Urology Medical News about Topoisomerase II α renal medullary carcinoma

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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.

Methods

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.

Results

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.