Analysis of the neoplastic nature and biological potential of sporadic and nevoid basal cell carcinoma syndrome-associated keratocystic odontogenic tumor

Tumor angiogenesis in keratocystic odontogenic tumor assessed by using CD-105 antigen

“…The VEGF expression by epithelial cells in KCOT may promote growth via an autocrine proliferative effect on the cystic epithelium and while paracrine stimulation of the vascular network may maintain survival and promote growth, enlargement and expansion. Thus, findings of previous studies (44, 49, 50, 52) were confirmed by immunohistochemically in the current study by observing the positive correlation between MVD, TVA and MVA and Ki‐67 LI in KCOT. This could explains role of tumor angiogenesis in the biological locally aggressive behavior of the KCOT such as: (i) the locally aggressive biological behavior, manifested by a large lesion extending along the cancellous bone without producing any noteworthy expansion of cortical plates (2, 4, 5) (ii) tendency to recur, suggesting increased epithelial activity, although the rate of recurrence may depend on the method of treatment, (recurrence up to 62% was found) (1–3) Although DC can become a large lesion and expand the cortical bone of the maxilla or mandible, no recurrence of DC was usually reported after surgical enucleation.…”

“…Katase N et al. (50) have suggested that heparanase may be involved in the aggressive behavior of KCOT, particularly in nevoid basal cell carcinoma syndrome associated KCOT. Heparanase is an endo‐D‐glucuronidase enzyme that specifically cleaves heparin sulphate and the increase of its level in tumors promotes invasion, angiogenesis and metastasis (51).…”

Potential relevance of cyclooxygenase-2 expression in keratocystic odontogenic tumours - an immunohistochemical study

“…The fact that no correlation was found between the expression of COX‐2 and any of the clinical features only shows that the pathogenic mechanism involved in these tumours is not ‘clinical‐related’. In fact, it unveils an intrinsic characteristic of the tumor that bares no association either with its syndromic or primary nature, thus substantiating previous molecular studies which have established an identical mechanism involving the development of both sporadic and NBCCS‐associated KCOTs and therefore establishing the neoplastic nature of the KCOT (17, 35, 42).…”

Odontogenic Keratocystic Tumor: A Clinical and Histopathologic Retrospective Study Based on the New WHO Classification

“…These loci are related to DNA unbalance, revealing deletion of tumor suppressor genes (Agaram et al;Henley et al, 2005). In addition, cell proliferation markers, such as p53, Ki67, and PCNA, as well as certain cytokeratins and suppression of apoptosis-related markers, such as bcl-2 and Bax were also identified (Koizumi;Ogden et al;Shear, 2002a;Shear, 2002b;Vered et al) In order to prove the KCOT tissue invasiveness, Heikinheimo et al (2007) observed reduction in the expression of genes responsible for the formation of extracellular matrix components, and Katase et al (2007) noticed increase of heparanase (enzyme that is frequently increased in tumors, promoting tissue invasion, angiogenesis, and metastasis) expression in the KCOT epithelial cells.…”