title: Two relatively distinct patterns of ameloblastoma: an anti-apoptotic proliferating site in the outer layer (periphery) and a pro-apoptotic differentiating site in the inner layer (centre).
abstract: OBJECTIVE
  This study was performed to determine the apoptotic behaviour of ameloblastomas by analysing the role of bcl-2 family proteins in ameloblastomas and the location of terminally apoptotic cells in the ameloblastoma epithelial tissues.
  
  
  RESULTS
  For immunohistochemistry, tissue sections of 32 patients were treated with an antigen-retrieval
  
  
  METHODS
  Primary antibodies against the apoptosis-related proteins, bcl-2, bcl-X, bax, and bak were applied. Besides immunohistochemistry, Western blotting and TUNEL were also performed. Most of the outer layer cells were predominantly stained by the bcl-2 antibody, while most of the inner layer cells were stained by antibodies against the apoptosis-modulating proteins, bax and bak. Among the bcl-2 family, bcl-2 was the most ubiquitously expressed protein in ameloblastomas, while bcl-X was expressed in the greatest concentrations. The major bcl-X protein was bcl-XL. Some of the inner layer cells entered the terminal apoptotic stage, which were revealed by TUNEL. The acanthomatous areas over-expressed the apoptosis-modulating proteins, especially bak.
  
  
  CONCLUSIONS
  Ameloblastoma has much more apoptosis-inhibiting protein than the apoptosis-modulating protein. Ameloblastoma has two relatively distinct patterns, an anti-apoptotic proliferating site in the outer layer (periphery) and a pro-apoptotic differentiating site in the inner layer (centre). The acanthomatous area, which was stained strongly by bak antibody and contained numerous terminally apoptotic cells, was considered as the differentiated area.
authors.affiliation: Section of Oral and Maxillofacial Oncology, Faculty of Dental Science, Kyushu University, Fukuoka, Japan. ferry@dent.kyushu-u.ac.jp
authors.forename: F
authors.initials: F
authors.lastname: Sandra
authors.forename: N
authors.initials: N
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Mitsuyasu
authors.forename: Y
authors.initials: Y
authors.lastname: Shiratsuchi
authors.forename: M
authors.initials: M
authors.lastname: Ohishi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000564:Ameloblastoma / Q000378:metabolism / Q000473:pathology*; D017209:Apoptosis; D015153:Blotting, Western; D002454:Cell Differentiation; D002455:Cell Division; D002648:Child; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D008339:Mandibular Neoplasms / Q000378:metabolism / Q000473:pathology*; D008565:Membrane Proteins / Q000032:analysis; D008875:Middle Aged; D011518:Proto-Oncogene Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein
chemical_list: C494772:BAK1 protein, human; C494826:BAX protein, human; C494811:BCL2L1 protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein