The term 'cellular senescence' has often been applied indiscriminately to a
ny form of growth arrest of cultured cells that occurs either after some pe
riod in culture or following insults such as the overexpression of oncogene
s. Recent reports have suggested there may be many mechanisms of cellular s
enescence. Our increasing understanding of the role of telomere shortening
in the replicative aging of cultured fibroblasts now permits a re-examinati
on of what may reasonably be called cellular senescence, and what most like
ly represents artifacts of the culture environment and/or specific cell-cyc
le control mechanisms.