Sustained specificity

he rising incidence of senescent cells during aging may promote cancer development, according to Judith Campisi (Lawrence Berkeley National Laboratory, Berkeley, CA) and colleagues. They propose that evolution may have selected a useful function for cellular senescence early in life—the switching-off of cells that are prone to becoming cancerous— without any consideration of how these cells might behave later on in life. It is not the senescent cells themselves that become cancerous, however. Rather, these fibroblast cells produce soluble factors, matrix, and perhaps cell-surface molecules that cause cocultured preneoplastic or neoplastic epithelial cells to proliferate and form tumors in nude mice. Cocultured primary epithelial cells are not affected. The effect on proliferation may be an unwanted byproduct of the senescence expression program, which includes increased levels of an odd mixture of molecules. Only a few of these molecules are involved in cell cycle arrest, but a number may promote epithelial proliferation. Campisi says that the expression mix may have arisen when evolution co-opted an existing program involved in wound healing to shut down the cell division of senescent fibroblasts. Wounding eventually blocks fibroblast division, as is required T