Results of novel strategies for treatment of Wilms' tumor

Abstract

The postoperative chemotherapy in stage I disease can be reduced without compromising the cure rate. The treatment of unfavorable stage III and IV disease or relapsed tumor remains a challenge.

Developmental tumourigenesis: NCAM as a putative marker for the malignant renal stem/progenitor cell population

“…Having established the elevation of TOP2A in the NCAM cell fraction, we next determined whether in vitro treatment of heterogeneous WT cells with the topoisomerase inhibitors, Etoposide and Irinotecan influences expression of both TOP2A and NCAM. This was compared to treatment with Cisplatin, used in refractory childhood solid tumours [45, 46] and to untreated WT cells. Etoposide, a topoisomerase II inhibitor had a dramatic effect on TOP2A expression with concomitant reduction in NCAM expression in two of the three tumours evaluated (WOO2 and WOO4, but not in WO1O) in respect to the untreated control.…”

Treatment of Wilms tumor using carboplatin compared to therapy without carboplatin

“…Cyclophosphamide, ifosfamide, cisplatin, carboplatin, and etoposide have also been shown to be active against WT. Multiagent regimens containing these drugs, and particularly the ICE combination (ifosfamide, carboplatin, and etoposide), have raised post‐relapse survival levels to approximately 50–60% . A number of highly effective chemotherapy regimens, including ifosfamide‐carboplatin‐etoposide, cyclophosphamide‐etoposide, and carboplatin‐etoposide, are regarded as the treatment of choice in recurrent cases .…”