Evidence map›Paper›PMID 31395590›Full record

ArticleCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2019

Evidence for Etiologic Subtypes of Breast Cancer in the Carolina Breast Cancer Study.

Halei C Benefield, Emily C Zabor, Yue Shan, Emma H Allott, Colin B Begg, Melissa A Troester

Abstract read
In one paragraph

Article in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Can We Interpret Analyses of Etiologic Heterogeneity When Molecular Markers Are Used to Classify Tumors?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TP53 Pathway Function, Estrogen Receptor Status, and Breast Cancer Risk Factors in the Carolina Breast Cancer Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Halei C BenefieldDepartment of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. hcb10@med.unc.edu.ORCID 0000-0003-1400-5374
Emily C ZaborDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID 0000-0002-1402-4498
Yue ShanDepartment of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Emma H AllottCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, United Kingdom.ORCID 0000-0003-1227-3615
Colin B BeggDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Melissa A TroesterDepartment of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KATHERINE A. HOADLEY · 1992 to 2026
$59.3M
UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
Cancer Control Education ProgramT32CA057726 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa B Gilkey, Melissa A. Troester · 2017 to 2026
$3.7M
Biology of Race and Progression Associated Breast Tumor Gene ExpressionU01CA179715 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEROU, CHARLES M, TROESTER, MELISSA A. · 2014 to 2018
$1.6M
Statistical Strategies for Establishing Etiologic Heterogeneity of TumorsR01CA163251 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI BEGG, COLIN B · 2012 to 2015
$1.5M
The role of estrogen receptor in breast cancer outcomes and the effect of exposure historyF30CA236199 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BENEFIELD, HALEI · 2019 to 2021
$121k
NCI NIH HHS F30 CA236199NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA058223NCI NIH HHS R01 CA163251NCI NIH HHS T32 CA057726NCI NIH HHS U01 CA179715NIEHS NIH HHS P30 ES010126
6 · The paper itself

Abstract

backgroundDistinctions 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.

methodsWe 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.

resultsER 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

conclusionsClinical 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.

Indexed as

Biomarkers, TumorBreast NeoplasmsFemaleHumansRegistriesBiomarkers, Tumor

Identifiers

PMID31395590
PMCPMC6825567

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.