Evidence map›Paper›PMID 28152543›Full record

ArticleBritish journal of cancer2017

Asporin is a stromally expressed marker associated with prostate cancer progression.

Annie Rochette, Nadia Boufaied, Eleonora Scarlata, Lucie Hamel, Fadi Brimo, Hayley C Whitaker, Antonio Ramos-Montoya, David E Neal, Alice Dragomir, Armen Aprikian and 2 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

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  17. ASPORIN: A root of the matter in tumors and their host environment.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
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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

12 authors at 3 institutions in 2 countries.

Annie RochetteDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Nadia BoufaiedDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Eleonora ScarlataDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Lucie HamelDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Fadi BrimoDepartment of Pathology, Division of Urology, McGill University and The McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Hayley C WhitakerDepartment of Oncology, University of Cambridge, Box 279, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Antonio Ramos-MontoyaDepartment of Oncology, University of Cambridge, Box 279, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
David E NealDepartment of Oncology, University of Cambridge, Box 279, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Alice DragomirDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Armen AprikianDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Simone ChevalierDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
Axel A ThomsonDepartment of Surgery, Division of Urology, McGill University and the Cancer Research Program of the Research Institute of McGill University Health Centre, Montreal, Quebec H4A 3J1, Canada.
McGill University Health Centre · CAUniversity of Cambridge · GBAddenbrooke's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer shows considerable heterogeneity in disease progression and we propose that markers expressed in tumour stroma may be reliable predictors of aggressive tumour subtypes.

methodsWe have used Kaplan-Meier, univariate and multivariate analysis to correlate the expression of Asporin (ASPN) mRNA and protein with prostate cancer progression in independent cohorts. We used immunohistochemistry and H scoring to document stromal localisation of ASPN in a tissue microarray and mouse prostate cancer model, and correlated expression with reactive stroma, defined using Masson Trichrome staining. We used cell cultures of primary prostate cancer fibroblasts treated with serum-free conditioned media from prostate cancer cell lines to examine regulation of ASPN mRNA in tumour stromal cells.

resultsWe observed increased expression of ASPN mRNA in a data set derived from benign vs tumour microdissected tissue, and a correlation with biochemical recurrence using Kaplan-Meier and Cox proportional hazard analysis. ASPN protein localised to tumour stroma and elevated expression of ASPN was correlated with decreased time to biochemical recurrence, in a cohort of 326 patients with a median follow up of 9.6 years. Univariate and multivariate analysis demonstrated that ASPN was correlated with progression, as were Gleason score, and clinical stage. Additionally, ASPN expression correlated with the presence of reactive stroma, suggesting that it may be a stromal marker expressed in response to the presence of tumour cells and particularly with aggressive tumour subtypes. We observed expression of ASPN in the stroma of tumours induced by p53 inhibition in a mouse model of prostate cancer, and correlation with neuroendocrine marker expression. Finally, we demonstrated that ASPN transcript expression in normal and cancer fibroblasts was regulated by conditioned media derived from the PC3, but not LNCaP, prostate cancer cell lines.

conclusionsOur results suggest that ASPN is a stromally expressed biomarker that correlates with disease progression, and is observed in reactive stroma. ASPN expression in stroma may be part of a stromal response to aggressive tumour subtypes.

Indexed as

AdultAgedAnimalsBiomarkers, TumorCells, CulturedCohort StudiesCulture Media, ConditionedExtracellular Matrix ProteinsFetusFibroblastsFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesMaleMiceASPN protein, humanBiomarkers, TumorCulture Media, ConditionedExtracellular Matrix ProteinsRetinoblastoma ProteinRNA, MessengerTumor Suppressor Protein p53

Identifiers

PMID28152543
PMCPMC5355923
OpenAlexW2585568219

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.