Basetti Madhu1, Kenneth P. Olive2, Mae A. Goldgraben2, David A. Tuveson3, John R. Griffiths1
1Molecular Imaging, Cancer Research UK Cambridge Research Institute, Cambridge, England, UK; 2Tumour Modelling & Experimental Medicine , Cancer Research UK Cambridge Research Institute, Cambridge, England, UK; 3Tumour Modelling & Experimental Medicine, Cancer Research UK Cambridge Research Institute, Cambridge, England, UK
Pancreatic ductal adenocarcinoma (PDA) is profoundly insensitive to treatment with a broad variety of chemotherapeutic regimens but occasionally responds to gemcitabine (difluoro-deoxycytidine, dFdC). Tuveson and colleagues developed a genetically engineering mouse model of PDA that recapitulates the cardinal pathophysiological and molecular features of the cognate human disease. We have used 19F MR spectroscopy to follow the uptake of gemcitabine and formation of its active compound dFdCTP in primary and transplanted tumours of PDA and other tissues. Our data suggests that drug delivery and/or drug metabolism are critical features that influence the response to gemcitabine and potentially other agents in PDA.
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