Cellular senescence is characterized by stable cell cycle arrest that is 
triggered by various forms of stress stimuli. Senescent cells show a series of 
morphological and physiological alterations including a flat and enlarged 
morphology, an increase in acidic beta-galactosidase activity, chromatin 
condensation, and changes in gene expression pattern. These features are not 
observed in proliferating cells or quiescent cells in vitro. Using these 
senescence markers, cellular senescence has been shown to occur in benign or 
premalignant lesions but not in malignant lesions and to act as a 
tumor-suppressing mechanism in vivo. The onset and maintenance of the senescent 
state are regulated by two tumor suppressor proteins, p53 and Rb, which mediate 
senescence signals through p38 mitogen-activated protein kinase and 
cyclin-dependent kinase inhibitors. Alterations of chromatin structure are 
believed to contribute to the irreversible nature of the senescent state. 
Senescent cells form characteristic heterochromatin structure called 
senescence-associated heterochromatic foci (SAHFs), which may repress the 
expression of proliferation-promoting genes, such as E2F target genes. Recent 
studies have provided molecular insights into the structure and the mechanism of 
SAHF formation. In this paper, we review the role of cellular senescence in 
tumor suppression in vivo and the molecular mechanism of stable growth arrest in 
senescent cells, focusing on the special form of heterochromatin, SAHFs.