Evidence map›Paper›PMID 35798469›Full record

ArticleESMO open2022

ctDNA as a biomarker of progression in oesophageal adenocarcinoma.

V F Bonazzi, L G Aoude, S Brosda, J M Lonie, K Patel, J J Bradford, L T Koufariotis, S Wood, B Mark Smithers, N Waddell and 1 more

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

Article in ESMO open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 3 pooled it
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 3 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

V F BonazziThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia. Electronic address: v.bonazzi@uq.edu.au.
L G AoudeThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia.
S BrosdaThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia.
J M LonieThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia.
K PatelThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia.
J J BradfordThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia.
L T KoufariotisQIMR Berghofer Medical Research Institute, Herston, Australia.
S WoodQIMR Berghofer Medical Research Institute, Herston, Australia.
B Mark SmithersPrincess Alexandra Hospital, Woolloongabba, Australia; Faculty of Medicine, University of Queensland, Herston, Australia.
N WaddellQIMR Berghofer Medical Research Institute, Herston, Australia.
A P BarbourThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Australia; Princess Alexandra Hospital, Woolloongabba, Australia.
The University of Queensland · AUQIMR Berghofer Medical Research Institute · AUPrincess Alexandra Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of oesophageal adenocarcinoma (OAC) is rapidly increasing and despite improvements in treatment, the 5-year survival rate remains poor. Prognostic biomarkers that address the genomic heterogeneity in this highly complex disease will aid the development of precision therapeutics and improve patient survival. The aim of this study was to determine whether circulating tumour DNA (ctDNA) has prognostic significance as a biomarker in OAC patients. PATIENTS AND

methodsWe profiled 209 blood and tumour samples from 57 OAC patients. Using a panel of 77 cancer genes, we sequenced ctDNA in plasma samples (n = 127) which were taken at multiple time points before and after therapy. In parallel, we sequenced matched tumour samples from 39 patients using the same gene panel. To assess whether the ctDNA profile reflected the tumour heterogeneity, we sequenced additional multi-region primary tumour samples in 17 patients. In addition, we analysed whole-genome and whole-exome sequencing data from primary tumours for a subset of 18 patients.

resultsUsing a tumour-agnostic approach, we found that detectable ctDNA variants in post-treatment plasma samples were associated with worse disease-specific survival. To evaluate whether the ctDNA originated from the primary tumour, we carried out a tumour-informed analysis which confirmed post-treatment ctDNA variants were associated with worse survival. To determine whether ctDNA could be used as a clinical follow-up test, we assessed blood samples from multiple time points before and after treatment, in a subset of patients. Results showed that the variant allele frequency of ctDNA variants increased with disease recurrence.

conclusionThis study demonstrates that ctDNA variants can be detected in patients with OAC and this has potential clinical utility as a prognostic biomarker for survival.

Indexed as

AdenocarcinomaCirculating Tumor DNAEsophageal NeoplasmsBiomarkers, TumorHumansMutationBiomarkers, TumorCirculating Tumor DNAbiomarkerctDNAoesophageal adenocarcinomaprognosticsequencingsurvival

Identifiers

PMID35798469
PMCPMC9271467
OpenAlexW4220989359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.