Beham, A. and Dietmaier, W. and Vogel, M. and Rentsch, M. and Farkas, S. and Ruschof, J. and Jauch, Karl-Walter (1999) Loss of BAK expression correlates with MSI in colon cancer. LANGENBECKS ARCHIVES OF SURGERY. pp. 547-550. ISSN 1435-2443,
Full text not available from this repository.Abstract
Background: Genomic mutations of DNA mismatch repair enzymes are associated with genomic instability and are a common denominator of cancer resulting in familiar clustering of colon cancer also known as HNPCC. The tumors exhibit paradoxical low incidence of somatic mutations in the p53 tumor suppresser gene but defects of DNA repair enzymes are associated with frameshift mutations of the proapoptotic gene bar. Bar is member of the bcl-2 family which can be broadly categorized as death antagonists and death agonists of programmed cell death. Methods: To analyze expression of bcl-2 family members in the context of genomic instability samples of 61 patients with colon cancers were embedded in formalin. Expression of bcl-2 (6-C8), bcl-xl (Santa Cruz H-62), bcl-w (Santa Cruz N-19) and bak (Santa Cruz G-23) were analyzed by immunohistochemistry. Further genomic instability was assessed by PCR with the reference panel of the American Joint Commission of Cancer. Results: 22.9% of tumors showed evidence of genomic instability. No bak expression was seen in 56% of instable tumors and 32% of stable tumors. There was no difference in bcl-2 (14% vs. 12%) and bcl-w (0% vs. 0%) expression. Conclusion: These data suggest that genomic instability is associated with loss of bak expression in colon cancer. The lack of death agonists but not the overexpression of death antagonists might contribute to tumor progression in colon cancer with genomic instability.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | MUTATIONS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 30 Nov 2022 09:55 |
| Last Modified: | 30 Nov 2022 09:55 |
| URI: | https://pred.uni-regensburg.de/id/eprint/48689 |
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