About: MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer

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type	http://eprints.org/ontology/ArticleEPrint http://eprints.org/ontology/EPrint Article Academic Article
seeAlso	HTML Summary of #77398 MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer
sameAs	MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer
http://eprints.org/ontology/hasAccepted	MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (PDF)
http://eprints.org/ontology/hasDocument	MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (PDF) MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (Other) MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (Other) MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (Other) MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (Other) MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (Other)
dc:hasVersion	MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer (PDF)
Title	MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer
described by	https://demo.openlinksw.com/about/id/entity/https/www.cs.kent.ac.uk/people/staff/akj22/materials/CO644/export_kar_RDFN3.n3
Date	2018-01-23
Creator	Mohammed A Aleskandarany Ian O. Ellis Kiu Wai Cheng Rokaya El-Ansari Madeleine L Craze Christopher C Nolan Nuno DM Coimbra Maria Diez-Rodriguez Hayley Cheung Natasha Jewa D. Soria Andrew R. Green Emad A Rakha
status	peer reviewed published
Publisher	Nature Publishing Group
abstract	Background: Altered cellular metabolism is a hallmark of cancer and some are reliant on glutamine for sustained proliferation and survival. We hypothesise that the glutamine–proline regulatory axis has a key role in breast cancer (BC) in the highly proliferative classes. Methods: Glutaminase (GLS), pyrroline-5-carboxylate synthetase (ALDH18A1), and pyrroline-5-carboxylate reductase 1 (PYCR1) were assessed at DNA/mRNA/protein levels in large, well-characterised cohorts. Results: Gain of PYCR1 copy number and high PYCR1 mRNA was associated with Luminal B tumours. High ALDH18A1 and high GLS protein expression was observed in the oestrogen receptor (ER)+/human epidermal growth factor receptor (HER2)– high proliferation class (Luminal B) compared with ER+/HER2– low proliferation class (Luminal A) (P=0.030 and P=0.022 respectively), however this was not observed with mRNA. Cluster analysis of the glutamine–proline regulatory axis genes revealed significant associations with molecular subtypes of BC and patient outcome independent of standard clinicopathological parameters (P=0.012). High protein expression of the glutamine–proline enzymes were all associated with high MYC protein in Luminal B tumours only (P<0.001). Conclusions: We provide comprehensive clinical data indicating that the glutamine–proline regulatory axis plays an important role in the aggressive subclass of luminal BC and is therefore a potential therapeutic target.
Is Part Of	British Journal of Cancer https://kar.kent.ac.uk/id/repository
list of authors	https://kar.kent.ac.uk/id/eprint/77398#authors
issue	2
volume	118
is topic of	https://www.cs.kent.ac.uk/people/staff/akj22/materials/CO644/export_kar_RDFN3.n3
is primary topic of	HTML Summary of #77398 MYC regulation of glutamine--proline regulatory axis is key in luminal B breast cancer

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