The fibrosing BCC subtype was associated with a higher degree of inflammation (p < 0.001) and revealed a higher COX-2 immunoreactivity than nodular BCC (p = 0.012).
COX-2 common variants -765G-->C and -1195A-->G appear to be associated with risk of NMSC, although in different ways in the SCC and BCC subgroups, indicating that environmental and genetic risk factors may play different roles in the outcome leading to these two phenotypes.
While it cannot beruled out that the present findings are due to chance, the results indicate that high COX-2 expression may increase risk of BCC while NSAID use may be protective.
COX-2 was not detected in MCF-7 cells, but its expression in RMTCs was inhibited by SA treatment, which also significantly reduced BCC growth, but failed to cause cell death by necrosis or apoptosis.