Evidence map›Paper›PMID 38195591›Full record

ReviewMolecular cancer2024

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age.

Gillian Seaton, Hannah Smith, Andrea Brancale, Andrew D Westwell, Richard Clarkson

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Gillian SeatonEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ, UK.
Hannah SmithEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ, UK.
Andrea BrancaleUCT Prague, Technická 5, 166 28, 6 - Dejvice, IČO: 60461337, Prague, Czech Republic.
Andrew D WestwellCardiff University School of Pharmacy and Pharmaceutical Sciences, Redwood Building, King Edward VII Avenue, Cardiff, CF10 3NB, UK.
Richard ClarksonEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ, UK. clarksonr@cf.ac.uk.
Cardiff University · GBUniversity of Chemistry and Technology, Prague · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the early 1990's a group of unrelated genes were identified from the sites of recurring translocations in B-cell lymphomas. Despite sharing the nomenclature 'Bcl', and an association with blood-borne cancer, these genes have unrelated functions. Of these genes, BCL2 is best known as a key cancer target involved in the regulation of caspases and other cell viability mechanisms. BCL3 on the other hand was originally identified as a non-canonical regulator of NF-kB transcription factor pathways - a signaling mechanism associated with important cell outcomes including many of the hallmarks of cancer. Most of the early investigations into BCL3 function have since focused on its role in NF-kB mediated cell proliferation, inflammation/immunity and cancer. However, recent evidence is coming to light that this protein directly interacts with and modulates a number of other signaling pathways including DNA damage repair, WNT/β-catenin, AKT, TGFβ/SMAD3 and STAT3 - all of which have key roles in cancer development, metastatic progression and treatment of solid tumours. Here we review the direct evidence demonstrating BCL3's central role in a transcriptional network of signaling pathways that modulate cancer biology and treatment response in a range of solid tumour types and propose common mechanisms of action of BCL3 which may be exploited in the future to target its oncogenic effects for patient benefit.

Indexed as

Hematologic NeoplasmsNF-kappa BCell ProliferationHumansNeoplasm Recurrence, LocalProto-OncogenesNF-kappa BBCL3C-MycHallmarksNF-kappaBSMAD3STAT3Targeted therapyTranscriptionWNT

Identifiers

PMID38195591
PMCPMC10775530
OpenAlexW4390726158

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.