title: Ameloblastoma, calcifying epithelial odontogenic tumor, and glandular odontogenic cyst show a distinctive immunophenotype with some myoepithelial antigen expression.
abstract: BACKGROUND
  Odontogenic neoplasms have some morphologic overlap with salivary gland neoplasms, many of which show myoepithelial differentiation. In the 1980s, an ultrastructural study identified a population of myoepithelial-like cells in calcifying epithelial odontogenic tumor. Myoepithelial derived tumors have since been shown to have distinct immunohistochemical profiles.
  
  
  METHODS
  We examined a series of odontogenic neoplasms, including 11 ameloblastomas, four calcifying epithelial odontogenic tumors, five glandular odontogenic cysts (GOCs), and five keratocystic odontogenic tumors with a panel of myoepithelial-associated immunohistochemical stains. We also assessed representative control examples of oral mucosa, odontogenic rests, and dentigerous cysts.
  
  
  RESULTS
  All of the neoplastic and non-neoplastic oral epithelium-derived entities share a p63-positive, high molecular weight cytokeratin (CK5/6)-positive immunophenotype. Calponin reactivity was at least focally present in two of four calcifying epithelial odontogenic tumors, three of five GOCs, and 10 of 11 ameloblastomas; the sole completely non-reactive ameloblastoma represents a lung metastasis. One case of calcifying epithelial odontogenic tumor was focally positive for glial fibrillary acidic protein. However, other more definitive markers of myoepithelial differentiation, including S-100 and smooth muscle actin, were negative. Two of three calcifying epithelial odontogenic tumors and five of five GOCs were also positive for a low molecular weight cytokeratin (CK7).
  
  
  CONCLUSIONS
  Ameloblastomas, GOCs, and calcifying epithelial odontogenic tumors show a distinctive immunophenotype which overlaps with that of myoepithelial-derived salivary gland neoplasms but does not provide definitive support for myoepithelial differentiation.
authors.affiliation: Department of Surgical Pathology, Stanford University School of Medicine, Stanford, CA 94305-5324, USA. ditag@stanford.edu
authors.forename: Dita
authors.initials: D
authors.lastname: Gratzinger
authors.forename: Mohamed E
authors.initials: ME
authors.lastname: Salama
authors.forename: Catherine F
authors.initials: CF
authors.lastname: Poh
authors.forename: Robert V
authors.initials: RV
authors.lastname: Rouse
mesh_terms: D000564:Ameloblastoma / Q000473:pathology*; D000951:Antigens, Neoplasm / Q000096:biosynthesis; D002135:Calcium-Binding Proteins / Q000096:biosynthesis; D002454:Cell Differentiation; D004847:Epithelial Cells / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D016130:Immunophenotyping; D053531:Keratins, Type II / Q000096:biosynthesis / Q000276:immunology; D008565:Membrane Proteins / Q000096:biosynthesis; D008840:Microfilament Proteins / Q000096:biosynthesis; D032342:Muscle Cells / Q000473:pathology; D009124:Muscle Proteins / Q000096:biosynthesis; D009807:Odontogenic Cysts / Q000473:pathology*; D009808:Odontogenic Tumors / Q000473:pathology*; D012189:Retrospective Studies; D012468:Salivary Gland Neoplasms / Q000473:pathology*; D000096985:Calponins
chemical_list: D000951:Antigens, Neoplasm; D002135:Calcium-Binding Proteins; D053531:Keratins, Type II; D008565:Membrane Proteins; D008840:Microfilament Proteins; D009124:Muscle Proteins; D000096985:Calponins; C081876:CKAP4 protein, human