title: Apoptosis: future directions in cancer therapy.
abstract: Cancer as a multifactorial disease results in gain of immortality due to defective apoptosis. The primary mode of cell death by apoptosis induced by various modes of treatment often fail in vivo. The in vitro environment is less complex while the in vivo environment is influenced by various external regulatory signals besides the existence of multiple, parallel and independent apoptotic pathways. Further, specific preference for an apoptotic pathway in a certain cell type would significantly alter the apoptotic responses. Identification of defects in preferred pathways and choosing alternative and potentially inducible pathways would help in deciding on apoptosis-based treatment protocols. Mechanisms involved in the execution of apoptosis may also not be unique to apoptotic pathways since similar events, possibly with strict control, do occur during mitosis. Further evaluation may yield new dimensions to apoptosis and apoptosis-based therapy.
authors.affiliation: Regional Cancer Centre, Kerala, India.
authors.forename: D
authors.initials: D
authors.lastname: Ravi
authors.forename: K R
authors.initials: KR
authors.lastname: Panikkar
authors.forename: M K
authors.initials: MK
authors.lastname: Nair
authors.forename: M R
authors.initials: MR
authors.lastname: Pillai
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D019008:Drug Resistance, Neoplasm / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000502:physiology; D009369:Neoplasms / Q000188:drug therapy / Q000503:physiopathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53