title: Expression of molecules related to AKT pathway as putative regulators of ameloblastoma local invasiveness.
abstract: BACKGROUND
  Ameloblastoma is an odontogenic neoplasm with local invasiveness and high recurrence. We previously suggested that growth factors, matrix metalloproteinases (MMPs), and TIMPs influence ameloblastoma invasiveness (Pathol. Res. Pract., 208, 2012, 225; Oral. Surg. Oral. Med. Oral. Pathol. Oral Radiol. Endod., 111, 2011, 474). Signals generated by this molecular network would be transduced by ERK 1/2 pathway (Oral. Surg. Oral. Med. Oral. Pathol. Oral Radiol. Endod., 111, 2011, 474). Others signaling pathways may influence ameloblastoma biology. Here, we studied expression of AKT and related molecules in ameloblastoma.
  
  
  METHODS
  Fourteen cases of solid/multicystic ameloblastomas were examined. Immunohistochemistry was carried out to detected AKT (phospho-AKT), NF-қB (phospho-NF-қB), β-catenin, cyclin-D1, and COX-2 in ameloblastoma samples. These molecules were evaluated in neoplastic cells and stroma.
  
  
  RESULTS
  All proteins were detected in ameloblastoma. Expression of these markers was quantified and compared. Spearman's rank test was carried out to address positive correlations between proteins (P < 0.05). Ameloblastoma had a significant positive correlation of AKT (phospho-AKT) with β-catenin. β-catenin correlated with Cyclin-D1 and COX-2 in neoplastic cells. AKT (phospho-AKT) correlated with β-catenin; β-catenin with Cyclin-D1; AKT (phospho-AKT) with NF-қB (phospho-NF-қB); and NF-қB (phospho-NF-қB) with COX-2 in stromal cells.
  
  
  CONCLUSIONS
  Results suggest that proteins studied are present and probably involved in a functional pathway in neoplastic cells and stroma and may therefore influence the local invasiveness of ameloblastoma.
authors.affiliation: Department of Oral Pathology, School of Dentistry, Federal University of Pará, Belem, Brazil.
authors.forename: Rodolpho L
authors.initials: RL
authors.lastname: Cecim
authors.forename: Hicso A F
authors.initials: HA
authors.lastname: Carmo
authors.forename: Maria S S
authors.initials: MS
authors.lastname: Kataoka
authors.forename: Vanessa M
authors.initials: VM
authors.lastname: Freitas
authors.forename: Sérgio
authors.initials: S
authors.lastname: de Melo Alves Júnior
authors.forename: Erick N
authors.initials: EN
authors.lastname: Pedreira
authors.forename: Ruy G
authors.initials: RG
authors.lastname: Jaeger
authors.forename: Joao J V
authors.initials: JJ
authors.lastname: Pinheiro
mesh_terms: D000564:Ameloblastoma / Q000473:pathology*; D002467:Cell Nucleus / Q000473:pathology; D019938:Cyclin D1 / Q000032:analysis; D051546:Cyclooxygenase 2 / Q000032:analysis; D003593:Cytoplasm / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016328:NF-kappa B / Q000032:analysis; D009361:Neoplasm Invasiveness; D051057:Proto-Oncogene Proteins c-akt / Q000032:analysis*; D015398:Signal Transduction / Q000502:physiology; D017154:Stromal Cells / Q000473:pathology; D051176:beta Catenin / Q000032:analysis
chemical_list: C530104:CCND1 protein, human; D016328:NF-kappa B; D051176:beta Catenin; D019938:Cyclin D1; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D051057:Proto-Oncogene Proteins c-akt
keywords: AKT pathway; ameloblastoma; molecular markers; odontogenic tumors