Abstract
Neuroblastoma is one of the most common extra cranial solid tumours of childhood. The tumours are derived from the neural crest and have a high degree of heterogeneity1. Success of current therapies is modest. New pharmaceuticals have to be developed and their mechanism of action evaluated. As neuroblastoma cells are rapidly proliferating cells, they rely to a great extend on CTP synthetase for the synthesis of CTP. CTP synthetase catalyses the conversion of UTP into CTP and an increased CTP synthetase activity may cause an imbalance in the pyrimidine ribonucleotide pool2. The gene coding for CTP synthetase is located on chromosome 1p343, which is often deleted in neuroblastoma causing LOH. Despite 1p-deletion neuroblastoma cells have a high CTP synthetase activity, making CTP synthetase an attractive target for chemotherapy. Cyclopentenyl cytosine (CPEC) is a cytidine analogue that is readily metabolised to its active form: CPEC-triphosphate, which potently inhibits CTP synthetase causing rapid depletion of the intracellular cytidine nucleotides4 . In this study, we
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