• ABSTRACT
    • Carcinogenesis can be triggered by a diverse range of molecular lesions, a variety of which can be illustrated by Wilm's tumor (WT), a pediatric kidney cancer. Molecular defects observed in WTs include several independent targets and mechanisms best exemplified by changes on the short arm of chromosome 11. This article will review the molecular pathology of WT and emphasize the broader ramifications for cancer genetics. Consideration will be given to carcinogenic pathways, novel cellular molecules, and technologies that will assist in the rapid interpretation and assimilation of DNA sequence data arising from the sequencing of the human genome.