Evidence map›Paper›PMID 39020404›Full record

ArticleGenome medicine2024

Spatial intra-tumour heterogeneity and treatment-induced genomic evolution in oesophageal adenocarcinoma: implications for prognosis and therapy.

Sandra Brosda, Lauren G Aoude, Vanessa F Bonazzi, Kalpana Patel, James M Lonie, Clemence J Belle, Felicity Newell, Lambros T Koufariotis, Venkateswar Addala, Marjan M Naeini and 5 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Genome medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
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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

15 authors.

Sandra BrosdaFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia. s.brosda@uq.edu.au.ORCID 0000-0002-0867-6166
Lauren G AoudeFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Vanessa F BonazziFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Kalpana PatelFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
James M LonieFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Clemence J BelleFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Felicity NewellQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Lambros T KoufariotisQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Venkateswar AddalaQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Marjan M NaeiniQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
AGITG DOCTOR Investigators
John V PearsonQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Lutz KrauseFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Nicola WaddellQIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Andrew P BarbourFrazer Institute, The University of Queensland, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.

Funding

Cancer Australia APP2010313Cancer Australia APP2012395Cure Cancer Australia Foundation CCAF2023-AoudeMetro South Health Research Support Scheme RSS_2022_039National Health and Medical Research Council APP1139071National Health and Medical Research Council APP2018244PA Research Foundation RSS_2020_040Royal Australasian College of Surgeons Mitchell Crouch FellowshipThe University of Queensland Philip Walker Surgery Research Scholarship
6 · The paper itself

Abstract

backgroundOesophageal adenocarcinoma (OAC) is a highly heterogeneous cancer with poor survival. Standard curative treatment is chemotherapy with or without radiotherapy followed by oesophagectomy. Genomic heterogeneity is a feature of OAC and has been linked to treatment resistance.

methodsWhole-genome sequencing data from 59 treatment-naïve and 18 post-treatment samples from 29 OAC patients was analysed. Twenty-seven of these were enrolled in the DOCTOR trial, sponsored by the Australasian Gastro-Intestinal Trials Group. Two biopsies from each treatment-naïve tumour were assessed to define 'shared' (between both samples) and 'private' (present in one sample) mutations.

resultsMutational signatures SBS2/13 (APOBEC) and SBS3 (BRCA) were almost exclusively detected in private mutation populations of treatment-naïve tumours. Patients presenting these signatures had significantly worse disease specific survival. Furthermore, mutational signatures associated with platinum-based chemotherapy treatment as well as high platinum enrichment scores were only detected in post-treatment samples. Additionally, clones with high putative neoantigen binding scores were detected in some treatment-naïve samples suggesting immunoediting of clones.

conclusionsThis study demonstrates the high intra-tumour heterogeneity in OAC, as well as indicators for treatment-induced changes during tumour evolution. Intra-tumour heterogeneity remains a problem for successful treatment strategies in OAC.

Indexed as

AdenocarcinomaEsophageal NeoplasmsMutationAgedEvolution, MolecularFemaleGenetic HeterogeneityGenomicsHumansMaleMiddle AgedPrognosisWhole Genome SequencingGeneticsOesophageal adenocarcinomaTreatment impactTumour evolutionWhole-genome sequencing

Identifiers

PMID39020404
PMCPMC11253399

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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.