Evidence map›Paper›PMID 28040694›Full record

ArticleJournal of the National Cancer Institute2017

Risk Factors That Increase Risk of Estrogen Receptor-Positive and -Negative Breast Cancer.

Karla Kerlikowske, Charlotte C Gard, Jeffrey A Tice, Elad Ziv, Steven R Cummings, Diana L Miglioretti, Breast Cancer Surveillance Consortium

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the National Cancer Institute, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% of its field
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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
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  3. Trial
  4. Observational
  5. Review
  6. Article
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  13. Extending the Breast Cancer Surveillance Consortium Model of Invasive Breast Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Article
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  19. Obesity and Breast Cancer Risk: The Oncogenic Implications of Metabolic Dysregulation.The Journal of clinical endocrinology and metabolism · 2022
    Article
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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

7 authors at 3 institutions in 1 country.

Karla KerlikowskeAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Charlotte C GardAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Jeffrey A TiceAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Elad ZivAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Steven R CummingsAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Diana L MigliorettiAffiliations of authors: Departments of Medicine and Epidemiology and Biostatistics (KK, JAT, EZ) and General Internal Medicine Section, Department of Veterans Affairs (KK), University of California, San Francisco, San Francisco, CA; Department of Economics, Applied Statistics, and International Business, New Mexico State University, Las Cruces, NM (CCG); San Francisco Coordinating Center, California Pacific Medical Center Research Institute, San Francisco, CA (SRC); Department of Public Health Sciences, University of California, Davis, Davis, CA (DLM); Group Health Research Institute, Group Health Cooperative, Seattle, WA (DLM).
Breast Cancer Surveillance Consortium
University of California, Davis · USSan Francisco VA Medical Center · USUniversity of California, San Francisco · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Gina M Dayton · 2002 to 2026
$84.9M
Risk-based Imaging Strategies to Improve Breast Cancer Surveillance OutcomesP01CA154292 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Diana L Miglioretti · 2011 to 2026
$52.9M
Vermont Screening Process Documentation UnitU54CA163303 · NCI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI SPRAGUE, BRIAN L · 2011 to 2017
$6.4M
Genetics of mammographic density and breast cancer risk in LatinasK24CA169004 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZIV, ELAD · 2012 to 2021
$1.8M
NCI NIH HHS K24 CA169004NCI NIH HHS P01 CA154292NCI NIH HHS P30 CA093373NCI NIH HHS U54 CA163303
6 · The paper itself

Abstract

Background: Risk factors may differentially influence development of estrogen receptor (ER)-positive vs -negative breast cancer. We examined associations with strong, prevalent risk factors by ER subtype. Methods: Of 1 279 443 women age 35 to 74 years participating in the Breast Cancer Surveillance Consortium, 14 969 developed ER-positive and 3617 developed ER-negative invasive breast cancer. We calculated hazard ratios (HRs) using Cox regression and compared ER subtype hazard ratios at representative ages or by menopausal status using Wald tests. All statistical tests were two-sided. Results: For women age 40 years, compared with no prior biopsy, ER-positive vs ER-negative HRs were 1.53 (95% CI = 1.30 to 1.81) vs 1.26 (95% CI = 0.90 to 1.76) for nonproliferative disease, 1.63 (95% CI = 1.23 to 2.17) vs 1.41 (95% CI = 0.78 to 2.57) for proliferative disease without atypia, and 4.47 (95% CI = 2.88 to 6.96) vs 0.20 (95% CI = 0.02 to 2.51) for proliferative disease with atypia. Benign disease proliferation risk was stronger for ER-positive than ER-negative cancer for women age 35 years (Wald P = .04), age 40 years (Wald P = .04), and age 50 years (Wald P = .06). Among pre/perimenopausal women, body mass index (BMI) had a stronger association with ER-negative than ER-positive cancer (obese II/III vs. normal weight: HR = 1.52, 95% CI = 1.19 to 1.94; vs 1.21, 95% CI = 1.08 to 1.36). Increasing BMI similarly increased ER-positive and ER-negative cancer risk among postmenopausal hormone users (Wald P = .15) and nonusers (Wald P = .08). Associations with ER subtype varied by race/ethnicity across all ages (P < .001) and by family history of breast cancer and breast density for specific ages. Conclusions: Strength of risk factor associations differed by ER subtype. Separate risk models for ER subtypes may improve identification of women for targeted prevention strategies.

Indexed as

Body Mass IndexMenopauseAdultAgedAge FactorsBlack or African AmericanBreast DensityBreast NeoplasmsEstrogen Replacement TherapyFemaleHumansMiddle AgedProportional Hazards ModelsReceptors, EstrogenRisk FactorsWhite PeopleReceptors, Estrogen

Identifiers

PMID28040694
PMCPMC6075570
OpenAlexW2565388110

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.