Evidence map›Paper›PMID 38203649›Full record

ReviewInternational journal of molecular sciences2023

Androgen Receptor in Hormone Receptor-Positive Breast Cancer.

Ashfia Fatima Khan, Samaneh Karami, Anthony S Peidl, Kacie D Waiters, Mariam Funmi Babajide, Tasneem Bawa-Khalfe

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  10. The role of phosphatidylcholine metabolism in tumors.Medical oncology (Northwood, London, England) · 2025
    Review
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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

6 authors at 1 institution in 1 country.

Ashfia Fatima KhanCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.ORCID 0000-0002-1730-5383
Samaneh KaramiCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.
Anthony S PeidlCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.
Kacie D WaitersCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.
Mariam Funmi BabajideCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.
Tasneem Bawa-KhalfeCenter for Nuclear Receptors & Cell Signaling, Department of Biology & Biochemistry, University of Houston, 3517 Cullen Blvd, SERC Bldg., Rm 3010, Houston, TX 77204-5056, USA.
University of Houston · US

Funding

Targeting Constitutively Active SUMO Modified Androgen Receptors in Endocrine Resistant Breast CancerR01CA256543 · NCI · UNIVERSITY OF HOUSTON · PI BAWA-KHALFE, TASNEEM · 2021 to 2025
$1.8M
NCI NIH HHS R01 CA256543NCI NIH HHS R01CA256543
6 · The paper itself

Abstract

Breast cancer subtypes expressing hormone receptors (HR+ BCa) have a good prognosis and respond to first-line endocrine therapy (ET). However, the majority of HR+ BCa patients exhibit intrinsic or acquired ET resistance (ET-R) and rapid onset of incurable metastatic BCa. With the failure of conventional ET, limited targeted therapy exists for ET-R HR+ BCa patients. The androgen receptor (AR) in HR-negative BCa subtypes is emerging as an attractive alternative target for therapy. The AR drives Luminal AR (LAR) triple-negative breast cancer progression, and LAR patients consistently exhibit positive clinical benefits with AR antagonists in clinical trials. In contrast, the function of the AR in HR+ BCa is more conflicting. AR in HR+ BCa correlates with a favorable prognosis, and yet, the AR supports the development of ET-R BCa. While AR antagonists were ineffective, ongoing clinical trials with a selective AR modulator have shown promise for HR+ BCa patients. To understand the incongruent actions of ARs in HR+ BCa, the current review discusses how the structure and post-translational modification impact AR function. Additionally, completed and ongoing clinical trials with FDA-approved AR-targeting agents for BCa are presented. Finally, we identify promising investigational small molecules and chimera drugs for future HR+ BCa therapy.

Indexed as

Receptors, AndrogenTriple Negative Breast NeoplasmsAndrogen AntagonistsAndrogen Receptor AntagonistsAndrogensHumansAndrogen AntagonistsAndrogen Receptor AntagonistsAndrogensReceptors, Androgenandrogen receptor 1AR-targeting drugs 5clinical trials 6hormone-positive breast cancer 2post-translational modification 3SUMOylation 4

Identifiers

PMID38203649
PMCPMC10779387
OpenAlexW4390404647

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.