Apoptosis and mitosis in oral and oropharyngeal epithelia: Evidence for a topographical switch in premalignant lesions

Birchall, M., Winterford, C., Tripconi, L., Gobe, G. and Harmon, B. (1996) Apoptosis and mitosis in oral and oropharyngeal epithelia: Evidence for a topographical switch in premalignant lesions. Cell Proliferation, 29 8: 447-456. doi:10.1111/j.1365-2184.1996.tb00987.x


Author Birchall, M.
Winterford, C.
Tripconi, L.
Gobe, G.
Harmon, B.
Title Apoptosis and mitosis in oral and oropharyngeal epithelia: Evidence for a topographical switch in premalignant lesions
Journal name Cell Proliferation   Check publisher's open access policy
ISSN 0960-7722
Publication date 1996-08
Sub-type Article (original research)
DOI 10.1111/j.1365-2184.1996.tb00987.x
Volume 29
Issue 8
Start page 447
End page 456
Total pages 10
Place of publication Oxford, United Kingdom
Publisher Wiley-Blackwell
Language eng
Abstract Apoptosis (programmed cell death) may play a part in carcinogenesis. The mucosa of the oral cavity, a common site for the development of dysplasia and squamous cell carcinoma, is ideal for the study of carcinogenesis in vivo. Earlier work suggested that apoptosis falls with the development of carcinoma, and that carcinogenesis is preceded by topographical changes in apoptosis. To explore these hypotheses, 72 paraffin sections were obtained: 15 normal (N), nine mild dysplasia (D), 15 severe dysplasia/carcinoma in situ (CIS), 30 squamous cell carcinoma (SCC: power analysis suggested 15 per group). Apoptotic (AI) and mitotic (MI) indices and AT/MI ratio were calculated (1000 cells/slide). These, with age, sex, alcohol and smoking habits, and anatomical subsite, were entered into a regression model with histological group as dependent. Vertical cell position (cp) was plotted, and resultant frequency curves were compared. MI significantly increased (mean N 0.39, 95% confidence interval 0-0.35; D 0.63, 0.23-0.98; SCC 0.86, 0.51-1.21, P < 0.0001) and AI/MI significantly decreased (D 0.54, 0.20-0.86; SCC 0.28, 0.05-0.61, P < 0.05) progressing from D, through CIS, to SCC. However, after inclusion of all variables, only MI remained significant (P < 0.0001). Peak incidence of mitosis shifted downwards in CIS relative to N and D, whilst peak apoptosis shifted upwards. Thus, programmed cell death remains static as mitosis increases in carcinogenesis of the oral cavity. However, there is an alteration in the topographical relationship of these events in CIS which may make homeostatic mechanisms involving apoptosis less efficient.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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