Evidence map›Paper›PMID 25956172›Full record

ArticleJournal of the National Cancer Institute2015

Practical problems with clinical guidelines for breast cancer prevention based on remaining lifetime risk.

Anne S Quante, Alice S Whittemore, Tom Shriver, John L Hopper, Konstantin Strauch, Mary Beth Terry

Abstract readComparative Study
In one paragraph

Article in Journal of the National Cancer Institute, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Plasma metabolomics profiles and breast cancer risk.Breast cancer research : BCR · 2024
    Article
  3. Article
  4. Article
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  7. The Steroid Metabolome and Breast Cancer Risk in Women with a Family History of Breast Cancer: The Novel Role of Adrenal Androgens and Glucocorticoids.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  8. Article
  9. Article
  10. Comparison of Questionnaire-Based Breast Cancer Prediction Models in the Nurses' Health Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
  11. Article
  12. Article
  13. Review
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  16. Breast Cancer Risk Prediction Using Clinical Models and 77 Independent Risk-Associated SNPs for Women Aged Under 50 Years: Australian Breast Cancer Family Registry.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016
    Article
  17. 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.

Anne S Quante: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT).
Alice S Whittemore: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT).
Tom Shriver: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT).
John L Hopper: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT).
Konstantin Strauch: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT).
Mary Beth Terry: Joseph L. Mailman School of Public Health, Columbia University, New York, NY (ASQ, TS, MBT); Institute of Medical Informatics, Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany (ASQ, KS); Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany (ASQ, KS); Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ASW); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Carlton, Victoria, Australia (JLH); Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea (JLH); Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY (MBT). mt146@columbia.edu.

Funding

True Metal fac coreP30ES009089 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MATTHEW S PERZANOWSKI · 1998 to 2026
$44.7M
Breast Cancer Family Registry CohortUM1CA164920 · NCI · CANCER PREVENTION INSTIT OF CALIFORNIA · PI ANDRULIS, IRENE, BUYS, SAUNDRA S · 2012 to 2017
$12.7M
Genes, environment and breast cancer risk: The 15 year follow-up of the Prof-SC (Diversity Supplement)R01CA159868 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HOPPER, JOHN L, TERRY, MARY BETH · 2011 to 2015
$9.0M
Statistical Methods for Genetic EpidemiologyR01CA094069 · NCI · STANFORD UNIVERSITY · PI WHITTEMORE, ALICE · 2002 to 2016
$7.7M
NCI NIH HHS R01 CA094069NCI NIH HHS R01 CA 159868NCI NIH HHS R01 CA159868NCI NIH HHS UM1CA164920NIEHS NIH HHS P30 ES009089
6 · The paper itself

Abstract

backgroundClinical guidelines for breast cancer chemoprevention and MRI screening involve estimates of remaining lifetime risk (RLR); in the United States, women with an RLR of 20% or higher meet "high-risk" criteria for MRI screening.

methodsWe prospectively followed 1764 women without breast cancer to compare the RLRs and 10-year risks assigned by the risk models International Breast Cancer Intervention Study (IBIS) and Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA) and to compare both sets of model-assigned 10-year risks to subsequent incidence of breast cancer in the cohort. We used chi-square statistics to assess calibration and the area under the receiver operating characteristic curve (AUC) to assess discrimination. All statistical tests are two-sided.

resultsThe models classified different proportions of women as high-risk (IBIS = 59.3% vs BOADICEA = 20.1%) using the RLR threshold of 20%. The difference was smaller (IBIS = 52.9% vs BOADICEA = 43.2%) using a 10-year risk threshold of 3.34%. IBIS risks (mean = 4.9%) were better calibrated to observed breast cancer incidence (5.2%, 95% confidence interval (CI) = 4.2% to 6.4%) than were those of BOADICEA (mean = 3.7%) overall and within quartiles of model risk (P = .20 by IBIS and P = .07 by BOADICEA). Both models gave similar discrimination, with AUCs of 0.67 (95% CI = 0.61 to 0.73) using IBIS and 0.68 (95% CI = 0.62 to 0.74) using BOADICEA. Model sensitivities at thresholds for a 20% false-positive rate were also similar, with 41.8% using IBIS and 38.0% using BOADICEA.

conclusionRLR-based guidelines for high-risk women are limited by discordance between commonly used risk models. Guidelines based on short-term risks would be more useful, as models are generally developed and validated under a short fixed time horizon (≤10 years).

Indexed as

Genetic TestingHeterozygoteLife ExpectancyMutationAdultAgedAged, 80 and overArea Under CurveBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsFemaleGenetic Predisposition to DiseaseHumansIncidenceKaplan-Meier EstimateBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, human

Identifiers

PMID25956172
PMCPMC4554256

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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.