Cellular senescence is a critical mechanism in mammalian cells that suppresses tumorigenesis. It is characterized by a stable loss of proliferative capacity, despite continued viability and metabolic activity. Replicative senescence occurs due to telomere shortening, which triggers a DNA damage response (DDR), leading to cell cycle arrest. This process is mediated by the p53 and p16INK4A-RB pathways. Senescence can also be induced by oncogene activation (oncogene-induced senescence, OIS), DNA damage, or loss of tumor suppressors. OIS is distinct from replicative senescence as it cannot be bypassed by telomerase expression. Senescence is associated with morphological changes, increased SA-β-GAL activity, and the formation of senescence-associated heterochromatic foci (SAHF). Senescent cells also secrete factors that can promote tumor growth, highlighting the dual role of senescence in both tumor suppression and tumor promotion. Senescence is identified by various biomarkers, including cell cycle arrest, increased SA-β-GAL activity, and the accumulation of p16INK4A, p53, and other cell cycle inhibitors. However, these markers are not sufficient on their own to identify senescent cells. The role of senescence in vivo is complex, with evidence of its involvement in aging and age-related diseases, as well as its tumor-suppressive function. Senescence can be reversed in some cases, but it is generally irreversible. The study of senescence has important implications for cancer biology, as it provides a mechanism for tumor suppression and may be a target for cancer therapy. The identification of reliable biomarkers for senescent cells remains a challenge, particularly in vivo. Overall, cellular senescence is a multifaceted process that plays a critical role in maintaining cellular homeostasis and preventing tumorigenesis.Cellular senescence is a critical mechanism in mammalian cells that suppresses tumorigenesis. It is characterized by a stable loss of proliferative capacity, despite continued viability and metabolic activity. Replicative senescence occurs due to telomere shortening, which triggers a DNA damage response (DDR), leading to cell cycle arrest. This process is mediated by the p53 and p16INK4A-RB pathways. Senescence can also be induced by oncogene activation (oncogene-induced senescence, OIS), DNA damage, or loss of tumor suppressors. OIS is distinct from replicative senescence as it cannot be bypassed by telomerase expression. Senescence is associated with morphological changes, increased SA-β-GAL activity, and the formation of senescence-associated heterochromatic foci (SAHF). Senescent cells also secrete factors that can promote tumor growth, highlighting the dual role of senescence in both tumor suppression and tumor promotion. Senescence is identified by various biomarkers, including cell cycle arrest, increased SA-β-GAL activity, and the accumulation of p16INK4A, p53, and other cell cycle inhibitors. However, these markers are not sufficient on their own to identify senescent cells. The role of senescence in vivo is complex, with evidence of its involvement in aging and age-related diseases, as well as its tumor-suppressive function. Senescence can be reversed in some cases, but it is generally irreversible. The study of senescence has important implications for cancer biology, as it provides a mechanism for tumor suppression and may be a target for cancer therapy. The identification of reliable biomarkers for senescent cells remains a challenge, particularly in vivo. Overall, cellular senescence is a multifaceted process that plays a critical role in maintaining cellular homeostasis and preventing tumorigenesis.