Abstract
This different perspective on Tang et al. (beginning on p. 25 in this issue of the journal) discusses the pivotal role of cyclooxygenase (COX) signaling in the pathogenesis of basal cell carcinoma (BCC). These investigators conducted elegant experiments showing increased BCC burden in patch heterozygous mice overexpressing COX-2 in the epidermis. Genetic deletion of COX-1 or COX-2 resulted in a robust decrease in BCC burden in patch heterozygote mice. They then studied pharmacologic COX inhibition in mice and humans with loss of patch, finding a trend in humans toward decreased BCC burden. This finding has implications for public health.