Evidence map›Paper›PMID 37077714›Full record

ArticleMolecular therapy oncolytics2023

Efficacy of coxsackievirus A21 against drug-resistant neoplastic B cells.

Matthew Holmes, Gina B Scott, Samuel Heaton, Tyler Barr, Basem Askar, Louise M E Müller, Victoria A Jennings, Christy Ralph, Cathy Burton, Alan Melcher and 3 more

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

Article in Molecular therapy oncolytics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
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

13 authors at 4 institutions in 1 country.

Matthew HolmesLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Gina B ScottLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Samuel HeatonLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Tyler BarrLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Basem AskarLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Louise M E MüllerLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Victoria A JenningsLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Christy RalphLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Cathy BurtonHaematological Malignancy Diagnostic Service, Leeds Teaching Hospitals, Beckett Street, Leeds LS9 7TF, UK.
Alan MelcherThe Institute of Cancer Research, Division of Radiotherapy and Imaging, Chester Beatty Laboratories, London SW3 6JB, UK.
Peter HillmenLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
Christopher ParrishSt James's University Hospital, Leeds Teaching Hospital, Beckett Street, Leeds LS9 7TF, UK.
Fiona Errington-MaisLeeds Institute of Medical Research, University of Leeds, Beckett Street, Leeds LS9 7TF, UK.
University of Leeds · GBInstitute of Cancer Research · GBLeeds Teaching Hospitals NHS Trust · GBSt James's University Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary drug resistance and minimal residual disease are major challenges in the treatment of B cell neoplasms. Therefore, this study aimed to identify a novel treatment capable of eradicating malignant B cells and drug-resistant disease. Oncolytic viruses eradicate malignant cells by direct oncolysis and activation of anti-tumor immunity, have proven anti-cancer efficacy, and are safe and well tolerated in clinical use. Here, we demonstrate that the oncolytic virus coxsackievirus A21 can kill a range of B cell neoplasms, irrespective of an anti-viral interferon response. Moreover, CVA21 retained its capacity to kill drug-resistant B cell neoplasms, where drug resistance was induced by co-culture with tumor microenvironment support. In some cases, CVA21 efficacy was actually enhanced, in accordance with increased expression of the viral entry receptor ICAM-1. Importantly, the data confirmed preferential killing of malignant B cells and CVA21 dependence on oncogenic B cell signaling pathways. Significantly, CVA21 also activated natural killer (NK) cells to kill neoplastic B cells and drug-resistant B cells remained susceptible to NK cell-mediated lysis. Overall, these data reveal a dual mode of action of CVA21 against drug-resistant B cells and support the development of CVA21 for the treatment of B cell neoplasms.

Indexed as

B cell neoplasmBurkitt lymphomaChronic Lymphocytic Leukemiacoxsackievirus A21Diffuse large B cell lymphomadrug resistanceNon hodgkin lymphomaoncolytic virustumor microenvironment

Identifiers

PMID37077714
PMCPMC10106520
OpenAlexW4360602211

What OpenQuestion holds

Textmetadata
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.