LAUSR

Objectives Adenomatoid odontogenic tumors (AOT) are benign tumors derived from odontogenic epithelium, and they account for 2-7% of all odontogenic tumors. Intraosseous AOTs are thought to be associated with unerupted permanent teeth, although their pathogenesis is still unclear.KRAS mutation, which is involved in the pathogenesis of some malignant tumors as driver mutation, was recently detected in AOT suggesting its association with tumorigenesis.The aim of this study was to assess the frequency of KRAS mutation and his association with the presence of the MAPK / ERK signaling pathway proteins. Finding Paraffin-embedded tissue samples from 9 AOT patients (3-47 years old, mean 24.7 years) were obtained for this study. Genomic DNA was extracted from each sample, and in one case, genetic mutations in 50 cancer-associated genes were examined by next-generation sequencing. A KRAS G12D missense mutation was detected in the DNA sequence of the tumor cells, but it was not detected in that of the stroma tissue. Based on this result, hotspot mutations in the RAS family were analyzed by PCR-rSSO using the remaining 8 cases. KRAS G12V and KRAS G12R mutations were detected in 2 and 4 cases, respectively. Subsequently, in the paraffin blocks, immunohistochemistry was performed to visualize the presence of the proteins involved in the MAPK / ERK signaling pathway. All the cases were EGFR, KRAS,CRAF, BRAF positive, one case was ERK negative, and one case was MEK and ERK negative, all the other remaining cases were MEK and ERK positive. Conclusions In conclusion, KRAS mutation was frequently detected in AOT, suggesting its association with tumorigenesis of AOT. However, since EGFR was positive, how the mutation affects the tumor development is still unclear.