Evidence map›Paper›PMID 30217566›Full record

ReviewCancer letters2018

Targeting the turnover of oncoproteins as a new avenue for therapeutics development in castration-resistant prostate cancer.

Shan Wang, Dede N Ekoue, Ganesh V Raj, Ralf Kittler

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. How Oncovirus Affects Drug Resistance in Cancer Cells.Recent patents on anti-cancer drug discovery · 2026
    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

4 authors at 2 institutions in 1 country.

Shan WangEugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: Shan.Wang@utsouthwestern.edu.
Dede N EkoueDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ganesh V RajDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ralf KittlerEugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, TX, USA; Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: Ralf.Kittler@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

Development of small molecules for ERG ablation in prostate cancerR01CA200787 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KITTLER, RALF · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA200787
6 · The paper itself

Abstract

The current therapeutic armamentarium for castration-resistant prostate cancer (CRPC) includes second-generation agents such as the Androgen Receptor (AR) inhibitor enzalutamide and the androgen synthesis inhibitor abiraterone acetate, immunotherapies like sipuleucel-T, chemotherapies including docetaxel and cabazitaxel and the radiopharmaceutical radium 223 dichloride. However, relapse of CRPC resistant to these therapeutic modalities occur rapidly. The mechanisms of resistance to these treatments are complex, including specific mutations or alternative splicing of oncogenic proteins. An alternative approach to treating CRPC may be to target the turnover of these molecular drivers of CRPC. In this review, the mechanisms by which protein stability of several oncoproteins such as AR, ERG, GR, CYP17A1 and MYC, will be discussed, as well as how these findings could be translated into novel therapeutic agents.

Indexed as

Androgen Receptor AntagonistsAntineoplastic AgentsDrug Resistance, NeoplasmHumansMaleMutationNeoplasm Recurrence, LocalOncogene ProteinsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAndrogen Receptor AntagonistsAntineoplastic AgentsOncogene ProteinsReceptors, AndrogenAndrogen receptorERGOncoproteinProstate cancerProtein turnoverUbiquitination

Identifiers

PMID30217566
PMCPMC6186492
OpenAlexW2889668071

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.