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Evidence for post‐transcriptional down‐regulation of the apoptosis‐related gene bcl‐2 in human colorectal cancer
Author(s) -
Berney Christophe R.,
Downing Sean R.,
Yang JiaLin,
Russell Pamela J.,
Crowe Philip J.
Publication year - 2000
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(200005)191:1<15::aid-path566>3.0.co;2-e
Subject(s) - dysplasia , immunohistochemistry , oncogene , adenoma , messenger rna , colorectal cancer , in situ hybridization , cancer , cancer research , biology , pathology , colorectal adenoma , microbiology and biotechnology , medicine , gene , cell cycle , genetics
This retrospective study was undertaken to investigate the expression of bcl‐2 protein and messenger RNA in colorectal cancer (CRC). Immunohistochemical analysis using a monoclonal mouse antibody to the bcl‐2 protein and in situ hybridization using a digoxigenin‐labelled bcl‐2 cRNA probe were carried out on formalin‐fixed and paraffin‐embedded specimens from 53 colorectal adenocarcinomas, 27 liver secondaries, and 60 adenomas with various degrees of dysplasia. Normal human tonsil sections were used as positive controls. Expression of bcl‐2 protein and of messenger RNA was evaluated semiquantitatively. The expression of bcl‐2 protein was gradually and significantly lost during the progression from moderately dysplastic adenoma to primary CRC (moderate/severe dysplasia: Mann–Whitney U ‐test, p =0.0001; severe dysplasia/primary CRC: p =0.027), whereas the cellular expression of bcl‐2 mRNA was gradually increased during the dysplasia/adenoma–carcinoma neoplastic sequence. These observations suggest that in a proportion of colorectal cancer cases, the bcl‐2 proto‐oncogene expression may be down‐regulated at a post‐transcriptional level. Copyright © 2000 John Wiley & Sons, Ltd.