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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
MYC functions are specific in biological subtypes of breast cancer and confers resistance to endocrine therapy in luminal tumours
British Journal of Cancer, Volume 114, No. 8, Year 2016
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Description
Background:MYC 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.Methods:We 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 immunuohistochemistry. 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.Results:High 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.Conclusions:c-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. © 2016 Cancer Research UK.
Authors & Co-Authors
Green, Andew R.
United Kingdom, Nottingham
Nottingham City Hospital
Aleskandarany, Mohammed A.
United Kingdom, Nottingham
Nottingham University Hospitals Nhs Trust
Agarwal, Devika
United Kingdom, Nottingham
Nottingham Trent University
Elsheikh, Somaia Elbauomy
United Kingdom, Nottingham
Nottingham City Hospital
United Kingdom, Nottingham
Nottingham University Hospitals Nhs Trust
Nolan, Christopher C.
United Kingdom, Nottingham
Nottingham City Hospital
Diez-Rodriguez, Maria
United Kingdom, Nottingham
Nottingham City Hospital
MacMillan, Robert Douglas
United Kingdom, Nottingham
Nottingham University Hospitals Nhs Trust
Ball, Graham Roy
United Kingdom, Nottingham
Nottingham Trent University
Caldas, Carlos
United Kingdom, Cambridge
Cancer Research uk Cambridge Institute
Madhusudan, Srinivasan
United Kingdom, Nottingham
Nottingham City Hospital
Ellis, Ian O.
United Kingdom, Nottingham
Nottingham City Hospital
United Kingdom, Nottingham
Nottingham University Hospitals Nhs Trust
Rakha, Emad A.
United Kingdom, Nottingham
Nottingham City Hospital
United Kingdom, Nottingham
Nottingham University Hospitals Nhs Trust
Statistics
Citations: 83
Authors: 12
Affiliations: 4
Identifiers
Doi:
10.1038/bjc.2016.46
ISSN:
00070920
Research Areas
Cancer
Study Design
Cohort Study