Tumor Suppressor Genes which Encode Transcriptional Repressors: Studies on the EGR and Wilms’ Tumor (WT1) Gene Products

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Abstract
Over the past 15 years a revolution has occurred in our understanding of the cellular and molecular bases of neoplastic transformation and subsequent tumor formation. The recognition that neoplastic cell growth is a stable, heritable cellular phenotype led directly to the cloning of specific genetic loci from human tumor DNAs (termed oncogenes) which could convert a normal cell into a malignant cell (reviewed in reference 1). The remarkable finding that many oncogenic murine and avian retroviruses carried mutated versions of these cellular oncogenes gave further support for the oncogene hypothesis.1 Support for the relevance of oncogenes to human disease has come from the realization that many of these cancer-genes are “activated” (either by mutation, over-expression, or inappropriate expression) in many human tumor specimens.2