Importantly, the administration of EGF-toxin to dogs with spontaneous bladder cancer, who had failed or were not eligible for other therapies, resulted in ~30% average tumor reduction after one treatment cycle.
Pancreatic secretory trypsin inhibitor causes autocrine-mediated migration and invasion in bladder cancer and phosphorylates the EGF receptor, Akt2 and Akt3, and ERK1 and ERK2.
Collectively, our results indicate that EGF may be able to potentiate AR transactivation that leads to enhancing BCa progression, which may help us to develop a better therapeutic approach to treat BCa via targeting both EGF and AR signaling.
Therefore, we examined the mRNA expression of all four EGF receptors with real-time polymerase chain reaction in biopsies from 88 patients with bladder cancer, where the survival was followed for a median of 38.5 months (range 1-117 months).
The CpG islands included exon 5 of PAX6, exon 2 of p16, the 5' end of the deleted in bladder cancer gene, and the 5' end of transmembrane protein containing epidermal growth factor and follistatin domains.