Targets in Apoptosis Signaling: Promise of Selective Anticancer Therapy
The human body is composed of approximately 1014 cells, each of which is capable of committing suicide by apoptosis. Normally, the processes of cell division and cell death are tightly coupled, so that no net increase in cell numbers occurs. However, alterations in the expression or function of the genes that control cell division and cell death can upset this delicate balance, contributing to expansion of neoplastic cells causing cancers. While the existing, conventional anticancer drugs either cause cell cycle perturbation or DNA damage, they do not interact directly with the intracellular machinery for apoptosis. Tumor selectivity of such agents is due largely to the increased sensitivity to apoptosis of tumor cells following DNA damage or cell cycle perturbation. The study of the molecular basis of cancer has generated the promise of identifying new targets for more selective and molecularly focused anticancer therapies. This chapter describes several novel therapeutic agents or strategies that target critical regulators or effectors of apoptosis. These agents or strategies have the potential to exert selective cytotoxicity against cancer cells and are currently under investigation.
- DNA-Dependent Protein Kinase in Apoptosis
- Mutational Analysis of Oncogenes and Tumor Suppressor Genes in Human Cancer Using Denaturing Gradient Gel Electrophoresis
- Cancer Screenings, Diagnostic Technology Evolution, and Cancer Control
- Morphological Assessment of Apoptosis in Human Lung Cells
- Cell Cycle and Drug Sensitivity
- Ligand-Coupled Lipoprotein for Ovarian Cancer-Specific Drug Delivery
- Analysis of Apoptosis in Tissue Sections
- Targeted Alpha Therapy of Prostate Cancer
- Apoptosis: A Technical Overview
- Chimerization of a Monoclonal Antibody for Treating Hodgkin's Lymphoma