A framework for drug-induced apoptosis can now be articulated, in which intrinsic and extrinsic survival signals, as well as drug-induced death signals, are balanced. Pro-apoptotic members of the Bcl-2 family of proteins are influenced by pro-apoptotic signals, which ultimately govern cellular fate. This approach identifies many places where therapeutic interventions could be performed to overcome medication resistance, as well as new biological targets for cancer cell death induction. Chemotherapy has had a great deal of success in the treatment of several cancers. Before 1980, the five-year disease-free survival rate in children with acute lymphoblastic leukemia was 39%; by the end of the 1990s, it had risen to 63%. Chemotherapy, on the other hand, has had a negative impact on adult epithelial malignancies such as breast, colon, and lung carcinomas. The expectation that a better understanding of how cells, both normal and malignant, die following drug-induced damage will lead to advancements in chemotherapy was one motivation for the growing interest in apoptosis research.
