Evidence map›Paper›PMID 39561272›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2025

Hormone Receptor-Positive HER2-Negative/MammaPrint High-2 Breast Cancers Closely Resemble Triple-Negative Breast Cancers.

Alejandro Rios-Hoyo, Kaitlyn Xiong, Jiawei Dai, Christina Yau, Michal Marczyk, Rolando Garcia-Milian, Denise M Wolf, Laura A Huppert, Rita Nanda, Gillian L Hirst and 4 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2025. 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. Review
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  4. Observational
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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

14 authors.

Alejandro Rios-Hoyo *Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut.ORCID 0000-0001-5344-9168
Kaitlyn Xiong *Yale School of Medicine, New Haven, Connecticut.ORCID 0000-0001-9764-6745
Jiawei DaiYale Cancer Center, Yale School of Medicine, New Haven, Connecticut.ORCID 0000-0003-3806-5160
Christina YauDepartment of Surgery, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-1937-0859
Michal MarczykYale Cancer Center, Yale School of Medicine, New Haven, Connecticut.ORCID 0000-0003-2508-5736
Rolando Garcia-MilianBioinformatics Support Program, Research and Education Services, Cushing/Whitney Medical Library, Yale University, New Haven, Connecticut.ORCID 0000-0003-1557-566X
Denise M WolfDepartment of Laboratory Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-3676-653X
Laura A HuppertUniversity of California San Francisco Comprehensive Cancer Center, San Francisco, California.ORCID 0000-0002-8512-5608
Rita NandaSection of Hematology and Oncology, Department of Medicine, University of Chicago Medicine and Biological Sciences, Chicago, Illinois.ORCID 0000-0001-5248-0876
Gillian L HirstDepartment of Surgery, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-4502-0035
Erin F CobainUniversity of Michigan, Ann Arbor, Michigan.ORCID 0000-0001-9602-8611
Laura J van 't VeerDepartment of Laboratory Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-9838-8298
Laura J EssermanDepartment of Surgery, University of California, San Francisco, San Francisco, California.ORCID 0000-0001-9202-4568
Lajos PusztaiYale Cancer Center, Yale School of Medicine, New Haven, Connecticut.ORCID 0000-0001-9632-6686

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
The I SPY 2.2 TRIAL: Evolving to Imaging and Molecular Biomarker Response Directed Adaptive Sequential Treatment to Optimize Breast Cancer OutcomesP01CA210961 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Laura J Van't Veer · 2017 to 2026
$22.9M
UCSF Paul Calabresi K12 Career Development Program in Clinical OncologyK12CA260225 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BERGSLAND, EMILY K, BIVONA, TREVER G · 2021 to 2025
$2.6M
Immune biological differences between Triple Negative Breast Cancer in African American and non-African American women and potential immunotherapy opportunities to improve treatment outcomeR01CA219647 · NCI · YALE UNIVERSITY · PI PUSZTAI, LAJOS · 2017 to 2020
$2.0M
preoprative chemotherapy for breast cancerR01CA106290 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PUSZTAI, LAJOS · 2005 to 2007
$570k
Breast Cancer Research Foundation (BCRF) BCRF-22-133NCATS NIH HHS UL1 TR001863NCI NIH HHS K12 CA260225NCI NIH HHS P01 CA210961NCI NIH HHS R01 CA106290NCI NIH HHS R01 CA219647Sociedad Española de Oncología Médica (SEOM)Susan Komen Leadership Award SAC220225
6 · The paper itself

Abstract

purposeThe MammaPrint (MP) prognostic assay categorizes breast cancers into high- and low-risk subgroups, and the high-risk group can be further subdivided into high-1 (MP-H1), and very high-risk high-2 (MP-H2). The aim of this analysis was to assess clinical and molecular differences between the hormone receptor-positive (HR+)/HER2-negative MP-H1, -H2, and triple-negative (TN) MP-H1 and -H2 cancers. EXPERIMENTAL

designPretreatment gene expression data from 742 HER2-negative breast cancers enrolled in the I-SPY2 neoadjuvant trial were used. Prognostic risk categories were assigned using the MP assay. Transcriptional similarities across the four receptor and prognostic groups were assessed using principal component analyses and by identifying differentially expressed genes. We also examined pathologic complete response rates and event-free survivals by risk group.

resultsPrincipal component analysis showed that HR+/MP-H2 tumors clustered with TN/MP-H2 cancers. Only 125 genes showed differential expression between the HR+/MP-H2 and TN/MP-H2 cancers, whereas 1,465 genes were differentially expressed between HR+/MP-H2 and -H1. Gene set analysis revealed similarly high expression of cell cycle, DNA repair, and immune infiltration-related pathways in HR+/MP-H2 and TN/MP-H2 cancers. HR+/MP-H2 cancers also showed low estrogen receptor-related gene expression. Pathologic complete response rates were similarly high in TN/MP-H2 and HR+/MP-H2 cancers (42% vs. 30.5%; P = 0.11), and MP-H2 cancers with residual cancer had similarly poor event-free survival regardless of estrogen receptor status.

conclusionsIn conclusion, HR+/MP-H2 cancers closely resemble TN breast cancers in transcriptional and clinical features and benefit from similar treatment strategies.

Indexed as

Biomarkers, TumorBreast NeoplasmsErb-b2 Receptor Tyrosine KinasesReceptors, EstrogenReceptors, ProgesteroneTriple Negative Breast NeoplasmsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiddle AgedPrognosisBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesReceptors, EstrogenReceptors, Progesterone

Identifiers

PMID39561272
PMCPMC11747811

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.