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Editorial |

Harnessing Hedgehog for the Treatment of Basal Cell Carcinoma

Kelly L. Harms, MD, PhD; Andrzej A. Dlugosz, MD
JAMA Dermatol. 2013;149(5):607-608. doi:10.1001/jamadermatol.2013.448.
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Vismodegib, a first-in-class small-molecule hedgehog pathway inhibitor, was approved by the Food and Drug Administration in January 2012 for the treatment of metastatic and locally advanced basal cell carcinoma (BCC). The commentary by Wysong et al1 in this issue of JAMA Dermatology highlights the poor response of metastatic BCC to conventional forms of therapy, making hedgehog pathway antagonists an important addition to the therapeutic armamentarium for this rare but deadly type of BCC.

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Figure. Key components of hedgehog signaling pathway and inhibitors. Physiologic signaling takes place when hedgehog (HH) binds patched 1 (PTCH1) and derepresses smoothened (SMO), leading to activation of glioma-associated oncogene homologue (GLI) transcription factors and induction of HH target genes. In most basal cell carcinomas, PTCH1 is lost and SMO is constitutively active. Vismodegib and most other hedgehog pathway inhibitors act by binding and inhibiting SMO. Itraconazole also inhibits SMO but through a different mechanism, while arsenic trioxide and GLI antagonist molecules inhibit the function of GLI proteins.




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