title: Expression of proliferating cell nuclear antigen (PCNA) and Ki-67 in unicystic ameloblastoma.
abstract: The expression of proliferating cell nuclear antigen (PCNA) and Ki-67 was studied in unicystic and solid ameloblastoma (follicular and plexiform types) using a biotin-streptavidin method on routinely processed paraffin sections. To determine percentage PCNA and Ki-67 labelling indices, positive tumour cells and total tumour cells were counted in areas of each unicystic ameloblastoma corresponding to cystic linings, intraluminal nodules and invading tumour islands, and in solid ameloblastomas. Positive cells in basal and suprabasal layers of cystic tumour lining were also counted with respect to the length of basement membrane determined by image analysis. In unicystic ameloblastoma the invading islands exhibited a significantly higher PCNA labelling index (29.2 +/- 16.4%) than intraluminal nodules (13.6 +/- 5.4%; P < 0.05). Cystic tumour lining had relatively few PCNA positive cells and a labelling index (5.5 +/- 3.3%) significantly lower than invading islands (P < 0.001) or intraluminal nodules (P < 0.003). The labelling indices of solid ameloblastomas of follicular type (48.1 +/- 12.9%) were significantly higher than those of cystic tumour lining (P < 0.0001), intraluminal nodules (P < 0.001) and invading islands (P < 0.04) in unicystic ameloblastoma. Similar relationships were found for Ki-67 expression except that comparisons involving invading islands and intraluminal nodules were not significant, a finding probably due to the smaller number of specimens available for quantitative analysis. These results indicate differences in proliferative potential between different areas of unicystic ameloblastoma and between unicystic and solid lesions. The fact that invading tumour islands within the fibrous tissue wall showed high labelling indices is in agreement with the clinical observation that their presence may be related to recurrence after conservative surgery. This provides a biological basis for indicating more radical surgical excision as the treatment of choice for this subgroup of lesions.
authors.affiliation: Unit of Oral Pathology, School of Dentistry, University of Birmingham, UK.
authors.forename: T J
authors.initials: TJ
authors.lastname: Li
authors.forename: R M
authors.initials: RM
authors.lastname: Browne
authors.forename: J B
authors.initials: JB
authors.lastname: Matthews
mesh_terms: D000564:Ameloblastoma / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D002455:Cell Division; D006801:Humans; D007124:Immunoenzyme Techniques; D007573:Jaw Neoplasms / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins / Q000032:analysis / Q000096:biosynthesis*; D009687:Nuclear Proteins / Q000032:analysis / Q000096:biosynthesis*; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis / Q000096:biosynthesis*
chemical_list: D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen