Merlin: hanging tumor suppression on the Rac

Cancer can result from any number of abnormalities in the control of cell-c ycle progression, intracellular signaling and transduction of extracellular cues. Many insights into the crucial events that govern the regulation of cell growth have derived from studies of the gene products mutated in inher ited cancer syndromes. Recent work on the neurofibromatosis 2 (NF2) tumor s uppressor gene suggests that this negative growth regulator might function by modulating growth factor and extracellular matrix (ECM) signals that tri gger Rac1-dependent cytoskeleton-associated processes. In this article, we propose a molecular model for NF2 protein (merlin) function in the light of these and related new findings.