Evidence map›Paper›PMID 26728473›Full record

ReviewHormones & cancer2016

Moving Beyond the Androgen Receptor (AR): Targeting AR-Interacting Proteins to Treat Prostate Cancer.

Christopher Foley, Nicholas Mitsiades

Abstract readReview
In one paragraph

Review in Hormones & cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 57 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Christopher FoleyDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Suite R407, MS: BCM187, Houston, TX, 77030, USA.
Nicholas MitsiadesDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Suite R407, MS: BCM187, Houston, TX, 77030, USA. mitsiade@bcm.edu.
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
REGULATION OF UVEAL MELANOMA CELL FATE BY THE PKC PATHWAY VIA MITFR01CA193321 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MITSIADES, NICHOLAS · 2015 to 2019
$1.8M
NCI NIH HHS 1R01CA193321NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS R01 CA193321NIDDK NIH HHS P30 DK079638NIDDK NIH HHS P30-DK079638
6 · The paper itself

Abstract

Medical or surgical castration serves as the backbone of systemic therapy for advanced and metastatic prostate cancer, taking advantage of the importance of androgen signaling in this disease. Unfortunately, resistance to castration emerges almost universally. Despite the development and approval of new and more potent androgen synthesis inhibitors and androgen receptor (AR) antagonists, prostate cancers continue to develop resistance to these therapeutics, while often maintaining their dependence on the AR signaling axis. This highlights the need for innovative therapeutic approaches that aim to continue disrupting AR downstream signaling but are orthogonal to directly targeting the AR itself. In this review, we discuss the preclinical research that has been done, as well as clinical trials for prostate cancer, on inhibiting several important families of AR-interacting proteins, including chaperones (such as heat shock protein 90 (HSP90) and FKBP52), pioneer factors (including forkhead box protein A1 (FOXA1) and GATA-2), and AR transcriptional coregulators such as the p160 steroid receptor coactivators (SRCs) SRC-1, SRC-2, SRC-3, as well as lysine deacetylases (KDACs) and lysine acetyltransferases (KATs). Researching the effect of-and developing new therapeutic agents that target-the AR signaling axis is critical to advancing our understanding of prostate cancer biology, to continue to improve treatments for prostate cancer and for overcoming castration resistance.

Indexed as

AnimalsAntineoplastic AgentsClinical Trials as TopicHumansMaleMolecular ChaperonesMolecular Targeted TherapyProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionTranscription FactorsAntineoplastic AgentsAR protein, humanMolecular ChaperonesReceptors, AndrogenTranscription Factors

Identifiers

PMID26728473
PMCPMC5380740
OpenAlexW2225000706

What OpenQuestion holds

Textmetadata
LicenceTDM
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.