Evidence map›Paper›PMID 38369570›Full record

ArticleScientific reports2024

Real-time ex vivo monitoring of NK cell migration toward obesity-associated oesophageal adenocarcinoma following modulation of CX3CR1.

Eimear Mylod, Fiona O'Connell, Noel E Donlon, Maria Davern, Caroline Marion, Christine Butler, John V Reynolds, Joanne Lysaght, Melissa J Conroy

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
0.5field-weighted citation impact, top 38% 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, 2 citations in OpenAlex.

  1. Article
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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

9 authors at 2 institutions in 2 countries.

Eimear MylodCancer Immunology Research Group, Department of Anatomy, School of Medicine, Trinity Biomedical Sciences Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland.
Fiona O'ConnellDepartment of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland.
Noel E DonlonCancer Immunology and Immunotherapy Group, Department of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, St. James's Hospital, Trinity College Dublin, Dublin, Ireland.
Maria DavernCancer Immunology and Immunotherapy Group, Department of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, St. James's Hospital, Trinity College Dublin, Dublin, Ireland.
Caroline MarionCancer Immunology Research Group, Department of Anatomy, School of Medicine, Trinity Biomedical Sciences Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland.
Christine ButlerDepartment of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland.
John V ReynoldsDepartment of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland.
Joanne LysaghtCancer Immunology and Immunotherapy Group, Department of Surgery, School of Medicine, Trinity Translational Medicine Institute and Trinity St. James's Cancer Institute, St. James's Hospital, Trinity College Dublin, Dublin, Ireland.
Melissa J ConroyCancer Immunology Research Group, Department of Anatomy, School of Medicine, Trinity Biomedical Sciences Institute and Trinity St. James's Cancer Institute, Trinity College Dublin, Dublin, Ireland. meconroy@tcd.ie.
Trinity College Dublin · IESt. James's Hospital · IE

Funding

Breakthrough Cancer Research BCR-2019-02-PhD-TCDBreakthrough Cancer Research CIRF-2022-01
6 · The paper itself

Abstract

Oesophagogastric adenocarcinomas (OAC) are poor prognosis, obesity-associated cancers which may benefit from natural killer (NK) cell-based immunotherapies. Cellular immunotherapies encounter two key challenges to their success in OAC, namely recruitment to extratumoural tissues such as the omentum at the expense of the tumour and an immunosuppressive tumour microenvironment (TME) which can hamper NK cell function. Herein, we examined approaches to overcome the detrimental impact of obesity on NK cells and NK cell-based immunotherapies. We have demonstrated that NK cells migrate preferentially to the chemotactic signals of OAC patient-derived omentum over tumour in an ex vivo model of immune cell migration. We have identified CX3CR1 modulation and/or tumour chemokine profile remodelling as approaches to skew NK cell migration towards tumour. We also report targetable immunosuppressive facets of the obese OAC TME which dampen NK cell function, in particular cytotoxic capabilities. These data provide insights into approaches to therapeutically overcome key challenges presented by obesity and will inform superior design of NK cell-based immunotherapies for OAC.

Indexed as

AdenocarcinomaEsophageal NeoplasmsCell MovementCX3C Chemokine Receptor 1HumansImmunotherapyKiller Cells, NaturalObesityTumor MicroenvironmentCX3C Chemokine Receptor 1CX3CR1 protein, human

Identifiers

PMID38369570
PMCPMC10874956
OpenAlexW4391915749

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.