Evidence map›Paper›PMID 38519644›Full record

ArticleNPJ precision oncology2024

Identification of potentially actionable genetic variants in epithelial ovarian cancer: a retrospective cohort study.

Charlotte Fieuws, Joni Van der Meulen, Kristiaan Proesmans, Emiel A De Jaeghere, Siebe Loontiens, Jo Van Dorpe, Philippe Tummers, Hannelore Denys, Koen Van de Vijver, Kathleen B M Claes

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. High Frequency ofCancers · 2025
    Article
  3. 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

10 authors at 2 institutions in 1 country.

Charlotte FieuwsDepartment of Biomolecular Medicine, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-1567-2075
Joni Van der MeulenDepartment of Biomolecular Medicine, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-1916-2769
Kristiaan ProesmansDepartment of Bio-Analysis, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-7787-9397
Emiel A De JaeghereCancer Research Institute Ghent, Ghent, Belgium.
Siebe LoontiensDepartment of Biomolecular Medicine, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-4602-4580
Jo Van DorpeCancer Research Institute Ghent, Ghent, Belgium.ORCID http://orcid.org/0000-0001-8175-2930
Philippe TummersDepartment of Medical Oncology, Ghent University Hospital, Ghent, Belgium.
Hannelore DenysCancer Research Institute Ghent, Ghent, Belgium.ORCID http://orcid.org/0000-0002-8897-9430
Koen Van de VijverCancer Research Institute Ghent, Ghent, Belgium.
Kathleen B M ClaesDepartment of Biomolecular Medicine, Ghent University, Ghent, Belgium. kathleen.claes@ugent.be.ORCID http://orcid.org/0000-0003-0841-7372
Ghent University Hospital · BEGhent University · BE

Funding

Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 1S73622N
6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecologic malignancy, mainly due to late-stage diagnosis, frequent recurrences, and eventually therapy resistance. To identify potentially actionable genetic variants, sequencing data of 351 Belgian ovarian cancer patients were retrospectively captured from electronic health records. The cohort included 286 (81%) patients with high-grade serous ovarian cancer, 17 (5%) with low-grade serous ovarian cancer, and 48 (14%) with other histotypes. Firstly, an overview of the prevalence and spectrum of the BRCA1/2 variants highlighted germline variants in 4% (11/250) and somatic variants in 11% (37/348) of patients. Secondly, application of a multi-gene panel in 168 tumors revealed a total of 214 variants in 28 genes beyond BRCA1/2 with a median of 1 (IQR, 1-2) genetic variant per patient. The ten most often altered genes were (in descending order): TP53, BRCA1, PIK3CA, BRCA2, KRAS, ERBB2 (HER2), TERT promotor, RB1, PIK3R1 and PTEN. Of note, the genetic landscape vastly differed between the studied histotypes. Finally, using ESCAT the clinical evidence of utility for every genetic variant was scored. Only BRCA1/2 pathogenic variants were classified as tier-I. Nearly all patients (151/168; 90%) had an ESCAT tier-II variant, most frequently in TP53 (74%), PIK3CA (9%) and KRAS (7%). In conclusion, our findings imply that although only a small proportion of genetic variants currently have direct impact on ovarian cancer treatment decisions, other variants could help to identify novel (personalized) treatment options to address the poor prognosis of ovarian cancer, particularly in rare histotypes.

Identifiers

PMID38519644
PMCPMC10959961
OpenAlexW4393089398

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.