Evidence map›Paper›PMID 25134829›Full record

ReviewNature reviews. Urology2014

Autophagy as a modulator and target in prostate cancer.

Jason M Farrow, Joy C Yang, Christopher P Evans

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature reviews. Urology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03513211 (A Phase I/II Study of Hydroxychloroquine and Itraconazole as Therapy for Men With Androgen Normalised Prostate Cancer), which is not on this map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
–field-weighted citation impact
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.

NCT03513211 phase1 / phase2completednot on this mapstarted 2018, after this paper: background citation

A Phase I/II Study of Hydroxychloroquine and Itraconazole as Therapy for Men With Androgen Normalised Prostate Cancer

TypeinterventionalSponsorSt Vincent's Hospital, SydneyRan2018 to 2023Enrolled12ConditionsProstate CancerArmsSUBA-itraconazole, Hydroxychloroquine
3 · Its place in the literature

Who cites it

101 citing papers in PubMed.

  1. Review
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41 more citing papers are in PubMed but not listed here.

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

3 authors.

Jason M FarrowDepartment of Urology, School of Medicine, University of California, Davis, 4860 Y Street, Sacramento, CA 95817, USA.
Joy C YangDepartment of Urology, School of Medicine, University of California, Davis, 4860 Y Street, Sacramento, CA 95817, USA.
Christopher P EvansDepartment of Urology, School of Medicine, University of California, Davis, 4860 Y Street, Sacramento, CA 95817, USA.

Funding

UC Davis Clinical and Translational Science CenterUL1TR000002 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$12.2M
UC Davis Clinical and Translational Science CenterTL1TR000133 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$594k
NCATS NIH HHS TL1 TR000133NCATS NIH HHS UL1 TR000002
6 · The paper itself

Abstract

Autophagy, or 'self-eating', is an adaptive process that enables cells to cope with metabolic, toxic, and even infectious stressors. Although the adaptive capability of autophagy is generally considered beneficial, autophagy can also enhance nutrient utilization and improve growth characteristics of cancer cells. Moreover, autophagy can promote greater cellular robustness in the context of therapeutic intervention. In advanced prostate cancer, preclinical data provide evidence that autophagy facilitates both disease progression and therapeutic resistance. Notably, androgen deprivation therapy, taxane-based chemotherapy, targeted kinase inhibition, and nutrient restriction all induce significant cellular distress and, subsequently, autophagy. Understanding the context-dependent role of autophagy in cancer development and treatment resistance has the potential to improve current treatment of advanced prostate cancer. Indeed, preclinical studies have shown that the pharmacological inhibition of autophagy (with agents including chloroquine, hydroxychloroquine, metformin, and desmethylclomipramine) can enhance the cell-killing effect of cancer therapeutics, and a number of these agents are currently under investigation in clinical trials. However, many of these autophagy modulators are relatively nonspecific, and cytotoxicity in noncancerous tissues is still a concern. Moving forward, refinement of autophagy modulation is needed.

Indexed as

AutophagyHumansMaleProstatic Neoplasms

Identifiers

PMID25134829
PMCPMC4415606

What OpenQuestion holds

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Registered trials

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.