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Apoptosis occurs independently of bcl‐2 and p53 over‐expression in non‐small cell lung carcinoma
Author(s) -
O'NEILL A.J.,
STAUNTON M.J.,
GAFFNEY E.F.
Publication year - 1996
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.1996.d01-478.x
Subject(s) - apoptosis , biology , cancer research , mitosis , cell , carcinoma , oncogene , mitotic index , adenocarcinoma , pathology , cell cycle , cancer , medicine , microbiology and biotechnology , genetics
Certain oncogenes and tumour suppressor genes are known to modulate apoptosis. To investigate whether over‐expressed bcl‐2 and abnormally stabilized p53 are associated with reduced apoptosis in paraffin sections of non‐small cell lung carcinoma, apoptotic, mitotic, and Ki‐67 labelling indices were determined and correlated with bcl‐2 and p53 immunoreactivity in 54 squamous cell carcinomas and 22 adenocarcinomas. Nineteen 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 correlation between apoptotic indices and mitotic indices. bcl‐2 over‐expression and p53 over‐expression were not associated with attenuated apoptosis, or altered mitotic or Ki‐67 labelling indices in either tumour type. Neither bcl‐2 nor p53 was of prognostic significance. These results suggest that apoptosis in non‐small cell lung carcinoma occurs independently, and is not modulated primarily by, bcl‐2 or p53. It is likely that the effects on apoptosis of bcl‐2 and p53 are countered by those of other oncogene products and/or additional factors that regulate apoptosis in vivo