Meeting Banner
Abstract #2699

Dichloroacetate Treatment Resulted in Altered Phospholipid Metabolism and Compromised Tumour Bioenergetics in Human Colon Carcinoma Xenografts

Yuen-Li Chung1, Helen Troy1, Geoffrey S. Payne1, Marion Stubbs2, Ian R. Judson3, John R. Griffiths2, Martin O. Leach1

1CR-UK and ESPRC Cancer Imaging Centre, Institute of Cancer Research, Sutton, Surrey, United Kingdom; 2Cancer Research UK Cambridge Research Institute, Cambridge, United Kingdom; 3CR-UK Centre for Cancer Therapeutics, Institute of Cancer Research, Sutton, Surrey, United Kingdom

Dichloroacetate (DCA) is a pyruvate dehydrogenase kinase (PDK) inhibitor and is found to be an anti-cancer agent. The aim of this work was to develop a non-invasive and robust biomarker for tumour response following PDK inhibition. In vivo and in vitro 1H- and 31P-MRS of HT29 xenografts and tumour extracts were used. DCA treatment caused tumour growth inhibition and altered phospholipid metabolism and tumour bioenergetics. The drop in total choline and phosphomonoesters may have potential as non-invasive markers for tumour response following treatment with DCA or other PDK inhibitors.