These substrates can modulate cell behavior,45 which suggests that matrilysin may have a central role in the process of invasion and tumor metastasis.46 PLX 4720 MMP-26 is frequently expressed in both normal cells and endometrium, placenta, and kidney, as well as in epithelial neoplasms from various anatomic sites. It shows proteolytic activity on various ECM components, including fibronectin, collagen IV, gelatin,

and fibrinogen.7 and 47 Cavalcante et al. (2008)25 evaluated the expression of MMP-7 and MMP-26 in syndromic and nonsyndromic keratocystic odontogenic tumors, and observed a strong epithelial expression in cases associated with Gorlin syndrome compared to non-syndromic cases, which may explain the more aggressive behavior of syndrome-associated KOTs. Studies were also performed on the immunohistochemical expression of these matrilysins in ameloblastomas and adenomatoid odontogenic tumors, trying to correlate with distinct tumor biologic behavior

of these pathologies. However, Freitas et al. (2009)26 found no statistically significant differences between the immunostaining of both lesions, but there was a significant staining for MMP-7 and MMP-26 in both the parenchyma and the stroma, suggesting a role in the process of remodeling and growth of these tumors. In our results, the immunostaining of MMP-7 in the parenchyma scores were 2 in 100% of cases, whereas MMP-26 showed some variability. In the stroma, we observed 100% staining of the matrilysins, buy Inhibitor Library thereby demonstrating the involvement of these proteins in the interaction between epithelial cells and stroma in the process of tumor growth and expansion.9 and 41 Besides Progesterone degrading ECM components, MMP-7 and MMP-26 are also able to activate other metalloproteinases, such as MMP-9. MMP-7 activates MMPs 2 and 9.48 and 49 MMPs 2 and 9 degrade collagen type IV, and these gelatinases are involved in processes of tumor invasion and metastasis,50 as referenced above. The positivity evidenced by metalloproteinases 1, 7, 9, and 26 in stromal cells

demonstrates that these enzymes are also produced by fibroblasts, endothelial cells, inflammatory lymphocytes, plasma cells, and neutrophils, which are also involved in the degradation of ECM. Similar results were found in ameloblastomas,22 and 24 adenomatoid odontogenic tumors (AOTs),26 and 27 and odontogenic cysts.28 Ghost cells are necessary prerequisites for the diagnosis of CCOT, though not pathognomonic of these lesions.19 There is still much controversy about the nature of these cells. Some researchers believe that they represent a normal or atypical keratinization,51 simple cellular degeneration, or a product of the abortive enamel matrix,52 or that they derive from apoptotic processes of odontogenic cells and originate from metaplastic transformation of odontogenic tumors.