Expression of a functional NAT after in vitro transfection of bladder cancer cells with the NAT gene under the control of telomerase promoters leads to active uptake of [131I]MIBG and dose-dependent cell kill.
Loss of 8p22 and genetic instability involving chromosome 8 indicate that this chromosome is important in bladder cancer and that NAT genes will act as important genetic landmarks in defining deletions in this disease.
In this study, paclitaxel was selected to test the inhibition of NAT activity (N-acetylation of AF) and NAT gene expression in a human bladder cancer cell line (T24).
Defective glutathione S-transferase (GST) and N-acetyltransferase (NAT) enzymes have been associated with an increased risk of developing lung and bladder cancer.