Molecular cytogenetic identification of cyclin D1 gene amplification in a renal pelvic tumor attributed to phenacetin abuse.

Abstract

Despite extensive epidemiologic evidence of phenacetin abuse as a risk factor for renal pelvic carcinomas, genetic alterations in the resultant tumors remain largely unclear. In this report, a phenacetin-associated renal pelvic carcinoma (histologically a transitional-cell carcinoma) from an 80-year-old female patient was evaluated by molecular cytogenetic methods. Fluorescence in situ hybridization was used to identify chromosome gains or losses for the cyclin D1, p53, Rb and c-myc genes and the ploidy of their respective chromosomes. Cyclin D1 gene amplification, but normal copy numbers of p53, Rb and c-myc, and normal ploidy of chromosomes 8, 11, 13 and 17 were observed. Expression of cyclin D1 protein was confirmed by immunohistochemistry. In the absence of p53, Rb or c-myc abnormalities, the results suggested that cyclin D1 gene amplification and its protein overexpression may be involved in the genesis of renal pelvic carcinomas associated with phenacetin abuse.

• Authors: C C Lee, H Wanibuchi, S Yamamoto, M Hirose, Y Hayashi, S Fukushima
• Journal: Pathology international (Pathol Int) Vol. 49 Issue 7 Pg. 648-52 (Jul 1999) ISSN: 1320-5463 [Print] Australia
• PMID: 10504527 (Publication Type: Case Reports, Journal Article)

Chemical References

• Analgesics, Non-Narcotic
• Cyclin D1
• Phenacetin

Topics

• Aged
• Aged, 80 and over
• Analgesics, Non-Narcotic (adverse effects)
• Carcinoma, Transitional Cell (chemically induced, genetics, pathology)
• Chromosomes, Human (genetics)
• Cyclin D1 (analysis)
• Fatal Outcome
• Female
• Genes, Retinoblastoma (genetics)
• Genes, bcl-1 (genetics)
• Genes, myc (genetics)
• Genes, p53 (genetics)
• Humans
• Immunoenzyme Techniques
• In Situ Hybridization, Fluorescence
• Kidney Neoplasms (chemically induced, genetics, pathology)
• Kidney Pelvis (drug effects, pathology)
• Phenacetin (adverse effects)
• Ploidies