du résumé
BACKGROUND
Distinctions in the etiology of triple-negative versus luminal breast cancer have become well established using immunohistochemical surrogates [notably estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2)]. However, it is unclear whether established immunohistochemical subtypes are the sole or definitive means of etiologically subdividing breast cancers.
METHODS
We evaluated clinical biomarkers and tumor suppressor p53 with risk factor data from cases and controls in the Carolina Breast Cancer Study, a population-based study of incident breast cancers. For each individual marker and combinations of markers, we calculated an aggregate measure to distinguish the etiologic heterogeneity of different classification schema. To compare schema, we estimated subtype-specific case-control odds ratios for individual risk factors and fit age-at-incidence curves with two-component mixture models. We also evaluated subtype concordance of metachronous contralateral breast tumors in the California Cancer Registry.
RESULTS
ER was the biomarker that individually explained the greatest variability in risk factor profiles. However, further subdivision by p53 significantly increased the degree of etiologic heterogeneity. Age at diagnosis, nulliparity, and race were heterogeneously associated with ER/p53 subtypes. The ER
CONCLUSIONS
Clinical marker-based intrinsic subtypes have established value, yet other schema may also yield important etiologic insights.
IMPACT
Novel environmental or genetic risk factors may be identifiable by considering different etiologic schema, including cross-classification based on ER/p53.
Identifiants
pubmed: 31395590
pii: 1055-9965.EPI-19-0365
doi: 10.1158/1055-9965.EPI-19-0365
pmc: PMC6825567
mid: NIHMS1536983
doi:
Substances chimiques
Biomarkers, Tumor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1784-1791Subventions
Organisme : NCI NIH HHS
ID : U01 CA179715
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES010126
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA163251
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA057726
Pays : United States
Organisme : NCI NIH HHS
ID : F30 CA236199
Pays : United States
Informations de copyright
©2019 American Association for Cancer Research.
Références
J Natl Cancer Inst. 2014 Aug 12;106(8):
pubmed: 25118203
Int J Cancer. 2011 Aug 15;129(4):931-7
pubmed: 20949563
Nature. 2011 Jun 29;474(7353):609-15
pubmed: 21720365
Nature. 2012 Oct 4;490(7418):61-70
pubmed: 23000897
Cancer Med. 2015 Sep;4(9):1432-9
pubmed: 25974664
Epidemiol Rev. 1993;15(1):169-76
pubmed: 8405200
Cancer Epidemiol Biomarkers Prev. 1999 Mar;8(3):255-63
pubmed: 10090304
Biostatistics. 2008 Jan;9(1):137-51
pubmed: 17566074
J Natl Cancer Inst. 2004 Apr 7;96(7):516-23
pubmed: 15069113
Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):439-43
pubmed: 17372238
Cancer Res. 2010 Jan 15;70(2):575-87
pubmed: 20068186
BMC Cancer. 2010 May 26;10:237
pubmed: 20504346
J Natl Cancer Inst. 2018 Feb 1;110(2):
pubmed: 28859290
Cancer Epidemiol Biomarkers Prev. 2016 Mar;25(3):470-8
pubmed: 26711328
JAMA. 2006 Jun 7;295(21):2492-502
pubmed: 16757721
Clin Cancer Res. 2002 Nov;8(11):3427-32
pubmed: 12429630
NPJ Breast Cancer. 2018 Jun 25;4:13
pubmed: 29951581
Cancer Causes Control. 2003 Sep;14(7):609-18
pubmed: 14575358
PLoS Med. 2016 Dec 6;13(12):e1002174
pubmed: 27923045
Breast Cancer Res Treat. 2016 Dec;160(3):531-537
pubmed: 27757717
Cancer Epidemiol Biomarkers Prev. 2006 Oct;15(10):1899-905
pubmed: 17035397
Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):855-61
pubmed: 10548312
Cancer. 2014 Jul 15;120(14):2174-82
pubmed: 24911404
J Am Stat Assoc. 2017;112(517):54-63
pubmed: 28603323
Breast Cancer Res Treat. 2010 Feb;120(1):217-27
pubmed: 19629680
Cancer Epidemiol Biomarkers Prev. 2007 Jul;16(7):1437-42
pubmed: 17627009
Breast Cancer Res Treat. 2007 Oct;105(2):195-207
pubmed: 17186360
Breast Cancer Res Treat. 2008 May;109(1):123-39
pubmed: 17578664
Cancer Res. 2017 Jul 1;77(13):3708-3717
pubmed: 28512241
BMC Med Res Methodol. 2014 Dec 22;14:138
pubmed: 25532962
Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):829-35
pubmed: 12223426
Breast Cancer Res Treat. 2004 Jun;85(3):255-61
pubmed: 15111764
Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1558-68
pubmed: 15466970
Cancer Res. 2018 Oct 15;78(20):6011-6021
pubmed: 30185547
J Natl Cancer Inst. 2004 Feb 4;96(3):218-28
pubmed: 14759989
Arch Surg. 2005 Jan;140(1):58-62
pubmed: 15655207
J Natl Cancer Inst. 2016 Dec 31;109(5):
pubmed: 28040694
Sci Rep. 2018 May 16;8(1):7735
pubmed: 29769535
Epidemiol Rev. 1993;15(1):17-35
pubmed: 8405201
Nat Clin Pract Oncol. 2007 Jul;4(7):415-23
pubmed: 17597706
Stat Med. 2013 Dec 20;32(29):5039-52
pubmed: 23857589
Arch Pathol Lab Med. 2007;131(1):18-43
pubmed: 19548375
J Clin Invest. 2018 Apr 2;128(4):1371-1383
pubmed: 29480819
Cancer. 1988 Jul 1;62(1):109-13
pubmed: 3383109
Breast Cancer Res Treat. 1995 Jul;35(1):51-60
pubmed: 7612904