Evidence map›Paper›PMID 39794353›Full record

ArticleNPJ genomic medicine2025

Assessment of candidate high-grade serous ovarian carcinoma predisposition genes through integrated germline and tumour sequencing.

Deepak N Subramanian, Maia Zethoven, Kathleen I Pishas, Evanny R Marinović, Simone McInerny, Simone M Rowley, Prue E Allan, Lisa Devereux, Dane Cheasley, Paul A James and 1 more

Abstract read
In one paragraph

Article in NPJ genomic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Deepak N SubramanianCancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-0891-9324
Maia ZethovenBioinformatics Core Facility, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Kathleen I PishasCancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Evanny R MarinovićCancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Simone McInernyParkville Familial Cancer Centre, Peter MacCallum Cancer Centre and The Royal Melbourne Hospital, Melbourne, VIC, Australia.
Simone M RowleyCancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Prue E AllanDepartment of Pathology, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Lisa DevereuxSir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0003-2435-5888
Dane CheasleyCancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-1170-4690
Paul A James *Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-4361-4657
Ian G Campbell *Cancer Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia. ian.campbell@petermac.org.ORCID http://orcid.org/0000-0002-7773-4155

Funding

Department of Health | National Health and Medical Research Council (NHMRC) APP1092856Department of Health | National Health and Medical Research Council (NHMRC) GNT1134107National Breast Cancer Foundation (NBCF) IIRS-22-027
6 · The paper itself

Abstract

High-grade serous ovarian carcinoma (HGSOC) has a significant hereditary component, only half of which is explained. Previously, we performed germline exome sequencing on BRCA1 and BRCA2-negative HGSOC patients, revealing three proposed and 43 novel candidate genes enriched with rare loss-of-function variants. For validation, we undertook case-control analyses using genomic data from disease-free controls. This confirms enrichment for nearly all previously identified genes. Additionally, one-hundred-and-eleven HGSOC tumours from variant carriers were sequenced alongside other complementary studies, seeking evidence of biallelic inactivation as supportive evidence. PALB2 and ATM validate as HGSOC predisposition genes, with 6/8 germline carrier tumours exhibiting biallelic inactivation accompanied by characteristic mutational signatures. Among candidate genes, only LLGL2 consistently shows biallelic inactivation and protein expression loss, supporting it as a novel HGSOC susceptibility gene. The remaining candidate genes fail to validate. Integrating case-control analyses with tumour sequencing is thus crucial for accurate gene discovery in familial cancer studies.

Identifiers

PMID39794353
PMCPMC11724014

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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.