Evidence map›Paper›PMID 26943587›Full record

ArticleOncotarget2016

A BRCA1 deficient, NFκB driven immune signal predicts good outcome in triple negative breast cancer.

Niamh E Buckley, Paula Haddock, Ricardo De Matos Simoes, Eileen Parkes, Gareth Irwin, Frank Emmert-Streib, Stephen McQuaid, Richard Kennedy, Paul Mullan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 34 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

9 authors at 1 institution in 1 country.

Niamh E BuckleyCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Paula HaddockCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Ricardo De Matos SimoesCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Eileen ParkesCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Gareth IrwinCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Frank Emmert-StreibCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Stephen McQuaidCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Richard KennedyCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Paul MullanCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.
Queen's University Belfast · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple negative (TNBCs) and the closely related Basal-like (BLBCs) breast cancers are a loosely defined collection of cancers with poor clinical outcomes. Both show strong similarities with BRCA1-mutant breast cancers and BRCA1 dysfunction, or 'BRCAness', is observed in a large proportion of sporadic BLBCs. BRCA1 expression and function has been shown in vitro to modulate responses to radiation and chemotherapy. Exploitation of this knowledge in the treatment of BRCA1-mutant patients has had varying degrees of success. This reflects the significant problem of accurately detecting those patients with BRCA1 dysfunction. Moreover, not all BRCA1 mutations/loss of function result in the same histology/pathology or indeed have similar effects in modulating therapeutic responses. Given the poor clinical outcomes and lack of targeted therapy for these subtypes, a better understanding of the biology underlying these diseases is required in order to develop novel therapeutic strategies.We have discovered a consistent NFκB hyperactivity associated with BRCA1 dysfunction as a consequence of increased Reactive Oxygen Species (ROS). This biology is found in a subset of BRCA1-mutant and triple negative breast cancer cases and confers good outcome. The increased NFκB signalling results in an anti-tumour microenvironment which may allow CD8+ cytotoxic T cells to suppress tumour progression. However, tumours lacking this NFκB-driven biology have a more tumour-promoting environment and so are associated with poorer prognosis. Tumour-derived gene expression data and cell line models imply that these tumours may benefit from alternative treatment strategies such as reprogramming the microenvironment and targeting the IGF and AR signalling pathways.

Indexed as

Signal TransductionAdultBRCA1 ProteinCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMiddle AgedMutationNF-kappa BOutcome Assessment, Health CarePrognosisReactive Oxygen SpeciesTriple Negative Breast NeoplasmsBRCA1 ProteinBRCA1 protein, humanNF-kappa BReactive Oxygen SpeciesBRCA1microenvironmentNFkBpredictive biomarkertriple negative breast cancer

Identifiers

PMID26943587
PMCPMC4991425
OpenAlexW2289044916

What OpenQuestion holds

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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.