Evidence map›Paper›PMID 23925999›Full record

ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2013

Functional proteomics characterization of residual triple-negative breast cancer after standard neoadjuvant chemotherapy.

J Sohn, K A Do, S Liu, H Chen, G B Mills, G N Hortobagyi, F Meric-Bernstam, A M Gonzalez-Angulo

Abstract read
In one paragraph

Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Trial
  2. Review
  3. Tumor P70S6K hyperactivation is inversely associated with tumor-infiltrating lymphocytes in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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  12. IGFBP-2 - taking the lead in growth, metabolism and cancer.Journal of cell communication and signaling · 2015
    Article
  13. Review
  14. Article
  15. Review
  16. Article
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  20. Differences in gene and protein expression and the effects of race/ethnicity on breast cancer subtypes.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    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

8 authors.

J SohnDepartments of Breast Medical Oncology.
K A DoBiostatistics.
S LiuDepartments of Breast Medical Oncology.
H ChenDepartments of Breast Medical Oncology.
G B MillsSystems Biology.
G N HortobagyiDepartments of Breast Medical Oncology.
F Meric-BernstamSurgical Oncology (FMB), The University of Texas MD Anderson Cancer Center, Houston, USA.
A M Gonzalez-AnguloDepartments of Breast Medical Oncology; Systems Biology. Electronic address: agonzalez@mdanderson.org.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
The PI3K/PTEN/AKT Signal Transduction Cascade in Breast CancerK23CA121994 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GONZALEZ-ANGULO, ANA M. · 2006 to 2010
$680k
NCI NIH HHS K23CA121994-01PHS HHS KG090341
6 · The paper itself

Abstract

backgroundIn this study, we used functional proteomics to determine the molecular characteristics of residual triple receptor-negative breast cancer (TNBC) patients after neoadjuvant systemic chemotherapy (NCT) and their relationship with patient outcomes in order to identify potential targets for therapy. PATIENTS AND

methodsProtein was extracted from 54 residual TNBCs, and 76 proteins related to breast cancer signaling were measured by reverse phase protein arrays (RPPAs). Univariable and multivariable Cox proportional hazard models were fitted for each protein. Survival outcomes were estimated by the Kaplan-Meier product limit method. Training and cross validation were carried out. The coefficients estimated from the multivariable Cox model were used to calculate a risk score (RS) for each sample.

resultsMultivariable analysis using the top 25 proteins from univariable analysis at a false discovery rate (FDR) of 0.3 showed that AKT, IGFBP2, LKB1, S6 and Stathmin were predictors of recurrence-free survival (RFS). The cross-validation model was reproducible. The RS model calculated based on the multivariable analysis was -1.1086 × AKT + 0.2501 × IGFBP2 - 0.6745 × LKB1+1.0692 × S6 + 1.4086 × stathmin with a corresponding area under the curve, AUC = 0.856. The RS was an independent predictor of RFS (HR = 3.28, 95%CI = 2.07-5.20, P < 0.001).

conclusionsWe found a five-protein model that independently predicted RFS risk in patients with residual TNBC disease. The PI3 K pathway may represent potential therapeutic targets in this resistant disease.

Indexed as

Neoadjuvant TherapyAdultAgedAMP-Activated Protein Kinase KinasesAnthracyclinesAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBridged-Ring CompoundsDisease-Free SurvivalFemaleHumansInsulin-Like Growth Factor Binding Protein 2Middle AgedProtein Serine-Threonine KinasesProteomicsAMP-Activated Protein Kinase KinasesAnthracyclinesAntineoplastic AgentsBiomarkers, TumorBridged-Ring CompoundsIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRibosomal Protein S6StathminSTK11 protein, humantaxaneTaxoidsmolecular characterizationneoadjuvant chemotherapyresidual diseaseresistancetriple receptor-negative breast cancer

Identifiers

PMID23925999
PMCPMC3784335

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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.