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dc.contributor.authorSivalingam, Vanitha
dc.contributor.authorMcVey, R
dc.contributor.authorGilmour, K
dc.contributor.authorAli, S
dc.contributor.authorRoberts, C
dc.contributor.authorRenehan, Andrew G
dc.contributor.authorKitchener, Henry C
dc.contributor.authorCrosbie, Emma J
dc.date.accessioned2015-09-17T11:09:57Zen
dc.date.available2015-09-17T11:09:57Zen
dc.date.issued2015-02-26en
dc.identifier.citationA presurgical window-of-opportunity study of metformin in obesity-driven endometrial cancer. 2015, 385 Suppl 1:S90 Lanceten
dc.identifier.issn1474-547Xen
dc.identifier.pmid26312913en
dc.identifier.doi10.1016/S0140-6736(15)60405-6en
dc.identifier.urihttp://hdl.handle.net/10541/577426en
dc.description.abstractMetformin use is associated with reduced cancer risk in several observational studies of patients with type 2 diabetes. Results from preclinical studies in endometrial cancer show that metformin reduces cellular proliferation by inhibition of the PI3K-AKT-mTOR pathway. We tested the hypothesis that metformin would reduce cellular proliferation in vivo in atypical endometrial hyperplasia and endometrial endometrioid adenocarcinoma.
dc.language.isoenen
dc.rightsArchived with thanks to Lancet (London, England)en
dc.titleA presurgical window-of-opportunity study of metformin in obesity-driven endometrial cancer.en
dc.typeArticleen
dc.contributor.departmentInstitute of Cancer Sciences, University of Manchester, Manchester, UKen
dc.identifier.journalLanceten
html.description.abstractMetformin use is associated with reduced cancer risk in several observational studies of patients with type 2 diabetes. Results from preclinical studies in endometrial cancer show that metformin reduces cellular proliferation by inhibition of the PI3K-AKT-mTOR pathway. We tested the hypothesis that metformin would reduce cellular proliferation in vivo in atypical endometrial hyperplasia and endometrial endometrioid adenocarcinoma.


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