Evidence map›Paper›PMID 23077249›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Estrogen receptor prevents p53-dependent apoptosis in breast cancer.

Shannon T Bailey, Hyunjin Shin, Thomas Westerling, Xiaole Shirley Liu, Myles Brown

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 145 citations in OpenAlex.

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  10. Mutational landscape of TP53 and CDH1 in gastric cancer.World journal of gastrointestinal surgery · 2024
    Article
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  14. The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
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29 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Shannon T BaileyCenter for Functional Cancer Epigenetics and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Hyunjin Shin
Thomas Westerling
Xiaole Shirley Liu
Myles Brown
Brigham and Women's Hospital · USHarvard University · USDana-Farber Cancer Institute · US

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0M
Computational Models for Mechanisms of Global Transcription RegulationR01HG004069 · NHGRI · DANA-FARBER CANCER INST · PI LIU, XIAOLE SHIRLEY · 2006 to 2013
$3.6M
Comprehensive Analysis of Estrogen Receptor Genomic ActionR01DK074967 · NIDDK · DANA-FARBER CANCER INST · PI BROWN, MYLES A · 2007 to 2011
$2.9M
NCI NIH HHS P01 CA080111NHGRI NIH HHS R01 HG004069NHGRI NIH HHS R01HG004069NIDDK NIH HHS R01 DK074967
6 · The paper itself

Abstract

More than two-thirds of breast cancers express the estrogen receptor (ER) and depend on estrogen for growth and survival. Therapies targeting ER function, including aromatase inhibitors that block the production of estrogens and ER antagonists that alter ER transcriptional activity, play a central role in the treatment of ER+ breast cancers of all stages. In contrast to ER- breast cancers, which frequently harbor mutations in the p53 tumor suppressor, ER+ breast cancers are predominantly wild type for p53. Despite harboring wild-type p53, ER+ breast cancer cells are resistant to chemotherapy-induced apoptosis in the presence of estrogen. Using genome-wide approaches, we have addressed the mechanism by which ER antagonizes the proapoptotic function of p53. Interestingly, both ER agonists such as estradiol and the selective ER modulator (SERM) tamoxifen promote p53 antagonism. In contrast, the full ER antagonist fulvestrant blocks the ability of ER to inhibit p53-mediated cell death. This inhibition works through a mechanism involving the modulation of a subset of p53 and ER target genes that can predict the relapse-free survival of patients with ER+ breast cancer. These findings suggest an improved strategy for the treatment of ER+ breast cancer using antagonists that completely block ER action together with drugs that activate p53-mediated cell death.

Indexed as

ApoptosisBreast NeoplasmsFemaleHumansReceptors, EstrogenTumor Suppressor Protein p53Receptors, EstrogenTumor Suppressor Protein p53

Identifiers

PMID23077249
PMCPMC3497783
OpenAlexW2141280707

What OpenQuestion holds

Textmetadata
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.