Evidence map›Paper›PMID 29210989›Full record

ReviewCancers2017

Supraphysiologic Testosterone Therapy in the Treatment of Prostate Cancer: Models, Mechanisms and Questions.

Osama S Mohammad, Michael D Nyquist, Michael T Schweizer, Stephen P Balk, Eva Corey, Stephen Plymate, Peter S Nelson, Elahe A Mostaghel

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 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

8 authors at 3 institutions in 2 countries.

Osama S MohammadFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. osamasaad89@live.com.
Michael D NyquistFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. mnyquist@fhcrc.org.
Michael T SchweizerFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. scwheize@uw.edu.
Stephen P BalkBeth Israel Deaconess Medical Center, Boston, MA 02215, USA. sbalk@bidmc.org.
Eva CoreyDepartment of Urology, University of Washington, Seattle, WA 98195, USA. ecorey@u.washington.edu.
Stephen PlymateSchool of Medicine, University of Washington, Seattle, WA 98195, USA. splymate@uw.edu.
Peter S NelsonFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. pnelson@fhcrc.org.
Elahe A MostaghelFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. emostagh@fhcrc.org.
Fred Hutch Cancer Center · USUniversity of Washington · USBeth Israel Deaconess Medical Center · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Steven P. Balk · 2013 to 2026
$25.0M
Exploring high-does testosterone as a potential treatment for abiraterone-resistant prostate cancerR21CA194798 · NCI · UNIVERSITY OF WASHINGTON · PI COREY, EVA · 2016 to 2017
$370k
Targeting the Metabolome in Androgen Receptor-driven Castration-resistant Prostate CancerI01BX003324 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI PLYMATE, STEPHEN R. · 2016 to 2024
–
BLRD VA I01 BX003324NCI NIH HHS P01 CA163227NCI NIH HHS P50 CA097186NCI NIH HHS R21 CA194798
6 · The paper itself

Abstract

Since Huggins defined the androgen-sensitive nature of prostate cancer (PCa), suppression of systemic testosterone (T) has remained the most effective initial therapy for advanced disease although progression inevitably occurs. From the inception of clinical efforts to suppress androgen receptor (AR) signaling by reducing AR ligands, it was also recognized that administration of T in men with castration-resistant prostate cancer (CRPC) could result in substantial clinical responses. Data from preclinical models have reproducibly shown biphasic responses to T administration, with proliferation at low androgen concentrations and growth inhibition at supraphysiological T concentrations. Many questions regarding the biphasic response of PCa to androgen treatment remain, primarily regarding the mechanisms driving these responses and how best to exploit the biphasic phenomenon clinically. Here we review the preclinical and clinical data on high dose androgen growth repression and discuss cellular pathways and mechanisms likely to be involved in mediating this response. Although meaningful clinical responses have now been observed in men with PCa treated with high dose T, not all men respond, leading to questions regarding which tumor characteristics promote response or resistance, and highlighting the need for studies designed to determine the molecular mechanism(s) driving these responses and identify predictive biomarkers.

Indexed as

BATbiphasicbipolar androgen therapycastration resistant prostate cancerCRPChigh dose testosteronesupraphysiologic androgen

Identifiers

PMID29210989
PMCPMC5742814
OpenAlexW2773273196

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.