Nature 389, 876–881 (1997)

The contents summary page in the issue of 23 October included an item on this Letter that was somewhat misleading. A more accurate summary reads: “Patients with basal cell nevus syndrome develop basal cell carcinomas (BCCs) early in life and carry mutations in the Patched gene, which encodes a receptor for the Sonic hedgehog ligand. These findings implicated the activation of the Sonic hedgehog signalling pathway in the familial or inherited form of BCC. However, the molecular mechanisms underlying the development of sporadic BCCs, the commonest form of skin cancer in fair-skinned adults with over a million cases a year worldwide, remained unknown. Now Dahmane et al. provide compelling evidence that virtually all sporadic BCCs have the Shh signalling pathway activated as determined by the expression of the zinc finger transcription factor Gli1, the final target and mediator of Shh signalling. The work predicts that any mutations that lead to the activation of this pathway in basal cells, and thus to Gli1 transcription and function, will cause basal cell cancer. Moreover, work in model organisms shows that inappropriate expression of Gli1 in the skin leads to the development of epidermal tumours. Gli1 may thus be both a marker and cause of BCC formation, making prospects for early diagnosis and possible treatment of this widespread type of skin cancer feasible.”