Abstract

This presentation will summarize data derived from Drosophila tumour models on how unscheduled gene expression impinge on tumour initiation and malignant growth. Most of the malignant tumours that can be experimentally induced in flies are larval brain tumors caused by loss-of-function of any of several genes that control the asymmetric division of neural precursors. However, there is a different type of fly cancer model that derives from the neuroepithelium. In the latter, genes that are normally expressed in germline cells become aberrantly activated. In the human oncology literature, these genes are referred to as cancer-testis, or cancer-germline genes. Direct proof of the functional relevance of such genes in human malignancy is still lacking, but research on the fly models is unveiling unsuspected functions of these genes that may have direct therapeutic implications. Another key aspect of human malignant growth that Drosophila tumour models recapitulate well is genome instability. Through ongoing experiments on this front we are currently addressing the cause-effect relation between genome instability and malignant growth and how the former can be used to inhibit the latter.