Prior studies have evaluated p16INK4a expression in odontogenic keratocyst and ameloblastoma, but data regarding other odontogenic cysts and tumors have been sparse.
In addition, we investigated the relationship between BRAFV600E mutations and epithelial-mesenchymal transition, which has not been studied in ameloblastoma.
Expression of CKs was consistent with other histological variants of ameloblastoma (AM), but AM-BC had significantly higher p53 and Ki-67 (p < 0.05) labeling indices than other histological variants of AM.Two patients had BRAF gene mutations.
Most ameloblastomas (AM) in humans harbour mutually-exclusive driving mutations in BRAF, HRAS, KRAS, NRAS or FGFR2 that activate MAPK signalling, and in SMO that activates Hedgehog signalling.
While ameloblastomas show BRAFp.V600E mutations, adenomatoid odontogenic tumours harbour either KRAS p.G12R or p.G12 V. The lack of understanding of the core molecular changes involved in tumour initiation and progression represents a critical barrier to developing new strategies for cancer detection and prevention.
BRAFV600E mutation is common in mandibular ameloblastomas, especially in cases of tumours larger than 4 cm and in the posterior region of the mandible.
<b>Conclusions:</b> The complete response observed here illustrate the role of molecular profiling in complicate clinical situation of rare head and neck cancer and the potential benefit of BRAF-targeted therapy in ameloblastoma carrying <i>BRAF</i> V600E mutation.
The presence of BRAF-V600E mutations in ameloblastoma was related to decreased levels of glycerol in comparison with tumors carrying only wild-type alleles of this gene.
High-throughput DNA sequencing methods, such as next-generation sequencing using Illumina have yielded advancements in studies on MAPK signaling pathways and their association with AM; in particular, BRAFV600E is mediated by the activation of the Ras/Raf/MAPK pathway.
Most ameloblastomas (AM) in humans harbour mutually-exclusive driving mutations in BRAF, HRAS, KRAS, NRAS or FGFR2 that activate MAPK signalling, and in SMO that activates Hedgehog signalling.
Expression of CKs was consistent with other histological variants of ameloblastoma (AM), but AM-BC had significantly higher p53 and Ki-67 (p < 0.05) labeling indices than other histological variants of AM.Two patients had BRAF gene mutations.
IL-8 also increased total β-catenin and p-β-catenin expression in ameloblastoma tumor cells, and β-catenin knockdown partially inhibited the EMT process in tumor cells, as evidenced by increased E-cadherin, and decreased vimentin and zeb1 levels.
In conclusion, the present results indicated various expression and correlation of p63 with the proliferation of odontogenic epithelial cells in DC, OKC, and AB.
Adamantinoma-like Ewing sarcoma (ALES) is a rare tumor that demonstrates the EWSR1-FLI1 translocation characteristic of Ewing sarcoma despite overt epithelial differentiation including diffuse expression of cytokeratins and p40.
In conclusion, the present results indicated various expression and correlation of p63 with the proliferation of odontogenic epithelial cells in DC, OKC, and AB.
IL-8 also increased total β-catenin and p-β-catenin expression in ameloblastoma tumor cells, and β-catenin knockdown partially inhibited the EMT process in tumor cells, as evidenced by increased E-cadherin, and decreased vimentin and zeb1 levels.
In conclusion, the present results indicated various expression and correlation of p63 with the proliferation of odontogenic epithelial cells in DC, OKC, and AB.
In conclusion, the present results indicated various expression and correlation of p63 with the proliferation of odontogenic epithelial cells in DC, OKC, and AB.
Adamantinoma-like Ewing sarcoma (ALES) is a rare tumor that demonstrates the EWSR1-FLI1 translocation characteristic of Ewing sarcoma despite overt epithelial differentiation including diffuse expression of cytokeratins and p40.
Nerve sparing enucleation and curettage was employed for the established cases of Odontogenic Cysts; Enucleation and curettage, peripheral ostectomy, followed by chemical cauterization was employed for the Unicystic Ameloblastomas and other Odontogenic tumours with a low Ki-67 and PCNA Proliferation Index (PI)/Labelling index (LI ≤ 3); Marginal resection was carried out for the tumours with a higher Labelling Index (LI >3 ≤5), and Segmental resection (including partial/complete Maxillectomy, Hemimandibulectomy with/without disarticulation) for the aggressive pathologies with high Labelling Index (LI > 5).