Expression of SHH, PTCH and SMO to the Hedgehog signal in keratocystic odontogenic tumor

Abstract

In 1960, Gorlin and Goltz established that the keratocystic odontogenic tumor (KCOT) is one of the main lesions of nevoid basal cell carcinoma syndrome (NBCCS). In 1996, Hahn and Johnson reported that 9q22.3 is a causative gene of NBCCS, and Patched 1 (PTCH) was identified as the responsible gene. PTCH is a receptor for the signaling protein Hedgehog (HH). The HH signaling pathway regulates proliferation, differentiation and morphogenesis of cells. Sonic hedgehog (SHH) has an important role in the process of morphogenesis during development. Loss of function mutations of PTCH and gain of function mutations in smoothened (SMO) result in constitutive activation of the pathway and are thought to facilitate oncogenesis. 9 Although the association between the pathogenesis of KCOT and PTCH has been investigated, there have been few studies that have simultaneously exExpression of SHH, PTCH and SMO to the Hedgehog signal in keratocystic odontogenic tumor