Evidence map›Paper›PMID 38604503›Full record

ArticleMolecular & cellular proteomics : MCP2024

Multi-Omic Analysis of Esophageal Adenocarcinoma Uncovers Candidate Therapeutic Targets and Cancer-Selective Posttranscriptional Regulation.

J Robert O'Neill, Marcos Yébenes Mayordomo, Goran Mitulović, Sofian Al Shboul, Georges Bedran, Jakub Faktor, Lenka Hernychova, Lukas Uhrik, Maria Gómez-Herranz, Mikołaj Kocikowski and 6 more

Open access · goldAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 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
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Human miRNAs in Cancer: Statistical Trends and Cross Kingdom Approach.International journal of molecular sciences · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. 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

16 authors at 6 institutions in 5 countries.

J Robert O'NeillCambridge Oesophagogastric Centre, Addenbrooke's Hospital, Cambridge, United Kingdom; Institute of Genetics and Cancer (IGC), University of Edinburgh, Edinburgh, Scotland. Electronic address: robertoneill@nhs.net.
Marcos Yébenes MayordomoInstitute of Genetics and Cancer (IGC), University of Edinburgh, Edinburgh, Scotland; International Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland. Electronic address: marcos.yebenes@gmail.com.
Goran MitulovićClinical Department of Laboratory Medicine Proteomics Core Facility, Medical University Vienna, Vienna, Austria; Bruker Austria, Wien, Austria.
Sofian Al ShboulDepartment of Pharmacology and Public Health, Faculty of Medicine, The Hashemite University, Zarqa, Jordan.
Georges BedranInternational Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland.
Jakub FaktorInternational Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland.
Lenka HernychovaResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Lukas UhrikResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Maria Gómez-HerranzInternational Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland.
Mikołaj KocikowskiInternational Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland.
Vicki SaveDepartment of Pathology, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom.
Bořivoj VojtěšekResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Mark J ArendsEdinburgh Pathology, Institute of Genetics and Cancer (IGC), University of Edinburgh, Edinburgh, Scotland.
OCCAMS Consortium
Ted HuppInstitute of Genetics and Cancer (IGC), University of Edinburgh, Edinburgh, Scotland; International Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland.
Javier Antonio AlfaroInternational Center for Cancer Vaccine Science (ICCVS), University of Gdansk, Gdansk, Poland; Institute for Adaptive and Neural Computation, School of Informatics, University of Edinburgh, Edinburgh, UK; International Centre for Cancer Vaccine Science, University of Gdańsk, Gdańsk, Poland; Department of Biochemistry and Microbiology, University of Victoria, Victoria, Canada; The Canadian Association for Responsible AI in Medicine, Victoria, BC, Canada. Electronic address: Javier.alfaro@proteogenomics.ca.
University of Gdańsk · PLEdinburgh Cancer Research · GBMasaryk Memorial Cancer Institute · CZEdinburgh Royal Infirmary · GBHashemite University · JOMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Efforts to address the poor prognosis associated with esophageal adenocarcinoma (EAC) have been hampered by a lack of biomarkers to identify early disease and therapeutic targets. Despite extensive efforts to understand the somatic mutations associated with EAC over the past decade, a gap remains in understanding how the atlas of genomic aberrations in this cancer impacts the proteome and which somatic variants are of importance for the disease phenotype. We performed a quantitative proteomic analysis of 23 EACs and matched adjacent normal esophageal and gastric tissues. We explored the correlation of transcript and protein abundance using tissue-matched RNA-seq and proteomic data from seven patients and further integrated these data with a cohort of EAC RNA-seq data (n = 264 patients), EAC whole-genome sequencing (n = 454 patients), and external published datasets. We quantified protein expression from 5879 genes in EAC and patient-matched normal tissues. Several biomarker candidates with EAC-selective expression were identified, including the transmembrane protein GPA33. We further verified the EAC-enriched expression of GPA33 in an external cohort of 115 patients and confirm this as an attractive diagnostic and therapeutic target. To further extend the insights gained from our proteomic data, an integrated analysis of protein and RNA expression in EAC and normal tissues revealed several genes with poorly correlated protein and RNA abundance, suggesting posttranscriptional regulation of protein expression. These outlier genes, including SLC25A30, TAOK2, and AGMAT, only rarely demonstrated somatic mutation, suggesting post-transcriptional drivers for this EAC-specific phenotype. AGMAT was demonstrated to be overexpressed at the protein level in EAC compared to adjacent normal tissues with an EAC-selective, post-transcriptional mechanism of regulation of protein abundance proposed. Integrated analysis of proteome, transcriptome, and genome in EAC has revealed several genes with tumor-selective, posttranscriptional regulation of protein expression, which may be an exploitable vulnerability.

Indexed as

AdenocarcinomaBiomarkers, TumorEsophageal NeoplasmsGene Expression Regulation, NeoplasticProteomicsFemaleHumansMaleMultiomicsProteomeRNA Processing, Post-TranscriptionalBiomarkers, TumorProteomebiomarkeresophageal adenocarcinomamultiomicsproteogenomicsproteomics

Identifiers

PMID38604503
PMCPMC11245951
OpenAlexW4394600866

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.