Cellular senescence is a stress response that blocks cell proliferation and plays a key role in cancer suppression. It is common in pre-malignant tumors and is essential for preventing tumor progression. Malignant tumors can still undergo senescence if oncogenes are inactivated or tumor suppressors are restored. Senescent tumor cells are cleared by immune cells, leading to efficient tumor regression. Chemotherapy can also induce senescence, contributing to its therapeutic effects. These concepts are well supported in mouse models but need further clinical validation. Senescence is characterized by cell cycle arrest, DNA damage, and telomere shortening. Oncogene-induced senescence (OIS) is a tumor suppressor mechanism similar to oncogene-induced apoptosis. Studies in mice and humans show that senescence is prevalent in pre-malignant tumors but absent in malignant ones. Senescence is induced by oncogenes such as HRAS, Kras, and BRAF, and is regulated by tumor suppressors like p53, INK4A, and ARF. Senescence can be triggered by oncogene inactivation, loss of tumor suppressors, or chemotherapy. Tumor suppressors like PTEN, VHL, NF1, and RB prevent excessive oncogenic signaling, while p53, INK4A, and ARF induce senescence when oncogenic signals are detected. Senescence is a critical barrier to tumor progression and can be harnessed for cancer therapy. Restoring p53 function can induce senescence and tumor regression. Senescence can also be induced by inactivating oncogenes like MYC or KRAS, leading to tumor regression. Senescence is cleared by immune cells, contributing to tumor regression. Senescence is a promising target for cancer therapy, as it can induce tumor cell death and prevent tumor progression. However, senescent cells can also release pro-inflammatory factors that may promote tumor growth. Further research is needed to understand the role of senescence in cancer and to develop effective therapies. Senescence markers such as beta-galactosidase, p16, p21, and p27 are used to detect senescent cells in tumors. These markers, combined with reduced proliferation, provide evidence of senescence in tumors. Senescence is a key mechanism in tumor suppression and may be a valuable target for cancer treatment.Cellular senescence is a stress response that blocks cell proliferation and plays a key role in cancer suppression. It is common in pre-malignant tumors and is essential for preventing tumor progression. Malignant tumors can still undergo senescence if oncogenes are inactivated or tumor suppressors are restored. Senescent tumor cells are cleared by immune cells, leading to efficient tumor regression. Chemotherapy can also induce senescence, contributing to its therapeutic effects. These concepts are well supported in mouse models but need further clinical validation. Senescence is characterized by cell cycle arrest, DNA damage, and telomere shortening. Oncogene-induced senescence (OIS) is a tumor suppressor mechanism similar to oncogene-induced apoptosis. Studies in mice and humans show that senescence is prevalent in pre-malignant tumors but absent in malignant ones. Senescence is induced by oncogenes such as HRAS, Kras, and BRAF, and is regulated by tumor suppressors like p53, INK4A, and ARF. Senescence can be triggered by oncogene inactivation, loss of tumor suppressors, or chemotherapy. Tumor suppressors like PTEN, VHL, NF1, and RB prevent excessive oncogenic signaling, while p53, INK4A, and ARF induce senescence when oncogenic signals are detected. Senescence is a critical barrier to tumor progression and can be harnessed for cancer therapy. Restoring p53 function can induce senescence and tumor regression. Senescence can also be induced by inactivating oncogenes like MYC or KRAS, leading to tumor regression. Senescence is cleared by immune cells, contributing to tumor regression. Senescence is a promising target for cancer therapy, as it can induce tumor cell death and prevent tumor progression. However, senescent cells can also release pro-inflammatory factors that may promote tumor growth. Further research is needed to understand the role of senescence in cancer and to develop effective therapies. Senescence markers such as beta-galactosidase, p16, p21, and p27 are used to detect senescent cells in tumors. These markers, combined with reduced proliferation, provide evidence of senescence in tumors. Senescence is a key mechanism in tumor suppression and may be a valuable target for cancer treatment.