Evidence map›Paper›PMID 28320414›Full record

ArticleJournal of translational medicine2017

Epidermal growth factor receptor and epididymis invasion as prognostic biomarkers in clinical stage I testicular germ cell tumours.

Miguel F Sanmamed, E Esteban, E Uriol, R Zarate, M Capelan, C Muriel, G Crespo, J P Berros, P Pardo-Coto, Q Perez and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

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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

14 authors at 6 institutions in 3 countries.

Miguel F SanmamedDepartment of Immunobiology, School of Medicine, Yale University, 300 George Street, Suite 203A, New Haven, CT, 06511, USA. miguel.sanmamed@yale.edu.ORCID 0000-0002-7295-6074
E EstebanDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
E UriolDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
R ZarateClinical Genetics Unit, Clínica Universidad de Navarra, Pamplona, Spain.
M CapelanBreast Unit, Royal Marsden NHS Foundation Trust, London, UK.
C MurielDepartment of Medical Oncology, Hospital Regional Universitario Carlos Haya, Málaga, Spain.
G CrespoDepartment of Medical Oncology, Hospital Universitario de Burgos, Burgos, Spain.
J P BerrosDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
P Pardo-CotoDepartment of Medical Oncology, Centro Médico de Asturias, Oviedo, Spain.
Q PerezDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
C Alvarez-FernándezDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
P Jiménez FonsecaDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
M LuqueDepartment of Medical Oncology, Hospital Universitario Central de Asturias, Oviedo, Spain.
A AstudilloDepartment of Pathology, Hospital Universitario Central de Asturias, Oviedo, Spain.
Hospital Universitario Central de Asturias · ESClinica Universidad de Navarra · ESHospital Regional Universitario de Málaga · ESHospital Universitario de Burgos · ESRoyal Marsden NHS Foundation Trust · GBYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInguinal orchiectomy is curative in 70-80% of clinical stage I testicular germ cell tumours (CS I TGCT). The identification of patients who are at low risk of relapse is critical to avoid unnecessary treatment. The aim of this study is to explore EGFR, hMLH-1/hMSH-2 and microsatellite instability (MSI) as potential prognostic factors of recurrence in CS I TGCT.

methodsFifty-six CS I TGCT patients who underwent inguinal orchiectomy were included in this study. We analysed the relationship between clinicopathological and molecular factors with survival. Analysis of hMLH1, hMSH2 and EGFR expression was carried out by immunohistochemistry. Methylation status of the hMLH1 promoter was determined by pyrosequencing analysis in selected cases. EGFR exons 19, 20, 21 were analysed by PCR labeled-fragments and MSI status was determined using standard Multiplex MSI assays.

resultsClassical pathological factors such as lymphovascular invasion, high percentage of embryonal carcinoma, rete testis invasion or tumour size ≥4 cm showed a significant relationship with a higher risk of relapse. Additionally, it was found that an epididymis invasion proved to be a significant independent poor prognostic factor of recurrence (p = 0.001). hMLH1 or hMSH2 expression showed no significant association with risk of relapse and no MSI was found. EGFR expression was observed in 30.4% of samples and its expression was associated with higher risk of relapse (HR 3.5; 95% CI 1.3-9.8; p = 0.016). None of the cases presented EGFR kinase domain mutations.

conclusionsEpididymis invasion and EGFR expression, but not hMLH-1/hMSH-2 or MSI, could be potentially useful as new prognostic factors of recurrence for CS I TGCT.

Indexed as

AdultBiomarkers, TumorDemographyDisease-Free SurvivalDNA MethylationEpididymisErbB ReceptorsExonsGenome, HumanHumansImmunohistochemistryKaplan-Meier EstimateMaleMicrosatellite InstabilityMutL Protein Homolog 1MutS Homolog 2 ProteinBiomarkers, TumorEGFR protein, humanErbB ReceptorsMLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutS Homolog 2 ProteinEGFREpididymis invasionhMLH-1hMSH-2MSITesticular germ cell tumour

Identifiers

PMID28320414
PMCPMC5358043
OpenAlexW2602802155

What OpenQuestion holds

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Registered trials

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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.