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In pancreatic ductal adenocarcinoma (PDAC), the lack of specific symptoms or diagnostic markers, the highly aggressive nature of the disease and high intrinsic and acquired therapy resistance all result in a virtually unchanged overall 5-year survival rate of around 5%.1 Thus, early detection of PDAC is a major task for improvement of prognosis and management of this fatal disease as surgery currently presents the only option for long-term survival.2 Conventional imaging techniques, including CT, proton-based MRI and endoscopic ultrasound, differentiate tumour tissue based on morphological and physiological (eg, reduced perfusion) changes, often not present in precursor lesions and early-stage tumours. Consequently, emerging innovative imaging technologies include molecular and metabolic approaches that allow the assessment of tumour biology.
Cancer phenotypes result from a host of mutational events, including signalling pathways that adapt tumour cell metabolism to support growth. One of these metabolic phenotypes observed in tumour cells is the Warburg effect, that is, ATP generation from glycolysis even under normal oxygen condition, converting most incoming glucose to lactate. Key pathways involved include phosphoinositide 3-kinase, hypoxia-inducible factor, p53, MYC and AMP-activated protein kinase. These alterations in glucose metabolism have been used in positron emission tomography (PET) imaging, in which the glucose analogue 18F-labelled fluorodeoxyglucose (18F-FDG) has been extensively applied in many cancer entities including PDAC. However, …
Contributors Both authors drafted the manuscript and the figure.
Funding This work was supported by funding from Deutsche Forschungsgemeinschaft (DFG SFB824 to JTS and RFB) and the European Union's Seventh Framework Program for research, technological development and demonstration (FP7/CAM-PaC under grant agreement 602783 to JTS).
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
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