Evidence map›Paper›PMID 27779230›Full record

ReviewNature reviews. Urology2017

The current evidence on statin use and prostate cancer prevention: are we there yet?

Mahmoud A Alfaqih, Emma H Allott, Robert J Hamilton, Michael R Freeman, Stephen J Freedland

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

Review in Nature reviews. Urology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 3 pooled it
6.2field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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26 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

5 authors at 4 institutions in 2 countries.

Mahmoud A AlfaqihDivision of Urology, Department of Surgery, Duke University School of Medicine, Box 2626, Durham, North Carolina 27710, USA.
Emma H AllottDepartment of Nutrition, CB 7461, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, North Carolina 27599, USA.
Robert J HamiltonDivision of Urology, Department of Surgical Oncology, University of Toronto, 610 University Avenue, Toronto, Ontario M5G 2M9, Canada.
Michael R FreemanDivision of Cancer Biology and Therapeutics, Departments of Surgery and Biomedical Sciences, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA.
Stephen J FreedlandDivision of Urology, Department of Surgery, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, 8635 West 3rd Street, Suite 1070W, Los Angeles, California 90048, USA.
Cedars-Sinai Medical Center · USDuke University · USUniversity of North Carolina at Chapel Hill · USUniversity of Toronto · CA

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI CHUNG, LELAND W.K. · 2003 to 2019
$24.0M
Midcareer Investigator AwardK24CA160653 · NCI · DUKE UNIVERSITY · PI FREEDLAND, STEPHEN JAY · 2012 to 2016
$877k
NCI NIH HHS K24 CA160653NCI NIH HHS P01 CA098912
6 · The paper itself

Abstract

An increasing amount of data supports an inverse association between statin use and cancer risk. The findings for prostate cancer, particularly advanced disease, are the most promising of all cancers studied. Use of these agents seems to also be associated with improved prostate- cancer-specific survival, particularly in men undergoing radiotherapy, suggesting usefulness of statins in secondary and tertiary prevention. Some study results might be influenced by increased PSA screening and health-conscious behaviour in statin users but these factors are unlikely to completely account for observed beneficial effects. The epidemiological evidence is supported by preclinical studies that show that statins directly inhibit prostate cancer development and progression in cell-based and animal-based models. The antineoplastic effect of statins might arise from a number of cholesterol-mediated and non-cholesterol-mediated mechanisms that affect pathways essential for cancer formation and progression. Understanding these mechanisms is instrumental in drug discovery research for the development of future prostate cancer therapeutics, as well as in designing clinical trials to test a role for statins in prostate cancer prevention. Currently, sufficient data are lacking to support the use of statins for the primary prevention of prostate cancer and further research is clearly warranted. Secondary and tertiary prevention trials in men who have been diagnosed with prostate cancer might soon be performed.

Indexed as

Evidence-Based MedicineFollow-Up StudiesHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMaleObservational Studies as TopicProstatic NeoplasmsHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID27779230
PMCPMC5830185
OpenAlexW2537437198

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.