DIET, SIGNAL-TRANSDUCTION AND CARCINOGENESIS

The defects in the regulation of cell growth and differentiation that manifest themselves as cancer result from multiple defective genes and their products, which are involved in the processes of cellular signa ling, regulation of gene expression and control of the cell through it s replication cycle. Each of these molecular defects represents a new target for development of novel therapeutic agents and prophylactic in terventions. Evidence suggests that such therapeutic agents will show great efficacy for cells made cancerous by the single targeted defect. However, poor anticancer efficacy for clinically presenting cancer ma y occur as a result of the multiple molecular lesions. A combined-agen t approach seems likely to be more successful, but this will require d iagnosis of each tumor in substantially greater detail, down to the mo lecular level. When such molecular diagnosis becomes generally feasibl e, it should be possible to use combinations of highly specific agents at very low doses for therapy and ultimately for prevention of tumor metastasis. Chemoprevention in general may be achieved more easily tha n therapy with mechanism-based interventions, as certain individual le sions, in theory, may be rate limiting for carcinogenesis but may not be a significant contributor to the neoplastic phenotype by the time t he tumor presents in the clinic.