Basal Cell Carcinoma and the Carcinogenic Role of Aberrant Hedgehog Signaling

Anna Saran

Future Oncol. 2010;6(6):1003-1014.

Future Perspective

Study of BCC tumorigenesis has been hampered by the inexplicable failure of mutagenic chemicals, UV or ionizing radiation to induce BCCs in mice, and by the difficulty in culturing BCC-derived materials. The identification of mutations in Hh components and other genes has expanded our understanding of the molecular pathogenesis of BCC and facilitated the development of in vivo models that recapitulate the etiology and the histopathology of the human disease. In a relatively short period, the information acquired has provided a basis for the molecular target-based therapeutic management of BCC, and clinical trials have been successfully concluded, while new ones are in progress. Further understanding of the molecular mechanisms of Hh, and of other pathways driving carcinogenesis in parallel or downstream of Hh, will be an essential advantage for effective therapy of the commonly occurring BCC, and of other cancers in which Hh signaling is deregulated.

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Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.

Cite this: Basal Cell Carcinoma and the Carcinogenic Role of Aberrant Hedgehog Signaling - Medscape - Jun 01, 2010.

Table 1. Frequencies of sporadic basal cell carcinoma-carrying mutations in hedgehog signaling molecules.
Gene^†	Mutations (%)	Ref.
Ptch1	12/36 (33.3)	^[19]
Ptch1	3/26 (11.5)	^[34]
Ptch1	29/60 (48.3)	^[35]
Ptch1	6/15 (40)	^[110]
Ptch1	3/9 (33.3)	^[33]
Ptch1 Smo	8/31 (25.8) 4/31 (13)	^[39]
Ptch1 Smo Sufu	28/42 (66.7) 4/42 (9.5) 2/42 (4.8)	^[40]
Smo	3/47 (6.4)	^[37]
Smo	20/97 (20.6)	^[38]

^†The majority of mutations were found in different exons of the genes analyzed.

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