title: Enhanced expression of podoplanin in ameloblastomas.
abstract: OBJECTIVE
  Podoplanin, a mucin-type transmembrane glycoprotein, is specifically expressed by lymphatic but not blood vascular endothelial cells, and is also widely expressed in various specialized cell types throughout the body. Recent studies have demonstrated that it mediates a pathway leading to collective cell migration and invasion in vivo and in vitro. In the present study, we carried out an immunohistochemical investigation of podoplanin to clarify whether it is expressed in human ameloblastomas (AMs), which are characterized by locally aggressive behavior with a high rate of recurrence. In addition, we examined the localization of the epithelial marker E-cadherin and the mesenchymal marker vimentin to clarify whether AMs show epithelial-mesenchymal transition (EMT).
  
  
  METHODS
  Paraffin-embedded tissue specimens of 38 AMs were examined immunohistochemically using antibodies against podoplanin, E-cadherin, and vimentin.
  
  
  RESULTS
  Immunohistochemical reactivity for podoplanin was detected in the cell membrane and cytoplasm of most odontogenic tumor epithelial cells in AMs. Podoplanin was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. E-cadherin was expressed in central stellate reticulum-like cells and showed decreased expression in peripheral columnar cells. Immunoreactivity for E-cadherin was weak or negative in keratinizing cells of acanthomatous AMs, suggesting terminal differentiation of the tumor cells. Immunohistochemical reactivity for vimentin was found in stromal cells, but partial or no reaction was observed in neoplastic cells.
  
  
  CONCLUSIONS
  Expression of podoplanin in AMs is considered to be associated with neoplastic odontogenic tissues; this molecule might play a role in the collective cell migration of tumor nests in AMs. The pattern of expression of E-cadherin and vimentin suggests that invasion in AMs occurs in the absence of EMT. The migration and invasion mediated by podoplanin in AMs could be related to cytoskeletal reorganization.
authors.affiliation: Division of Pathology, Department of Diagnostic and Therapeutic Sciences, Meikai University School of Dentistry, Saitama, Japan. patricia@dent.meikai.ac.jp
authors.forename: Patricia
authors.initials: P
authors.lastname: González-Alva
authors.forename: Akio
authors.initials: A
authors.lastname: Tanaka
authors.forename: Yuka
authors.initials: Y
authors.lastname: Oku
authors.forename: Yuji
authors.initials: Y
authors.lastname: Miyazaki
authors.forename: Eri
authors.initials: E
authors.lastname: Okamoto
authors.forename: Masahiro
authors.initials: M
authors.lastname: Fujinami
authors.forename: Noriaki
authors.initials: N
authors.lastname: Yoshida
authors.forename: Kentaro
authors.initials: K
authors.lastname: Kikuchi
authors.forename: Fumio
authors.initials: F
authors.lastname: Ide
authors.forename: Hideaki
authors.initials: H
authors.lastname: Sakashita
authors.forename: Kaoru
authors.initials: K
authors.lastname: Kusama
mesh_terms: D000564:Ameloblastoma / Q000473:pathology*; D015820:Cadherins / Q000032:analysis; D002454:Cell Differentiation; D002462:Cell Membrane / Q000648:ultrastructure; D002465:Cell Movement; D003593:Cytoplasm / Q000648:ultrastructure; D003803:Dentigerous Cyst / Q000473:pathology; D004847:Epithelial Cells / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D007365:Intercellular Junctions / Q000473:pathology; D008562:Membrane Glycoproteins / Q000032:analysis*; D009361:Neoplasm Invasiveness; D009364:Neoplasm Recurrence, Local / Q000473:pathology; D017154:Stromal Cells / Q000473:pathology; D014746:Vimentin / Q000032:analysis; D000098853:Podoplanin
chemical_list: D015820:Cadherins; D008562:Membrane Glycoproteins; D014746:Vimentin; C117468:PDPN protein, human; D000098853:Podoplanin