Evidence map›Paper›PMID 25072326›Full record

ArticlePloS one2014

Selective androgen receptor modulators (SARMs) negatively regulate triple-negative breast cancer growth and epithelial:mesenchymal stem cell signaling.

Ramesh Narayanan, Sunjoo Ahn, Misty D Cheney, Muralimohan Yepuru, Duane D Miller, Mitchell S Steiner, James T Dalton

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-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

38 citing papers in PubMed, 70 citations in OpenAlex.

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  20. Drug Repurposing for Triple-Negative Breast Cancer.Journal of personalized medicine · 2020
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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

7 authors at 1 institution in 1 country.

Ramesh NarayananPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
Sunjoo AhnPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
Misty D CheneyPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
Muralimohan YepuruPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
Duane D MillerPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
Mitchell S SteinerPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
James T DaltonPreclinical Research and Development, GTx, Inc., Memphis, Tennessee, United States of America.
GTx (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe androgen receptor (AR) is the most highly expressed steroid receptor in breast cancer with 75-95% of estrogen receptor (ER)-positive and 40-70% of ER-negative breast cancers expressing AR. Though historically breast cancers were treated with steroidal androgens, their use fell from favor because of their virilizing side effects and the emergence of tamoxifen. Nonsteroidal, tissue selective androgen receptor modulators (SARMs) may provide a novel targeted approach to exploit the therapeutic benefits of androgen therapy in breast cancer. MATERIALS AND

methodsSince MDA-MB-453 triple-negative breast cancer cells express mutated AR, PTEN, and p53, MDA-MB-231 triple-negative breast cancer cells stably expressing wildtype AR (MDA-MB-231-AR) were used to evaluate the in vitro and in vivo anti-proliferative effects of SARMs. Microarray analysis and epithelial:mesenchymal stem cell (MSC) co-culture signaling studies were performed to understand the mechanisms of action.

resultsDihydrotestosterone and SARMs, but not bicalutamide, inhibited the proliferation of MDA-MB-231-AR. The SARMs reduced the MDA-MB-231-AR tumor growth and tumor weight by greater than 90%, compared to vehicle-treated tumors. SARM treatment inhibited the intratumoral expression of genes and pathways that promote breast cancer development through its actions on the AR. SARM treatment also inhibited the metastasis-promoting paracrine factors, IL6 and MMP13, and subsequent migration and invasion of epithelial:MSC co-cultures.

conclusion1. AR stimulation inhibits paracrine factors that are important for MSC interactions and breast cancer invasion and metastasis. 2. SARMs may provide promise as novel targeted therapies to treat AR-positive triple-negative breast cancer.

Indexed as

AnimalsCell Line, TumorCell ProliferationDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHumansMesenchymal Stem CellsMiceMice, NudeNeoplasm MetastasisParacrine CommunicationReceptors, AndrogenSelective Estrogen Receptor ModulatorsSignal TransductionTriple Negative Breast NeoplasmsReceptors, AndrogenSelective Estrogen Receptor Modulators

Identifiers

PMID25072326
PMCPMC4114483
OpenAlexW1971822166

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.