Abstract
We have found that the anti-apoptotic Bcl-2 family protein, Bcl-w, was frequently expressed in colorectal adenocarcinomas, with 69/75 showing positive staining with anti-Bcl-w IgG. Adenomas demonstrated a much lower frequency of Bcl-w expression (only 1 of 17), as did adenocarcinomas from other epithelial tissues such as breast (0/8), stomach (1/12) and cervix (0/12). Bcl-w status could be related to the histopathological classification of the tumours, with TNM stage III tumours showing significantly higher levels of expression than tumours of better prognostic grade (at P = 0.009). Those patients with node involvement also had tumours with significantly elevated levels of Bcl-w (at P = 0.02), compared to those which were node-negative. The results suggest that Bcl-w could play a general role in the progression from adenoma to adenocarcinoma in the colorectal epithelium. Currently, more data are being collected to allow us to assess the importance of Bcl-w for disease progression and patient survival. © 2000 Cancer Research Campaign
Keywords: Bcl-w, colorectal cancer, p53
Full Text
The Full Text of this article is available as a PDF (1.5 MB).
Footnotes
Some of the data included in this study was originally presented as a poster at the joint IACR/BACR meeting, at Trinity College, Dublin, June 1998. The poster contained data from 50 cases and showed the same trends as reported here. The addition of new cases to the study has shown that the relationship between p53 and Bcl-w expression is significant, although we were unable to report this as such in the initial presentation. In the initial study we did report that tetraploid tumours had significantly elevated Bcl-w expression. Although we still see a strong association between increased ploidy and increased Bcl-w expression, we can no longer report this as being significant.
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- Gagos S., Hopwood V. L., Iliopoulos D., Kostakis A., Karayannakos P., Yatzides H., Skalkeas G. D., Pathak S. Chromosomal markers associated with metastasis in two colon cancer cell lines established from the same patient. Anticancer Res. 1995 Mar-Apr;15(2):369–378. [PubMed] [Google Scholar]
- Gibson L., Holmgreen S. P., Huang D. C., Bernard O., Copeland N. G., Jenkins N. A., Sutherland G. R., Baker E., Adams J. M., Cory S. bcl-w, a novel member of the bcl-2 family, promotes cell survival. Oncogene. 1996 Aug 15;13(4):665–675. [PubMed] [Google Scholar]
- Ross A. J., Waymire K. G., Moss J. E., Parlow A. F., Skinner M. K., Russell L. D., MacGregor G. R. Testicular degeneration in Bclw-deficient mice. Nat Genet. 1998 Mar;18(3):251–256. doi: 10.1038/ng0398-251. [DOI] [PubMed] [Google Scholar]
- Vindeløv L. L., Christensen I. J. A review of techniques and results obtained in one laboratory by an integrated system of methods designed for routine clinical flow cytometric DNA analysis. Cytometry. 1990;11(7):753–770. doi: 10.1002/cyto.990110702. [DOI] [PubMed] [Google Scholar]
- Watson A. J., Merritt A. J., Jones L. S., Askew J. N., Anderson E., Becciolini A., Balzi M., Potten C. S., Hickman J. A. Evidence of reciprocity of bcl-2 and p53 expression in human colorectal adenomas and carcinomas. Br J Cancer. 1996 Apr;73(8):889–895. doi: 10.1038/bjc.1996.178. [DOI] [PMC free article] [PubMed] [Google Scholar]