Serth, J. and Kuczyk, M. and Machtens, S. and Bokemeyer, C. and Herrmann, R. and Hartmann, J and Knuechel, Ruth and Jonas, U. (1999) Analysis of the cyclin-dependent kinase inhibitor p27(Kip1) in muscle invasive bladder cancer. ONCOLOGY REPORTS, 6 (1). pp. 229-233. ISSN 1021-335X,
Full text not available from this repository.Abstract
It has been suggested that a deregulated cell cycle control contributes to the development of human malignancies due to the lass of critical antiproliferative mechanisms. The cell cycle is controlled at two checkpoints, one at the G1-S and another at the G2-M transition. Several genes including the structurally related p21(WAF/CIP1) gene, the downstream mediator of the p53 tumor suppressor gene, and the p27(Kip1) gene have been identified as inducers of cell cycle arrest at the G1 checkpoint when substantial DNA damage has occurred to avoid further replication of the altered genome. Recently, a heat stable 27 kDa protein, the transcript of the p27(Kip1) gene, has been identified and was suggested to substantially participate in cell cycle control at the GI checkpoint. Previous investigations have correlated decreased expression of the p27(Kip1) protein with an increased biological aggressiveness of breast and small cell lung cancer. However, the moleculargenetic analysis of a variety of human malignancies including prostate cancer failed to identify any alteration at the p27(Kip1) gene locus, therefore suggesting a loss of p27(Kip1) protein expression to result from post-transcriptional/posttranslational events or from so far unknown regulatory mechanisms. So far, bladder cancer specimens have neither been investigated for p27(Kip1) alterations on the DNA level, nor has the result of moleculargenetic analysis been correlated with an immunohistochemically detected expression of the gene product, the p27(Kip1) protein. The present study is the first to describe p27(Kip1) gene alterations on the DNA level in 3 of 42 muscle invasive bladder cancer specimens. In contrast, loss of p27(Kip1) protein expression was observed in 14 of 42 (33%) tumors. According to the previously reported observation in a variety of human malignancies, in bladder cancer loss of p27(Kip1) protein expression seems to result from post-transcriptional or posttranslational events.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CELL-CYCLE; BREAST-CANCER; CDK INHIBITOR; EXPRESSION; ARREST; GENE; CARCINOMAS; FAMILY; P27; D1; bladder cancer; cell cycle control; cyclins; p27(Kip1) gene |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 05 Dec 2022 07:52 |
| Last Modified: | 05 Dec 2022 07:52 |
| URI: | https://pred.uni-regensburg.de/id/eprint/48710 |
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