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.
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).
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.
Defective glutathione S-transferase (GST) and N-acetyltransferase (NAT) enzymes have been associated with an increased risk of developing lung and bladder cancer.