Evidence map›Paper›PMID 31698248›Full record

ArticleiScience2019

Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers.

Suriyan Ponnusamy, Sarah Asemota, Lee S Schwartzberg, Fouzia Guestini, Keely M McNamara, Mariaelena Pierobon, Alba Font-Tello, Xintao Qiu, Yingtian Xie, Prakash K Rao and 13 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-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

28 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Hormone Signaling in Breast Development and Cancer.Advances in experimental medicine and biology · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Androgen Receptor in Hormone Receptor-Positive Breast Cancer.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Diverse role of androgen action in human breast cancer.Endocrine oncology (Bristol, England) · 2022
    Review
  20. Review
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

23 authors at 5 institutions in 2 countries.

Suriyan PonnusamyDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA.
Sarah AsemotaDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA.
Lee S SchwartzbergWest Cancer Center, Memphis, TN, USA.
Fouzia GuestiniDepartment of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Keely M McNamaraDepartment of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Mariaelena PierobonCenter for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, VA, USA.
Alba Font-TelloCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Xintao QiuCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Yingtian XieCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Prakash K RaoCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Thirumagal ThiyagarajanDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA.
Brandy GrimesWest Cancer Center, Memphis, TN, USA.
Daniel L JohnsonMolecular Informatics Core, University of Tennessee Health Science Center, Memphis, TN, USA.
Martin D FlemingDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA.
Frances E PritchardDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA.
Michael P BerryWest Cancer Center, Memphis, TN, USA.
Roy OswaksWest Cancer Center, Memphis, TN, USA.
Richard E FineWest Cancer Center, Memphis, TN, USA.
Myles BrownCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Hironobu SasanoDepartment of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Emanuel F PetricoinCenter for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, VA, USA.
Henry W LongCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Ramesh NarayananDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, 19, S. Manassas, Room 120, Memphis, TN 38103, USA; West Cancer Center, Memphis, TN, USA. Electronic address: rnaraya4@uthsc.edu.
University of Tennessee Health Science Center · USDana-Farber Cancer Institute · USWest Cancer Center · USTohoku University · JPGeorge Mason University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained treatment of estrogen receptor (ER)-positive breast cancer with ER-targeting drugs results in ER mutations and refractory unresponsive cancers. Androgen receptor (AR), which is expressed in 80%-95% of ER-positive breast cancers, could serve as an alternate therapeutic target. Although AR agonists were used in the past to treat breast cancer, their use is currently infrequent due to virilizing side effects. Discovery of tissue-selective AR modulators (SARMs) has renewed interest in using AR agonists to treat breast cancer. Using translational models, we show that AR agonist and SARM, but not antagonist, inhibit the proliferation and growth of ER-positive breast cancer cells, patient-derived tissues, and patient-derived xenografts (PDX). Ligand-activated AR inhibits wild-type and mutant ER activity by reprogramming the ER and FOXA1 cistrome and rendering tumor growth inhibition. These findings suggest that ligand-activated AR may function as a non-canonical inhibitor of ER and that AR agonists may offer a safe and effective treatment for ER-positive breast cancer.

Indexed as

CancerMolecular BiologyMolecular Mechanism of Gene Regulation

Identifiers

PMID31698248
PMCPMC6889594
OpenAlexW2981568031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.