Evidence map›Paper›PMID 39115191›Full record

ArticleMolecular oncology2024

Cell-free DNA from ascites identifies clinically relevant variants and tumour evolution in patients with advanced ovarian cancer.

Bonnita Werner, Elyse Powell, Jennifer Duggan, Marilisa Cortesi, Yeh Chen Lee, Vivek Arora, Ramanand Athavale, Michael Dean, Kristina Warton, Caroline E Ford

Abstract read
In one paragraph

Article in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
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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

10 authors.

Bonnita WernerGynaecological Cancer Research Group, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.ORCID 0000-0001-5208-1613
Elyse PowellGynaecological Cancer Research Group, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.
Jennifer DugganGynaecological Oncology Department, Royal Hospital for Women, Sydney, Australia.
Marilisa CortesiGynaecological Cancer Research Group, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.
Yeh Chen LeeGynaecological Oncology Department, Royal Hospital for Women, Sydney, Australia.
Vivek AroraSchool of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.
Ramanand AthavaleGynaecological Oncology Department, Royal Hospital for Women, Sydney, Australia.
Michael DeanLaboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.ORCID 0000-0003-2234-0631
Kristina WartonGynaecological Cancer Research Group, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.
Caroline E FordGynaecological Cancer Research Group, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.ORCID 0000-0002-4438-2309

Funding

Australian Academy of ScienceNIH
6 · The paper itself

Abstract

The emergence of targeted therapies has transformed ovarian cancer treatment. However, biomarker profiling for precision medicine is limited by access to quality, tumour-enriched tissue samples. The use of cell-free DNA (cfDNA) in ascites presents a potential solution to this challenge. In this study, next-generation sequencing was performed on ascites-derived cfDNA samples (26 samples from 15 human participants with ovarian cancer), with matched DNA from ascites-derived tumour cells (n = 5) and archived formalin-fixed paraffin-embedded (FFPE) tissue (n = 5). Similar tumour purity and variant detection were achieved with cfDNA compared to FFPE and ascites cell DNA. Analysis of large-scale genomic alterations, loss of heterozygosity and tumour mutation burden identified six cases of high genomic instability (including four with pathogenic BRCA1 and BRCA2 mutations). Copy number profiles and subclone prevalence changed between sequential ascites samples, particularly in a case where deletions and chromothripsis in Chr17p13.1 and Chr8q resulted in changes in clinically relevant TP53 and MYC variants over time. Ascites cfDNA identified clinically actionable information, concordant to tissue biopsies, enabling opportunistic molecular profiling. This advocates for analysis of ascites cfDNA in lieu of accessing tumour tissue via biopsy.

Indexed as

AscitesCell-Free Nucleic AcidsOvarian NeoplasmsAgedBiomarkers, TumorDNA Copy Number VariationsFemaleHigh-Throughput Nucleotide SequencingHumansLoss of HeterozygosityMiddle AgedMutationBiomarkers, TumorCell-Free Nucleic Acidsascitesbiomarkerscell‐free DNAhomologous recombination deficiencyovarian cancerprecision medicine

Identifiers

PMID39115191
PMCPMC11547227

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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.