Evidence map›Paper›PMID 29460925›Full record

ReviewNature reviews. Urology2018

Clinical implications of PTEN loss in prostate cancer.

Tamara Jamaspishvili, David M Berman, Ashley E Ross, Howard I Scher, Angelo M De Marzo, Jeremy A Squire, Tamara L Lotan

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Urology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 380 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
380citing papers in PubMed, 2 pooled it
24.1field-weighted citation impact, top 1% 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

380 citing papers in PubMed, 2 syntheses or guidelines pooled it, 635 citations in OpenAlex.

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  8. Immune Spatial Organization Predicts Distant Metastasis Risk in Aggressive Localized Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  18. Science advances · 2026
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320 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

7 authors at 4 institutions in 3 countries.

Tamara JamaspishviliDivision of Cancer Biology and Genetics, Cancer Research Institute, Queen's University, Kingston, Ontario, Canada.
David M BermanDivision of Cancer Biology and Genetics, Cancer Research Institute, Queen's University, Kingston, Ontario, Canada.
Ashley E RossDepartment of Urology, Johns Hopkins University, Baltimore, MD, USA.
Howard I ScherGenitourinary Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, NY, USA.
Angelo M De MarzoDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Jeremy A SquireDepartment of Pathology and Legal Medicine, University of Sao Paulo, Campus Universitario Monte Alegre, Ribeirão Preto, Brazil.
Tamara L LotanDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Johns Hopkins University · USQueen's University · CAMemorial Sloan Kettering Cancer Center · USUniversidade de São Paulo · BR

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
SPORE In Prostate CancerP50CA092629 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JAMES A EASTHAM · 2001 to 2026
$63.0M
NCI NIH HHS P30 CA006973NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA092629
6 · The paper itself

Abstract

Genomic aberrations of the PTEN tumour suppressor gene are among the most common in prostate cancer. Inactivation of PTEN by deletion or mutation is identified in ∼20% of primary prostate tumour samples at radical prostatectomy and in as many as 50% of castration-resistant tumours. Loss of phosphatase and tensin homologue (PTEN) function leads to activation of the PI3K-AKT (phosphoinositide 3-kinase-RAC-alpha serine/threonine-protein kinase) pathway and is strongly associated with adverse oncological outcomes, making PTEN a potentially useful genomic marker to distinguish indolent from aggressive disease in patients with clinically localized tumours. At the other end of the disease spectrum, therapeutic compounds targeting nodes in the PI3K-AKT-mTOR (mechanistic target of rapamycin) signalling pathway are being tested in clinical trials for patients with metastatic castration-resistant prostate cancer. Knowledge of PTEN status might be helpful to identify patients who are more likely to benefit from these therapies. To enable the use of PTEN status as a prognostic and predictive biomarker, analytically validated assays have been developed for reliable and reproducible detection of PTEN loss in tumour tissue and in blood liquid biopsies. The use of clinical-grade assays in tumour tissue has shown a robust correlation between loss of PTEN and its protein as well as a strong association between PTEN loss and adverse pathological features and oncological outcomes. In advanced disease, assessing PTEN status in liquid biopsies shows promise in predicting response to targeted therapy. Finally, studies have shown that PTEN might have additional functions that are independent of the PI3K-AKT pathway, including those affecting tumour growth through modulation of the immune response and tumour microenvironment.

Indexed as

MutationDNA Mutational AnalysisDNA, NeoplasmGenetic MarkersHumansMaleMembrane ProteinsProstatic NeoplasmsPTEN PhosphohydrolaseSignal TransductionTumor MicroenvironmentDNA, NeoplasmGenetic MarkersMembrane ProteinsPTEN PhosphohydrolaseTPTE protein, human

Identifiers

PMID29460925
PMCPMC7472658
OpenAlexW2788783025

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.