Evidence map›Paper›PMID 24345432›Full record

ArticleBreast cancer research : BCR2013

Progesterone receptor assembly of a transcriptional complex along with activator protein 1, signal transducer and activator of transcription 3 and ErbB-2 governs breast cancer growth and predicts response to endocrine therapy.

María C Díaz Flaqué, Natalia M Galigniana, Wendy Béguelin, Rocío Vicario, Cecilia J Proietti, Rosalía Russo, Martín A Rivas, Mercedes Tkach, Pablo Guzmán, Juan C Roa and 8 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Breast cancer research : BCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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  17. The HER2 Signaling Network in Breast Cancer--Like a Spider in its Web.Journal of mammary gland biology and neoplasia · 2014
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 2 countries.

María C Díaz Flaqué
Natalia M Galigniana
Wendy Béguelin
Rocío Vicario
Cecilia J Proietti
Rosalía Russo
Martín A Rivas
Mercedes Tkach
Pablo Guzmán
Juan C Roa
Esteban Maronna
Viviana Pineda
Sergio Muñoz
María Mercogliano
Eduardo H Charreau
Patricio Yankilevich
Roxana Schillaci
Patricia V Elizalde
Consejo Nacional de Investigaciones Científicas y Técnicas · ARExperimental Medicine and Biology Institute · ARUniversidad de La Frontera · CLBiomedicine Research Institute of Buenos Aires - CONICET - Partner Institute of the Max Planck Society · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe role of the progesterone receptor (PR) in breast cancer remains a major clinical challenge. Although PR induces mammary tumor growth, its presence in breast tumors is a marker of good prognosis. We investigated coordinated PR rapid and nonclassical transcriptional effects governing breast cancer growth and endocrine therapy resistance.

methodsWe used breast cancer cell lines expressing wild-type and mutant PRs, cells sensitive and resistant to endocrine therapy, a variety of molecular and cellular biology approaches, in vitro proliferation studies and preclinical models to explore PR regulation of cyclin D1 expression, tumor growth, and response to endocrine therapy. We investigated the clinical significance of activator protein 1 (AP-1) and PR interaction in a cohort of 99 PR-positive breast tumors by an immunofluorescence protocol we developed. The prognostic value of AP-1/PR nuclear colocalization in overall survival (OS) was evaluated using Kaplan-Meier method, and Cox model was used to explore said colocalization as an independent prognostic factor for OS.

resultsWe demonstrated that at the cyclin D1 promoter and through coordinated rapid and transcriptional effects, progestin induces the assembly of a transcriptional complex among AP-1, Stat3, PR, and ErbB-2 which functions as an enhanceosome to drive breast cancer growth. Our studies in a cohort of human breast tumors identified PR and AP-1 nuclear interaction as a marker of good prognosis and better OS in patients treated with tamoxifen (Tam), an anti-estrogen receptor therapy. Rationale for this finding was provided by our demonstration that Tam inhibits rapid and genomic PR effects, rendering breast cancer cells sensitive to its antiproliferative effects.

conclusionsWe here provided novel insight into the paradox of PR action as well as new tools to identify the subgroup of ER+/PR + patients unlikely to respond to ER-targeted therapies.

Indexed as

AnimalsBreast NeoplasmsCell NucleusCyclin D1Erb-b2 Receptor Tyrosine KinasesFemaleFollow-Up StudiesHumansMedroxyprogesterone AcetateMice, Inbred BALB CPhosphorylationPromoter Regions, GeneticReceptors, ProgesteroneRetrospective StudiesSelective Estrogen Receptor ModulatorsSTAT3 Transcription FactorCCND1 protein, humanCyclin D1ERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMedroxyprogesterone AcetateReceptors, ProgesteroneSelective Estrogen Receptor ModulatorsStat3 protein, mouseSTAT3 Transcription FactorTamoxifenTranscription Factor AP-1

Identifiers

PMID24345432
PMCPMC3978912
OpenAlexW2139866384

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.