Evidence map›Paper›PMID 31906898›Full record

ArticleBMC cancer2020

Increased levels of XPA might be the basis of cisplatin resistance in germ cell tumours.

Zuzana Cierna, Vera Miskovska, Jan Roska, Dana Jurkovicova, Lucia Borszekova Pulzova, Zuzana Sestakova, Lenka Hurbanova, Katarina Machalekova, Michal Chovanec, Katarina Rejlekova and 8 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Response of the Urothelial Carcinoma Cell Lines to Cisplatin.International journal of molecular sciences · 2022
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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

18 authors at 6 institutions in 2 countries.

Zuzana CiernaDepartment of Pathology, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Vera Miskovska1st Department of Oncology, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Jan RoskaDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Dana JurkovicovaDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Lucia Borszekova PulzovaDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Zuzana SestakovaDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Lenka HurbanovaDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Katarina MachalekovaSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Michal Chovanec2nd Department of Oncology, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Katarina RejlekovaSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Daniela SvetlovskaSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Katarina KalavskaSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Karol KajoSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Pavel BabalDepartment of Pathology, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Jozef MardiakSt. Elisabeth Cancer Institute, Bratislava, Slovakia.
Thomas A WardDepartment of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, UK.
Michal MegoDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Miroslav ChovanecDepartment of Genetics, Cancer Research Institute, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Bratislava, Slovakia. miroslav.chovanec@savba.sk.ORCID http://orcid.org/0000-0001-9120-5084
Cancer Research Institute of the Slovak Academy of Sciences · SKVysoká Škola Zdravotníctva a Sociálnej Práce sv. Alžbety · SKNational Institute of Cardiovascular Diseases · SKComenius University Bratislava · SKLancaster University · GBUniversity of Central Europe in Skalica · SK

Funding

Ministry of Health of the Slovak Republic 2019/57-BMCSAV-1Slovak Research and Development Agency APVV-0016-11Slovak Research and Development Agency APVV-15-0086Slovak Research and Development Agency APVV-17-0384VEGA Grant Agency of the Slovak Republic 1/0043/18VEGA Grant Agency of the Slovak Republic 2/0053/19VEGA Grant Agency of the Slovak Republic 2/0108/17
6 · The paper itself

Abstract

backgroundGerm cell tumours (GCTs) represent a highly curable malignity as they respond well to cisplatin (CDDP)-based chemotherapy. Nevertheless, a small proportion of GCT patients relapse or do not respond to therapy. As this might be caused by an increased capacity to repair CDDP-induced DNA damage, identification of DNA repair biomarkers predicting inadequate or aberrant response to CDDP, and thus poor prognosis for GCT patients, poses a challenge. The objective of this study is to examine the expression levels of the key nucleotide excision repair (NER) factors, XPA, ERCC1 and XPF, in GCT patients and cell lines.

methodsTwo hundred seven GCT patients' specimens with sufficient follow-up clinical-pathological data and pairwise combinations of CDDP-resistant and -sensitive GCT cell lines were included. Immunohistochemistry was used to detect the ERCC1, XPF and XPA protein expression levels in GCT patients' specimen and Western blot and qRT-PCR examined the protein and mRNA expression levels in GCT cell lines.

resultsGCT patients with low XPA expression had significantly better overall survival than patients with high expression (hazard ratio = 0.38, 95% confidence interval: 0.12-1.23, p = 0.0228). In addition, XPA expression was increased in the non-seminomatous histological subtype, IGCCCG poor prognosis group, increasing S stage, as well as the presence of lung, liver and non-pulmonary visceral metastases. Importantly, a correlation between inadequate or aberrant CDDP response and XPA expression found in GCT patients was also seen in GCT cell lines.

conclusionsXPA expression is an additional independent prognostic biomarker for stratifying GCT patients, allowing for improvements in decision-making on treatment for those at high risk of refractoriness or relapse. In addition, it could represent a novel therapeutic target in GCTs.

Indexed as

Antineoplastic AgentsBiomarkers, TumorCell Line, TumorCisplatinDNA-Binding ProteinsDNA DamageDNA RepairDrug Resistance, NeoplasmEndonucleasesHumansImmunohistochemistryMaleNeoplasm Recurrence, LocalNeoplasms, Germ Cell and EmbryonalPhosphorylationPrognosisAntineoplastic AgentsBiomarkers, TumorCisplatinDNA-Binding ProteinsEndonucleasesERCC1 protein, humanXeroderma Pigmentosum Group A Proteinxeroderma pigmentosum group F proteinXPA protein, humanDNA repairGerm cell tumoursNucleotide excision repairPrognostic markerXPA

Identifiers

PMID31906898
PMCPMC6945513
OpenAlexW3000707742

What OpenQuestion holds

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LicenceCC BY
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.