In conclusion, our results demonstrate that E1B-55 kD-deleted adenovirus caused more severe cytolytic effect and replicated more efficiently in bladder cancer cells with mutant p53 than in those with wild-type p53. In the bladder xenograft animal model, it also exerted antitumour effects, which could be augmented by combining with replication-defective adenoviral vector expressing K1–5. The gene discussed is TP53; the disease is urinary bladder cancer.