Apoptosis, a distinct mode of cell death, is responsible for the deletion of cells in normal tissues and occurs in specific pathological contexts. It is characterized by rapid condensation and budding of the cell, forming membrane-enclosed apoptotic bodies that are phagocytosed and digested by nearby cells without inflammation. Key biochemical features include double-strand cleavage of nuclear DNA at internucleosomal regions, leading to the production of oligonucleosomal fragments. Apoptosis is suppressed by inhibitors of mRNA and protein synthesis in many circumstances but can be regulated by certain proto-oncogenes and the p53 tumor suppressor gene. In tumors, apoptosis is often suppressed, but it can be induced by various treatments such as irradiation, cytotoxic chemotherapy, heating, and hormone ablation. The discovery that certain proto-oncogenes, like c-myc and bcl-2, and the p53 gene can regulate apoptosis has opened new avenues for cancer research and therapy. For example, c-myc expression can initiate apoptosis in some situations, while bcl-2 inhibits it. The involvement of the APO-1 or Fas antigen in apoptosis induction by antibodies and the role of p53 in enhancing apoptosis in tumor-derived cell lines are also discussed. Understanding the genetic regulation of apoptosis, including the roles of c-myc, c-fos, and bcl-2, is crucial for developing improved cancer treatments and overcoming resistance to therapy.Apoptosis, a distinct mode of cell death, is responsible for the deletion of cells in normal tissues and occurs in specific pathological contexts. It is characterized by rapid condensation and budding of the cell, forming membrane-enclosed apoptotic bodies that are phagocytosed and digested by nearby cells without inflammation. Key biochemical features include double-strand cleavage of nuclear DNA at internucleosomal regions, leading to the production of oligonucleosomal fragments. Apoptosis is suppressed by inhibitors of mRNA and protein synthesis in many circumstances but can be regulated by certain proto-oncogenes and the p53 tumor suppressor gene. In tumors, apoptosis is often suppressed, but it can be induced by various treatments such as irradiation, cytotoxic chemotherapy, heating, and hormone ablation. The discovery that certain proto-oncogenes, like c-myc and bcl-2, and the p53 gene can regulate apoptosis has opened new avenues for cancer research and therapy. For example, c-myc expression can initiate apoptosis in some situations, while bcl-2 inhibits it. The involvement of the APO-1 or Fas antigen in apoptosis induction by antibodies and the role of p53 in enhancing apoptosis in tumor-derived cell lines are also discussed. Understanding the genetic regulation of apoptosis, including the roles of c-myc, c-fos, and bcl-2, is crucial for developing improved cancer treatments and overcoming resistance to therapy.