title: Maspin, p53, p63, and Ki-67 in epithelial lesions of the tongue: from hyperplasia through dysplasia to carcinoma.
abstract: BACKGROUND
  The pattern of changes in the expression of mammary serine protease inhibitor (maspin) tumor suppressor protein in tongue epithelial lesions [hyperplasia (HP), mild dysplasia (MD), moderate-to-severe dysplasia (MSD) and squamous cell carcinoma (SCC)] was investigated and correlated to the expression of maspin-regulating factors p53 and p63, and the proliferation marker Ki-67.
  
  
  METHODS
  Cases of HP (n = 16), MD (n = 12), MSD (n = 11), and SCC (n = 22) were immunostained for maspin, p53, p63, and Ki-67. Maspin expression was scored separately for the basal, middle, and upper thirds of the epithelial width, and as the total sum of all 'thirds' (maspin-total). p53, p63, and Ki-67 were immuno-morphometrically assessed for the entire epithelial width.
  
  
  RESULTS
  Maspin expression was differential and progressive extending to higher epithelial layers as dysplastic changes aggravated and culminated in carcinoma. Strong expression was related to MSD in the middle third and to carcinoma in the upper third. It was frequently lost at the invasion front, where the tumor was less differentiated. The changes in mean scores of maspin-total in the different study groups were positively correlated to the mean scores of p63 (r = 0.5, P < 0.001), p53 (r = 0.4, P = 0.004), and Ki-67 (r = 0.5, P < 0.001).
  
  
  CONCLUSIONS
  Strong expression of maspin in the middle third of the epithelium may be considered a diagnostic sign of mild-to-moderate dysplasia and an indication of carcinoma in the upper third. The correlations between maspin and controlling factors (e.g. p63 and p53) may be events with key roles in the development of tongue carcinoma.
authors.affiliation: Department of Oral Pathology and Oral Medicine, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel. mvered@post.tau.ac.il
authors.forename: Marilena
authors.initials: M
authors.lastname: Vered
authors.forename: Irit
authors.initials: I
authors.lastname: Allon
authors.forename: Dan
authors.initials: D
authors.lastname: Dayan
mesh_terms: D014408:Biomarkers, Tumor / Q000096:biosynthesis*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology; D002471:Cell Transformation, Neoplastic; D004847:Epithelial Cells / Q000473:pathology; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism; D019394:Ki-67 Antigen / Q000096:biosynthesis; D007972:Leukoplakia, Oral / Q000378:metabolism* / Q000473:pathology; D015843:Serpins / Q000096:biosynthesis*; D014062:Tongue Neoplasms / Q000378:metabolism* / Q000473:pathology; D015534:Trans-Activators / Q000096:biosynthesis; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D025521:Tumor Suppressor Proteins / Q000096:biosynthesis
chemical_list: D014408:Biomarkers, Tumor; D019394:Ki-67 Antigen; C085344:SERPIN-B5; D015843:Serpins; C115051:TP63 protein, human; D015534:Trans-Activators; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins