APOPTOSIS OCCURS INDEPENDENTLY OF BCL-2 AND P53 OVER-EXPRESSION IN NONSMALL CELL LUNG-CARCINOMA

Citation
Aj. Oneill et al., APOPTOSIS OCCURS INDEPENDENTLY OF BCL-2 AND P53 OVER-EXPRESSION IN NONSMALL CELL LUNG-CARCINOMA, Histopathology, 29(1), 1996, pp. 45-50
Citations number
50
Categorie Soggetti
Cell Biology",Pathology
Journal title
ISSN journal
03090167
Volume
29
Issue
1
Year of publication
1996
Pages
45 - 50
Database
ISI
SICI code
0309-0167(1996)29:1<45:AOIOBA>2.0.ZU;2-A
Abstract
Certain oncogenes and tumour suppressor genes are known to modulate ap optosis. To investigate whether overexpressed bcl-2 and abnormally sta bilized p53 are associated with reduced apoptosis in paraffin sections of non-small cell lung carcinoma, apoptotic, mitotic, and Ki-67 label ling indices were determined and correlated with bcl-2 and p53 immunor eactivity in 54 squamous cell carcinomas and 22 adenocarcinomas. Ninet een squamous cell carcinomas (35.2%) showed over-expression of bcl-2, but all 22 adenocarcinomas were bcl-2 negative. Thirty-seven squamous cell carcinomas (68.5%) and 13 adenocarcinomas (59.1%) showed p53 over -expression. Apoptotic tumour cells were identified among p53 positive and bcl-2, positive tumour cells. There was a significant linear corr elation between apoptotic indices and mitotic indices, bcl-2 over-expr ession and p53 over-expression were not associated with attenuated apo ptosis, or altered mitotic or Ki-67 labelling indices in either tumour type. Neither bcl-2 nor p53 was of prognostic significance. These res ults suggest that apoptosis in non-small cell lung carcinoma occurs in dependently, and is not modulated primarily by, bcl-2 or p53. It is li kely that the effects on apoptosis of bcl-2 and p53 are countered by t hose of other oncogene products and/or additional factors that regulat e apoptosis in vivo.