Background Metabolic changes in tumour cells are used in clinical imaging and may provide potential therapeutic targets. Human papillomavirus (HPV) status is important in classifying head and neck cancers (HNSCC), identifying a distinct clinical phenotype; metabolic differences between these HNSCC subtypes remain poorly understood. Methods We used RNA sequencing to classify the metabolic expression profiles of HPV +ve and HPV −ve HNSCC, performed a meta-analysis on FDG-PET imaging characteristics and correlated results with in vitro extracellular flux analysis of HPV −ve and HPV +ve HNSCC cell lines. The monocarboxylic acid transporter-1 (MCT1) was identified as a potential metabolic target and tested in functional assays. Results Specific metabolic profiles were associated with HPV status, not limited to carbohydrate metabolism. There was dominance of all energy pathways in HPV-negative disease, with elevated expression of genes associated with glycolysis and oxidative phosphorylation. In vitro analysis confirmed comparative increased rates of oxidative phosphorylation and glycolysis in HPV-negative cell lines. PET SUV(max) scores however were unable to reliably differentiate between HPV-positive and HPV-negative tumours. MCT1 expression was significantly increased in HPV-negative tumours, and inhibition suppressed tumour cell invasion, colony formation and promoted radiosensitivity. Conclusion HPV-positive and negative HNSCC have different metabolic profiles which may have potential therapeutic applications.

Four consecutive infants and children with hepatoblastomas were treated with a combination of Adriamycin (doxorubicin) and cisplatin. Three patients had unresectable tumors and in each there was a dramatic decrease in tumor size and serum alpha-fetoprotein (AFP) levels. The tumors of two of these patients, including one with pulmonary metastases which cleared, were rendered resectable. The third patient's tumor remained unresectable but his AFP level returned to normal following radiotherapy. All three patients are disease-free, and both without metastases are off therapy from 9 to 24 months. A fourth child received the combination as adjuvant therapy following resection of an embryonal hepatoblastoma and he remains disease-free 7 months after its discontinuation. Therapy was tolerable in all patients and its principal toxicities were myelosuppression and magnesium wasting. Adriamycin and cisplatin in combination were very effective in these patients and deserve further trials, especially in unresectable and metastatic hepatoblastomas.