These results suggest that FAK may serve as a marker of cervical lymph node metastasis of tongue cancer and that RNAi targeting FAK could serve as a potential therapeutic for the treatment of tongue cancer.
Marsupialisation or decompression is frequently performed as a conservative therapy for keratocystic odontogenic tumours (KCOTs). Positive podoplanin (PDPN) expression in the epithelium of KCOT has been previously reported and may be associated with neoplastic invasion. In the present study, changes in PDPN expression were observed in the epithelium of KCOTs following decompression. In total, 16 pairs of paraffin-embedded tissue specimens obtained at the time of decompression and at two-stage curettage or enucleation were collected and immunohistochemically examined using an antibody against PDPN. The intensity of PDPN staining was evaluated with a semi-quantitative detection method and statistically analysed. The immunohistochemical reactivity of PDPN was consistently markedly positive in 93.8% of KCOT samples prior to decompression. The positive staining was immunolocalised to the cell membrane and cytoplasm of cells in the basal layer and extended into the suprabasal layer for two to three cell layers. At the time of curettage, 2 of the 16 (12.5%) cases were completely negative, 11 of the 16 (68.8%) cases were locally positive and 3 of the 16 (18.7%) cases showed a ‘linear staining’ pattern, as the PDPN-positive cells were restricted to within the single basal layer. The expression level of PDPN was significantly decreased (P<0.05) and a significant loss or reduction of PDPN expression was observed in KCOTs following decompression. Larger sample groups are required to further verify this result.
Abstract. Marsupialisation or decompression is frequently performed as a conservative therapy for keratocystic odontogenic tumours (KCOTs). Positive cyclooxygenase-2 (COX-2) expression in the epithelium of KCOTs was recently reported and may be associated with neoplastic invasion and progression. The aim of the present study was to investigate the change in COX-2 expression in the KCOT epithelium following decompression. In this study, 16 pairs of KCOT biopsy specimens obtained during decompression or enucleation were collected and analysed. Formalin-fixed, paraffin-embedded blocks were sectioned and immunohistochemically investigated using anti-COX-2 antibody. The molecular expression was semiquantitatively evaluated as follows: 0, negative; 1, weakly to moderately positive; and 2, strongly positive. In the samples obtained prior to decompression, the positive staining for COX-2 was immunolocalised to the cell membrane and the cytoplasm, it involved the full thickness of the epithelium and 15 of the 16 specimens (93.8%) exhibited mild to strong positivity. As regards the samples obtained following decompression, only 3 of the 16 specimens (18.8%) exhibited a mild positivity. The expression levels of COX-2 were significantly decreased following decompression (P<0.05). It may be concluded that loss or a significant reduction of COX-2 expression is associated with decompression in KCOTs. However, large-scale studies are required to verify these results and improve our knowledge of the possible involvement of COX-2 in the pathogenic mechanism underlying the development of KCOTs.
IntroductionUnlike other odontogenic cystic lesions, the odontogenic keratocyst (OKC) exhibits an intrinsic growth potential and a marked ability to destroy bone (1,2). Clinically, following conventional treatment such as enucleation, OKC exhibits a high tendency for recurrence (1,3). According to the 2005 World Health Organization classification, OKC was reclassified as a benign neoplasm, referred to as keratocystic odontogenic tumour (KCOT) (2,3).In the field of molecular biology, several immunohistochemical studies investigated the activity of the KCOT epithelium by using various markers of proliferation and apoptosis (4-7). The results of those studies demonstrated that p53 (4), PCNA (5) and Ki-67 (6) were more strongly expressed in the KCOT epithelium compared to other types of odontogenic cysts. Thus, it was concluded that the KCOT epithelium was highly proliferative, which may explain the high recurrence rate of KCOT and suggests that KCOTs have a different biological origin (7).Recently, marsupialisation or decompression combined with two-stage enucleation was proven to be an effective treatment for large KCOTs (3). According to data reported by Ninomiya et al (8), the size of the KCOT lesions was significantly decreased following decompression. To improve the outcome of decompression, investigation of the underlying molecular mechanisms of this type of therapy is required.Cyclooxygenase-2 (COX-2) levels were found to be elevated in...
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