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Topoisomerase II α status in renal medullary carcinoma: immuno-expression and gene copy alterations of a potential target of therapy
The Journal of Urology, 07/23/09

Albadine R et al. – In a study to evaluate topoisomerase II α expression in relation to the proliferation index and topoisomerase II α gene copy number status in a large series of pts with renal medullary carcinoma (RMC), it was found that topoisomerase II α is overexpressed in 85% of RMC, potentially supporting the use of topoisomerase II α inhibitor agents to treat this aggressive renal tumor. Topoisomerase II α overexpression in the RMC cohort was not due to gene amplification, but rather to transcriptional or post–transcriptional modifications.

• Archival tissues from 14 renal medullary carcinomas were retrieved.
• Immunohistochemistry was performed using monoclonal antibodies for topoisomerase II α and Ki67.
• The percent of cells with positive nuclear staining was assessed in the highest area of expression for each marker.
• A previously suggested >5% cutoff was used for topoisomerase II α overexpression.
• Topoisomerase II α gene copy number was evaluated using fluorescence in situ hybridization.
• Locus–specific topoisomerase II α gene and chromosome 17 centromere probes were used.
• Total number of topoisomerase II α and chromosome 17 centromere signals was counted in 150 cells per tumor and a topoisomerase II α–to–chromosome 17 centromere signal ratio was calculated in each tumor.
• A topoisomerase II α–to–chromosome 17 centromere ratio of ≥2.0 and <0.8 was used as a cutoff for amplification and deletion, respectively.
• Percent of tumor cells with polysomic, eusomic, or monosomic chromosome 17 status was also determined.

• On immuno–expression analysis, topoisomerase II α immunohistochemistry was technically inconclusive in 1 RMC.
• Topoisomerase II α was overexpressed in 11 of 13 RMCs (85%).
• High Ki67 proliferation index was noted in 13 of 14 tumors; Ki67 expression was greater than topoisomerase II α expression in all 13 informative tumors.
• A strong, statistically significant correlation was found for topoisomerase II α and Ki67 expression.
• Topoisomerase II α overexpression was associated with shorter survival.
• On fluorescence in situ hybridization, no topoisomerase II α amplification was detected in any of the 14 RMCs, including 11 with topoisomerase II α overexpression.
• Topoisomerase II α gene deletions were noted in 4 tumors.
• 2 of 4 deletions were associated with chromosome 17 monosomy and 2 were in eusomic chromosome 17 tumors.

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