Evidence map›Paper›PMID 33617937›Full record

Trial reportAnnals of oncology : official journal of the European Society for Medical Oncology2021

Predicted sensitivity to endocrine therapy for stage II-III hormone receptor-positive and HER2-negative (HR+/HER2-) breast cancer before chemo-endocrine therapy.

L Du, C Yau, L Brown-Swigart, R Gould, G Krings, G L Hirst, I Bedrosian, R M Layman, J M Carter, M Klein and 22 more

Registry-linked trialOpen access · bronzeAbstract readClinical Trial, Phase IIRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Annals of oncology : official journal of the European Society for Medical Oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01042379 (I-SPY Trial), which is not on this map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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.

NCT01042379 phase2recruitingnot on this map

I-SPY Trial (Investigation of Serial Studies to Predict Your Therapeutic Response With Imaging And moLecular Analysis 2)

TypeinterventionalSponsorQuantumLeap Healthcare CollaborativeRan2010 to 2031Enrolled5,000ConditionsBreast Neoplasms, Breast Cancer, Breast Tumors, AngiosarcomaArmsStandard Therapy, AMG 386 with or without Trastuzumab, AMG 479 (Ganitumab) plus Metformin, MK-2206 with or without Trastuzumab, AMG 386 and Trastuzumab
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Guideline
  2. Association Between theFrontiers in genetics · 2022
    Pooled it
  3. Trial
  4. Adjuvant Dose-Dense Chemotherapy in Hormone Receptor-Positive Breast Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025
    Trial
  5. Evaluation of the Sensitivity to Endocrine Therapy Index and 21-Gene Breast Recurrence Score in the SWOG S8814 Trial.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
    Trial
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  7. Article
  8. Review
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  13. Review
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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

32 authors at 11 institutions in 1 country.

L DuDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA.
C YauDepartment of Surgery, University of California, San Francisco, USA.
L Brown-SwigartDepartment of Pathology, University of California, San Francisco, USA.
R GouldDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA.
G KringsDepartment of Pathology, University of California, San Francisco, USA.
G L HirstDepartment of Surgery, University of California, San Francisco, USA.
I BedrosianDepartment of Breast Surgery, The University of Texas MD Anderson Cancer Center, Houston, USA.
R M LaymanDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA.
J M CarterDepartment of Pathology, Mayo Clinic, Rochester, USA.
M KleinDepartment of Pathology, University of Minnesota, Minneapolis, USA.
S VentersDepartment of Surgery, University of California, San Francisco, USA.
S ShadDepartment of Surgery, University of California, San Francisco, USA.
M van der NoordaaDepartment of Surgery, University of California, San Francisco, USA.
A J ChienDepartment of Medicine, University of California, San Francisco, USA.
T HaddadDepartment of Medicine, Mayo Clinic, Rochester, USA.
C IsaacsDepartment of Medicine, Georgetown University, Washington, USA.
L PusztaiDepartment of Medicine, Yale University School of Medicine, New Haven, USA.
K AlbainDepartment of Medicine, Loyola University, Chicago, USA.
R NandaDepartment of Medicine, University of Chicago, Chicago, USA.
D TripathyDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA.
M C LiuDepartment of Medicine, Mayo Clinic, Rochester, USA.
J BougheyDepartment of Surgery, Mayo Clinic, Rochester, USA.
R SchwabDepartment of Medicine, University of California, San Diego, USA.
N HyltonDepartment of Radiology, University of California, San Francisco, USA.
A DeMicheleDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, San Philadelphia, USA.
J PerlmutterGemini Group, Ann Arbor, USA.
D YeeDepartment of Medicine, University of Minnesota, Minneapolis, USA.
D BerryDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, USA.
L Van't VeerDepartment of Pathology, University of California, San Francisco, USA.
V ValeroDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA.
L J EssermanDepartment of Surgery, University of California, San Francisco, USA.
W F SymmansDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA; Department of Pathology, The University of Texas MD Anderson Cancer Center, San Francisco, USA. Electronic address: fsymmans@mdanderson.org.
University of California, San Francisco · USThe University of Texas MD Anderson Cancer Center · USMayo Clinic · USUniversity of Minnesota · USGemini Computers (United States) · USGeorgetown University · USLoyola University Chicago · USUniversity of California San Diego · USUniversity of Chicago · USUniversity of Pennsylvania · USYale University · US

Funding

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 Nola M. Hylton-Watson · 2017 to 2026
$22.9M
NCI NIH HHS P01 CA210961
6 · The paper itself

Abstract

backgroundWe proposed that a test for sensitivity to the adjuvant endocrine therapy component of treatment for patients with stage II-III breast cancer (SET2,3) should measure transcription related to estrogen and progesterone receptors (SET PATIENTS AND

methodsPatients with clinically high-risk, hormone receptor-positive (HR+), human epidermal growth factor receptor 2 (HER2)-negative (HR+/HER2-) breast cancer received neoadjuvant taxane-anthracycline chemotherapy, surgery with measurement of residual cancer burden (RCB), and then adjuvant endocrine therapy. SET2,3 was measured from pre-treatment tumor biopsies, evaluated first in an MD Anderson Cancer Center (MDACC) cohort (n = 307, 11 years' follow-up, U133A microarrays), cut point was determined, and then independent, blinded evaluation was carried out in the I-SPY2 trial (n = 268, high-risk MammaPrint result, 3.8 years' follow-up, Agilent-44K microarrays, NCI Clinical Trials ID: NCT01042379). Primary outcome measure was distant relapse-free survival. Multivariate Cox regression models tested prognostic independence of SET2,3 relative to RCB and other molecular prognostic signatures, and whether other prognostic signatures could substitute for SET

resultsSET2,3 added independent prognostic information to RCB in the MDACC cohort: SET2,3 [hazard ratio (HR) 0.23, P = 0.004] and RCB (HR 1.77, P < 0.001); and the I-SPY2 trial: SET2,3 (HR 0.27, P = 0.031) and RCB (HR 1.68, P = 0.008). SET2,3 provided similar prognostic information irrespective of whether RCB-II or RCB-III after chemotherapy, and in both luminal subtypes. Conversely, RCB was most strongly prognostic in cancers with low SET2,3 status (MDACC P < 0.001, I-SPY2 P < 0.001). Other molecular signatures were not independently prognostic; they could effectively substitute for RNA4 subtype within the BPI component of SET2,3, but they could not effectively substitute for SET

conclusionsSET2,3 added independent prognostic information to chemotherapy response (RCB) and baseline prognostic score or subtype. Approximately 40% of patients with clinically high-risk HR+/HER2- disease had high SET2,3 and could be considered for clinical trials of neoadjuvant endocrine-based treatment.

Indexed as

Breast NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorErb-b2 Receptor Tyrosine KinasesFemaleHormonesHumansNeoadjuvant TherapyNeoplasm Recurrence, LocalPrognosisReceptors, ProgesteroneBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesHormonesReceptors, Progesteronechemo-endocrinehormonalpredictionprognosisresponsetreatments

Identifiers

PMID33617937
PMCPMC12236464
OpenAlexW3131379307

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Registered trials

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.