Evidence map›Paper›PMID 42277179›Full record

ArticleOncogene2026

Mes/Stem-A ovarian cancer subtypes predict sensitivity to ATR inhibition.

Vignesh Sundararajan, Fang Ziyu, Gamal Ahmed Elfar, Tuan Zea Tan, Kuee Theng Kuay, Agnes Tan, Clemence Lai, Antje Margret Wengner, Huynh The Hung, Maili Qi and 3 more

Abstract read
In one paragraph

Article in Oncogene, 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

13 authors.

Vignesh SundararajanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0002-3982-3026
Fang ZiyuInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore.
Gamal Ahmed ElfarInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore.
Tuan Zea TanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0001-6624-1593
Kuee Theng KuayCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Agnes TanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Clemence LaiCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Antje Margret WengnerBayer AG, Pharmaceuticals, Berlin, Germany.
Huynh The HungLaboratory of Molecular Endocrinology, National Cancer Centre Singapore, Singapore, Singapore.
Maili QiDepartment of Gynecology Oncology, Singapore, Singapore.
Wen Yee ChayDivision of Medical Oncology, National Cancer Centre Singapore, Singapore, Singapore.
Chit Fang CheokInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore.
David Shao Peng TanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore. david_sp_tan@nuhs.edu.sg.ORCID http://orcid.org/0000-0001-9087-5262

Funding

MOH | National Medical Research Council (NMRC) CSASI21jun-0003National University Cancer Institute, Singapore (NCIS) NR22NMR112OM
6 · The paper itself

Abstract

High-grade serous ovarian cancer (HGSOC) remains one of the most common and lethal gynecological malignancies. Distinct gene expression molecular subtypes (GEMS) of HGSOC, with associated differences in outcome, have previously been described: Epithelial-A (Epi-A)/C3/Differentiated, Epithelial-B (Epi-B)/C2/Immunoreactive, Stem-like B (Stem-B)/C6, Mesenchymal (Mes)/C1, and Stem-like A (Stem-A)/C5/Proliferative. Notably, the Mes and Stem-A OC subtypes are associated with more advanced-stage tumors and poorer clinical outcomes, representing a molecular subtype of unmet clinical need. Hallmarks of HGSOC also include a high prevalence of genomic instability and increased replication stress. In this study, we demonstrate that HGSOC Mes/Stem-A (MSA) cell lines exhibit elevated levels of replication stress and increased sensitivity to ATR inhibitors. Additionally, through DNA fiber analysis, we observed significantly higher replication fork rates and ssDNA accumulation in MSA subtype cells. Consistent with the high levels of replication stress identified in these subtypes, MSA patient-derived xenograft models further validated the therapeutic vulnerability to ATR inhibition. The characteristic replication stress profile of the MSA subtype suggests its utility as a candidate biomarker for identifying patients most likely to benefit from ATR inhibition.

Indexed as

Ataxia Telangiectasia Mutated ProteinsOvarian NeoplasmsAnimalsCell Line, TumorDNA ReplicationFemaleGene Expression Regulation, NeoplasticHumansMiceNeoplastic Stem CellsXenograft Model Antitumor AssaysAtaxia Telangiectasia Mutated ProteinsATR protein, human

Identifiers

PMID42277179
PMCPMC13337489

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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.