Homozygous deletions of p16INK4 occur frequently in bilharziasis-associated bladder cancer
β Scribed by Yahya Tamimi; Pierre Paul Bringuier; Frank Smit; Adrie van Bokhoven; Ahmed Abbas; Frans M.J. Debruyne; Jack A. Schalken
- Book ID
- 102653691
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- French
- Weight
- 644 KB
- Volume
- 68
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
β¦ Synopsis
We have studied p16(INK4) mutation (by PCR-SSCP) and deletion (by Southern blotting and/or multiplex PCR) in a series of 47 bilharziasis-associated tumors from Egypt and compared the results with those obtained on a series of 17 established bladder cell lines and non-bilharziasis-associated bladder cancers from the Netherlands. In the cell lines we found 9 homozygous deletions and 1 mutation (59% of p16(INK4) alterations in cell lines), whereas in cases from the Netherlands deletions were found in 4 of 22 samples. No mutations were detected in the 46 samples screened. Interestingly, in bilharziasis-associated bladder cancer, deletions were present in 23 samples and mutations in a further 2 cases (53% of p16(INK4) alteration in bilharziasis-associated bladder cancer). No correlation was found between p16(INK4) alteration and histopathological data. Likewise, the same frequency of alteration was found in tumors with different differentiation patterns (squamous, transitional or adenocarcinoma). Three conclusions can be drawn from our findings: (i) p16(INK4) alterations are more frequent in cell lines than in primary tumors; (ii) in primary bladder tumors (bilharziasis-associated or not), p16(INK4) deletions are much more frequent than p16(INK4) mutations; (iii) p16(INK4) alterations are more frequent in bilharziasis-associated bladder tumors than in other bladder tumors. This high frequency of deletion is not related to a specific histological type but to the specific etiology of these tumors.
π SIMILAR VOLUMES
Inactivation of p16(INK4a) in the Rb pathway is among the most common somatic alterations observed in nonsmall cell lung cancers (NSCLCs). While epigenetic inactivation of the p16(INK4a) gene promoter has been shown to be associated with increased tobacco carcinogen exposure, little investigation of
Deletion of all or part of chromosome 9 is a well-described genetic alteration in bladder tumors. It has been proposed that inactivation of a tumor-suppressor gene on chromosome 9 is an important event in tumor development. Recent reports have supported cyclin-dependent kinase inhibitor 2 (CDKN2, al