Evidence map›Paper›PMID 26954716›Full record

ArticleBritish journal of cancer2016

MYC functions are specific in biological subtypes of breast cancer and confers resistance to endocrine therapy in luminal tumours.

Andrew R Green, Mohammed A Aleskandarany, Devika Agarwal, Somaia Elsheikh, Christopher C Nolan, Maria Diez-Rodriguez, R Douglas Macmillan, Graham R Ball, Carlos Caldas, Srinivasan Madhusudan and 2 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

81 citing papers in PubMed, 124 citations in OpenAlex.

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  16. Medulloblastoma: biology and immunotherapy.Frontiers in immunology · 2025
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21 more citing papers are in PubMed but not listed here.

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

12 authors at 5 institutions in 1 country.

Andrew R GreenDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Mohammed A AleskandaranyCellular Pathology, Nottingham University Hospitals NHS Trust, Hucknall Road, Nottingham NG5 1PB, UK.
Devika AgarwalSchool of Science and Technology, Nottingham Trent University, Nottingham NG11 8NS, UK.
Somaia ElsheikhDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Christopher C NolanDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Maria Diez-RodriguezDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
R Douglas MacmillanBreast Institute, Nottingham University Hospitals NHS Trust, Hucknall Road, Nottingham NG5 1PB, UK.
Graham R BallSchool of Science and Technology, Nottingham Trent University, Nottingham NG11 8NS, UK.
Carlos CaldasCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE.
Srinivasan MadhusudanDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Ian O EllisDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Emad A RakhaDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Nottingham City Hospital · GBNottingham University Hospitals NHS Trust · GBUniversity of Nottingham · GBNottingham Trent University · GBUniversity of Cambridge · GB

Funding

Cancer Research UK 16942Cancer Research UK 9675
6 · The paper itself

Abstract

backgroundMYC is amplified in approximately 15% of breast cancers (BCs) and is associated with poor outcome. c-MYC protein is multi-faceted and participates in many aspects of cellular function and is linked with therapeutic response in BCs. We hypothesised that the functional role of c-MYC differs between molecular subtypes of BCs.

methodsWe therefore investigated the correlation between c-MYC protein expression and other proteins involved in different cellular functions together with clinicopathological parameters, patients' outcome and treatments in a large early-stage molecularly characterised series of primary invasive BCs (n=1106) using immunohistochemistry. The METABRIC BC cohort (n=1980) was evaluated for MYC mRNA expression and a systems biology approach utilised to identify genes associated with MYC in the different BC molecular subtypes.

resultsHigh MYC and c-MYC expression was significantly associated with poor prognostic factors, including grade and basal-like BCs. In luminal A tumours, c-MYC was associated with ATM (P=0.005), Cyclin B1 (P=0.002), PIK3CA (P=0.009) and Ki67 (P<0.001). In contrast, in basal-like tumours, c-MYC showed positive association with Cyclin E (P=0.003) and p16 (P=0.042) expression only. c-MYC was an independent predictor of a shorter distant metastases-free survival in luminal A LN+ tumours treated with endocrine therapy (ET; P=0.013). In luminal tumours treated with ET, MYC mRNA expression was associated with BC-specific survival (P=0.001). In ER-positive tumours, MYC was associated with expression of translational genes while in ER-negative tumours it was associated with upregulation of glucose metabolism genes.

conclusionsc-MYC function is associated with specific molecular subtypes of BCs and its overexpression confers resistance to ET. The diverse mechanisms of c-MYC function in the different molecular classes of BCs warrants further investigation particularly as potential therapeutic targets.

Indexed as

AgedAtaxia Telangiectasia Mutated ProteinsBiomarkers, TumorBreast NeoplasmsClass I Phosphatidylinositol 3-KinasesCyclin B1Cyclin EDisease-Free SurvivalDrug Resistance, NeoplasmEndocrine CellsErb-b2 Receptor Tyrosine KinasesFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesAtaxia Telangiectasia Mutated ProteinsBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesCyclin B1Cyclin EErb-b2 Receptor Tyrosine KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-mycRNA, Messenger

Identifiers

PMID26954716
PMCPMC4984797
OpenAlexW2296031005

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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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.