Listeria monocytogenes causes apoptosis in dendritic cells and hepatocytes, thus reducing the risk of an effective host response until systemic infection has been established. Many viral pathogens trigger apoptotic events. Connections between viral latency and apoptosis are now being explored. Epstein-Barr virus appears to produce a bcl homologue during its cell cycle. Oncogenesis Apoptosis and the genes that control it have a profound effect on the malignant phenotype.
Some oncogenic mutations disrupt apoptosis and cause tumor initiation, progression or metastasis.
Other oncogenic changes promote apoptosis and override apoptosis during multistage carcinogenesis. The cellular and molecular processes that result in malignant cell proliferation are multiple and include upregulation of oncogenes as well as downregulation or arrest of tumour suppressor genes. Clearly the tumour suppressor protein p53 is important in a variety of carcinogenic processes. P53 probably acts as a corrective mechanism to counter hyperproliferative signals. As a rule, uncontrolled cell production and cell cycle alterations are a late phenom processes offers the prospect of new and improved cancer chemotherapy.