Evidence map›Paper›PMID 41702233›Full record

ArticleTranslational oncology2026

Clinicopathological and functional evaluation of replication protein A in epithelial ovarian cancers: A target validation study.

Mashael Algethami, Amera Sheha, Nehal Singhania, Shatha Alqahtani, Ahmed Shoqafi, Çağla Tosun, Jake Spicer, Michael S Toss, Adel Alblihy, Ayat Lashen and 4 more

Abstract read
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In one paragraph

Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mashael AlgethamiNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Sulaiman AlRajhi University, College of Applied Sciences, Department of Medical Laboratory Sciences, Al-Bukayriyah 51941, Qassim, Saudi Arabia.
Amera ShehaNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Histopathology Department, South Egypt Cancer Institute, Assiut University, Assiut, Egypt.
Nehal SinghaniaNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Shatha AlqahtaniNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Ahmed ShoqafiNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Çağla TosunNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Jake SpicerNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Michael S TossDepartment of Pathology, Nottingham University Hospital, City Campus, Hucknall Road, Nottingham NG51PB, UK.
Adel AlblihyNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Medical Center, King Fahad Security College (KFSC), Riyadh 11461, Saudi Arabia.
Ayat LashenNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Jennie N JeyapalanNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Faculty of medicine and Health Sciences, Centre for Cancer Sciences, University of Nottingham, Sutton Bonington Campus, Sutton Bonington, Leicestershire LE12 5RD, UK.
Nigel P MonganNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Faculty of medicine and Health Sciences, Centre for Cancer Sciences, University of Nottingham, Sutton Bonington Campus, Sutton Bonington, Leicestershire LE12 5RD, UK; Department of Pharmacology, Weill Cornell Medicine, NY, NY, 10065, USA.
Emad A RakhaNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Department of Pathology, Nottingham University Hospital, City Campus, Hucknall Road, Nottingham NG51PB, UK.
Srinivasan MadhusudanNaaz-Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK; Department of Oncology, Nottingham University Hospitals, Nottingham NG51PB, UK. Electronic address: srinivasan.madhusudan@nottingham.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replication Protein A (RPA), a single-stranded DNA (ssDNA)-binding protein is critically involved in DNA replication, checkpoint regulation and DNA repair. We evaluated RPA1, 2, and 3 sub-units protein expression in 331 ovarian tumours, transcripts in 1287 tumours and bioinformatics in the ovarian TCGA cohort (n = 379). Platinum resistant ovarian cancer cells were depleted for RPA 1 or 2 and tested for cisplatin, olaparib and talazoparib sensitivity. HAMNO (RPA1 protein-protein interaction inhibitor) was tested in sensitive and resistant cells. High nuclear RPA1 and RPA2 protein was significantly associated with high grade serous ovarian cancers (HGSOC), advanced stage, platinum resistance and worse progression free survival (PFS) (all ps <0.05). High RPA1 and RPA2 transcripts also linked with poor PFS. Preclinically, RPA1 or RPA 2 depletion increased sensitivity to cisplatin, olaparib and talazoparib treatment. HAMNO monotherapy was cytotoxic to sensitive and resistant cells. We conclude that RPA directed precision oncology strategy could be a viable strategy in HGSOC.

Indexed as

HAMNOOlaparibPARP inhibitorPARP inhibitor resistancePlatinum resistanceRPA1RPA2;RPA3Synthetic lethalityTalazoparib

Identifiers

PMID41702233
PMCPMC12925576

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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.