Evidence map›Paper›PMID 32522886›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2020

Genome Instability Profiles Predict Disease Outcome in a Cohort of 4,003 Patients with Breast Cancer.

Annette Lischka, Natalie Doberstein, Sandra Freitag-Wolf, Ayla Koçak, Timo Gemoll, Kerstin Heselmeyer-Haddad, Thomas Ried, Gert Auer, Jens K Habermann

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Genome stability disrupted by the circRBM39(4,5,6)-RPA2 axis represses breast tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 3 institutions in 3 countries.

Annette LischkaSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Campus Lübeck, Germany.ORCID 0000-0001-8042-4361
Natalie DobersteinSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Campus Lübeck, Germany.
Sandra Freitag-WolfInstitute of Medical Informatics and Statistics, Kiel University, University Hospital Schleswig-Holstein, Campus Kiel, Germany.
Ayla KoçakSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Campus Lübeck, Germany.
Timo GemollSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Campus Lübeck, Germany.ORCID 0000-0001-7400-5240
Kerstin Heselmeyer-HaddadGenetics Branch, NCI, NIH, Bethesda, Maryland.
Thomas RiedGenetics Branch, NCI, NIH, Bethesda, Maryland. riedt@mail.nih.gov.ORCID 0000-0002-0767-6009
Gert AuerDepartment of Pathology and Oncology, Karolinska University Hospital and Karolinska Institute, Stockholm, Sweden.
Jens K HabermannSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Campus Lübeck, Germany.
University Hospital Schleswig-Holstein · DEKarolinska University Hospital · SENational Institutes of Health · US

Funding

Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

purposeThe choice of therapy for patients with breast cancer is often based on clinicopathologic parameters, hormone receptor status, and EXPERIMENTAL

designWe retrospectively assessed clinical data of 4,003 patients with breast cancer with a minimum postoperative follow-up period of 10 years. For the entire cohort, we established genome instability profiles. We applied statistical methods, including correlation matrices, Kaplan-Meier curves, and multivariable Cox proportional hazard models, to ascertain the potential of standard clinicopathologic data and genome instability profiles as independent predictors of disease-specific survival in distinct subgroups, defined clinically or with respect to treatment.

resultsIn Cox regression analyses, two parameters of the genome instability profiles, the S-phase fraction and the stemline scatter index, emerged as independent predictors in premenopausal women, outperforming all clinicopathologic parameters. In postmenopausal women, age and hormone receptor status were the predominant prognostic factors. However, by including S-phase fraction and 2.5c exceeding rate, we could improve disease outcome prediction in pT1 tumors irrespective of the lymph node status. In pT3-pT4 tumors, a higher S-phase fraction led to poorer prognosis. In patients who received adjuvant endocrine therapy, chemotherapy or radiotherapy, or a combination, the ploidy profiles improved prognostication.

conclusionsGenome instability profiles predict disease outcome in patients with breast cancer independent of clinicopathologic parameters. This applies especially to premenopausal patients. In patients receiving adjuvant therapy, the profiles improve identification of high-risk patients.

Indexed as

Genomic InstabilityAdultAgedAged, 80 and overAge FactorsBreastBreast NeoplasmsChemotherapy, AdjuvantClinical Decision-MakingFemaleFollow-Up StudiesHumansKaplan-Meier EstimateMastectomyMiddle AgedPatient SelectionReceptors, EstrogenReceptors, Progesterone

Identifiers

PMID32522886
PMCPMC7483822
OpenAlexW3033659532

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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.