Evidence map›Paper›PMID 31930327›Full record

ReviewCarcinogenesis2020

The role of B-Cell Lymphoma-3 (BCL-3) in enabling the hallmarks of cancer: implications for the treatment of colorectal carcinogenesis.

Danny N Legge, Adam C Chambers, Christopher T Parker, Penny Timms, Tracey J Collard, Ann C Williams

Abstract readReview
In one paragraph

Review in Carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. A Critical Role of DC-SIGNImmunoTargets and therapy · 2025
    Article
  2. Review
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  16. Review
  17. Ferroptosis-RelatedPharmacogenomics and personalized medicine · 2022
    Article
  18. Article
  19. 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

6 authors.

Danny N LeggeColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.
Adam C ChambersColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.
Christopher T ParkerColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.
Penny TimmsColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.
Tracey J CollardColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.
Ann C WilliamsColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol, UK.

Funding

Medical Research Council MR/N001494/1Medical Research Council MR/R017247/1Wellcome Trust 203988/Z/16Z
6 · The paper itself

Abstract

With its identification as a proto-oncogene in chronic lymphocytic leukaemia and central role in regulating NF-κB signalling, it is perhaps not surprising that there have been an increasing number of studies in recent years investigating the role of BCL-3 (B-Cell Chronic Lymphocytic Leukaemia/Lymphoma-3) in a wide range of human cancers. Importantly, this work has begun to shed light on our mechanistic understanding of the function of BCL-3 in tumour promotion and progression. Here, we summarize the current understanding of BCL-3 function in relation to the characteristics or traits associated with tumourigenesis, termed 'Hallmarks of Cancer'. With the focus on colorectal cancer, a major cause of cancer related mortality in the UK, we describe the evidence that potentially explains why increased BCL-3 expression is associated with poor prognosis in colorectal cancer. As well as promoting tumour cell proliferation, survival, invasion and metastasis, a key emerging function of this proto-oncogene is the regulation of the tumour response to inflammation. We suggest that BCL-3 represents an exciting new route for targeting the Hallmarks of Cancer; in particular by limiting the impact of the enabling hallmarks of tumour promoting inflammation and cell plasticity. As BCL-3 has been reported to promote the stem-like potential of cancer cells, we suggest that targeting BCL-3 could increase the tumour response to conventional treatment, reduce the chance of relapse and hence improve the prognosis for cancer patients.

Indexed as

B-Cell Lymphoma 3 ProteinCarcinogenesisCell ProliferationColorectal NeoplasmsGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasm Recurrence, LocalNeoplastic Stem CellsNF-kappa BPrognosisProto-Oncogene MasSignal TransductionB-Cell Lymphoma 3 ProteinBCL3 protein, humanMAS1 protein, humanNF-kappa BProto-Oncogene Mas

Identifiers

PMID31930327
PMCPMC7221501

What OpenQuestion holds

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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.