Evidence map›Paper›PMID 27279911›Full record

ArticleTheranostics2016

Improvement of Prostate Cancer Diagnosis by Detecting PSA Glycosylation-Specific Changes.

Esther Llop, Montserrat Ferrer-Batallé, Sílvia Barrabés, Pedro Enrique Guerrero, Manel Ramírez, Radka Saldova, Pauline M Rudd, Rosa N Aleixandre, Josep Comet, Rafael de Llorens and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Theranostics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
15.6field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  6. High-MannoseJournal of proteome research · 2026
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  14. [Applications of chromatography in glycomics].Se pu = Chinese journal of chromatography · 2024
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Esther Llop1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Montserrat Ferrer-Batallé1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Sílvia Barrabés1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Pedro Enrique Guerrero1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Manel Ramírez2. Clinic Laboratory, Dr. J. Trueta University Hospital, 17007, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Radka Saldova5. NIBRT GlycoScience Group, National Institute for Bioprocessing Research and Training, Dublin, Ireland.
Pauline M Rudd5. NIBRT GlycoScience Group, National Institute for Bioprocessing Research and Training, Dublin, Ireland.
Rosa N Aleixandre2. Clinic Laboratory, Dr. J. Trueta University Hospital, 17007, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Josep Comet3. Urology Unit, Dr. J. Trueta University Hospital, 17007, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Rafael de Llorens1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Rosa Peracaula1. Biochemistry and Molecular Biology Unit. Department of Biology, University of Girona, Campus Montilivi, 17071, Girona, Spain.; 4. Biomedical Research Institute of Girona (IdIBGi). Dr. J. Trueta University Hospital, 17007, Girona, Spain.
Universitat de Girona · ESInstitut d'Investigació Biomèdica de Girona · ESNational Institute for Bioprocessing Research and Training · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

New markers based on PSA isoforms have recently been developed to improve prostate cancer (PCa) diagnosis. However, novel approaches are still required to differentiate aggressive from non-aggressive PCa to improve decision making for patients. PSA glycoforms have been shown to be differentially expressed in PCa. In particular, changes in the extent of core fucosylation and sialylation of PSA N-glycans in PCa patients compared to healthy controls or BPH patients have been reported. The objective of this study was to determine these specific glycan structures in serum PSA to analyze their potential value as markers for discriminating between BPH and PCa of different aggressiveness. In the present work, we have established two methodologies to analyze the core fucosylation and the sialic acid linkage of PSA N-glycans in serum samples from BPH (29) and PCa (44) patients with different degrees of aggressiveness. We detected a significant decrease in the core fucose and an increase in the α2,3-sialic acid percentage of PSA in high-risk PCa that differentiated BPH and low-risk PCa from high-risk PCa patients. In particular, a cut-off value of 0.86 of the PSA core fucose ratio, could distinguish high-risk PCa patients from BPH with 90% sensitivity and 95% specificity, with an AUC of 0.94. In the case of the α2,3-sialic acid percentage of PSA, the cut-off value of 30% discriminated between high-risk PCa and the group of BPH, low-, and intermediate-risk PCa with a sensitivity and specificity of 85.7% and 95.5%, respectively, with an AUC of 0.97. The latter marker exhibited high performance in differentiating between aggressive and non-aggressive PCa and has the potential for translational application in the clinic.

Indexed as

AgedAged, 80 and overHumansKallikreinsMaleMiddle AgedPolysaccharidesPrognosisProstate-Specific AntigenProstatic NeoplasmsProtein IsoformsKallikreinsKLK3 protein, humanPolysaccharidesProstate-Specific AntigenProtein Isoformsbenign prostatic hyperplasia (BPH)glycosylationPholiota squarrosa lectin (PhoSL)prostate cancer (PCa)prostate specific antigen (PSA)Sambucus nigra agglutinin (SNA).

Identifiers

PMID27279911
PMCPMC4893645
OpenAlexW2435326962

What OpenQuestion holds

Textmetadata
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.