title: Malignant worms: what cancer research can learn from C. elegans.
abstract: Developmental processes in the nematode C. elegans are controlled by pathways of gene functions that are analogous to those used in mammals. Hence, genetic studies in C. elegans have helped build the frameworks for these regulatory pathways. Many homologs of human genes that are targets for mutation in cancer have been found to function at distinct steps within such genetic pathways. This way, studies in C. elegans have provided important clues about the functions of human oncogenes and tumor suppressors. Understanding how human cancer genes function and act in signaling cascades is of great importance. This information reveals what kind of molecular changes contribute to the process of cell transformation. Moreover, additional candidate oncogenes and tumor suppressors may be revealed by identifying the functional partners of genes with an established role in cancer. Furthermore, identifying a cascade of gene functions increases the number of potential targets for therapeutic intervention, as blocking either one of multiple genes may interfere with signal transduction through the pathway. Simultaneous approaches in a number of different model systems act synergistically in solving pathways of gene functions. By using multiple models, the field takes advantage of the strengths of each system and circumvents its limitations. As one of the most powerful genetic animal systems, C. elegans will continue to reveal new mammalian signaling components. In addition, now that the C. elegans genome sequence has been completed, an increasing number of researchers are likely to discover homologs of human disease genes in the nematode and to analyze gene function in the worm model. Combined with the great potential of this animal in drug screens, it is simple to predict that C. elegans will worm its way deeper and deeper into cancer research.
authors.affiliation: Massachusetts General Hospital Cancer Center, Building 149, 13th Street, Charlestown, MA 02129, USA.
authors.forename: R Mako
authors.initials: RM
authors.lastname: Saito
authors.forename: Sander
authors.initials: S
authors.lastname: van den Heuvel
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D017173:Caenorhabditis elegans / Q000166:cytology / Q000235:genetics / Q000502:physiology*; D017124:Conserved Sequence; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*