Evidence map›Paper›PMID 15535853›Full record

ReviewBreast cancer research : BCR2004

The origins of estrogen receptor alpha-positive and estrogen receptor alpha-negative human breast cancer.

D Craig Allred, Powel Brown, Daniel Medina

Open access · goldAbstract readReview
In one paragraph

Review in Breast cancer research : BCR, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 5 pooled it
4.0field-weighted citation impact, top 6% 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

100 citing papers in PubMed, 5 syntheses or guidelines pooled it, 216 citations in OpenAlex.

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  14. Regulation of ERα-dependent breast cancer metastasis by a miR-29a signaling.Journal of experimental & clinical cancer research : CR · 2023
    Article
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40 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

3 authors at 2 institutions in 2 countries.

D Craig AllredBreast Center/Department of Pathology, Baylor College of Medicine, Houston, Texas, USA. dcallred@breastcenter.tmc.edu
Powel Brown
Daniel Medina
Baylor College of Medicine · USBreast Center · CH

Funding

TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OSBORNE, C KENT · 1992 to 2012
$30.9M
NCI NIH HHS P50 CA058183NCI NIH HHS P50-CA58183
6 · The paper itself

Abstract

Current hormonal therapies have benefited millions of patients with breast cancer. Their success, however, is often temporary and limited to a subset of patients whose tumors express estrogen receptor alpha (ER). The therapies are entirely ineffective in ER-negative disease. Recent studies suggest that there are many biological pathways and alterations involved in determining whether ER is expressed and how it is regulated during breast cancer evolution. Improving hormonal therapies, in addition to perfecting current strategies, will also target these newly discovered pathways and alterations, and others yet to be found. The present commentary will briefly highlight a few important observations and unanswered questions regarding ER status and growth regulation during breast cancer evolution, which hopefully will help to stimulate new thinking and progress in this important area of medial research.

Indexed as

Antineoplastic Agents, HormonalBreast NeoplasmsCell Growth ProcessesEstrogen Receptor alphaHumansAntineoplastic Agents, HormonalEstrogen Receptor alpha

Identifiers

PMID15535853
PMCPMC1064085
OpenAlexW2108725521

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.