title: Apoptosis and a re-investigation of the biologic basis for cancer therapy.
abstract: Antitumor therapy has expanded beyond the previous notions of cytotoxic or biologic therapy to now include agents that induce differentiation (e.g. all trans-retinoic acid for induction of complete remission in patients with acute promyelocytic leukemia [23]) or apoptosis [91]. In fact, the phenomenon of apoptosis may be fundamental to the current understanding of carcinogenesis [11] and may also underlie the effectiveness of some forms of chemotherapy [4,5,18,39,56,59,67], radiation therapy [19,44,52,60,64, 77,78,85] and the interferons [73]. The process of apoptosis has been shown to be responsible for the normal elimination of cells with damaged DNA [81] as well as other potentially dangerous cells such as autoreactive T-lymphocytes [14]. Therefore, although much attention has been given to oncogenes that induce cellular proliferation, one can easily see how the same result (i.e. neoplasia) could be obtained when the ability of a cell to undergo apoptosis is lost.
authors.affiliation: Department of Radiation Oncology, Hospital of the University of Pennsylvania, Philadelphia 19104.
authors.forename: A V
authors.initials: AV
authors.lastname: D'Amico
authors.forename: W G
authors.initials: WG
authors.lastname: McKenna
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D001695:Biology; D002455:Cell Division / Q000235:genetics; D004249:DNA Damage / Q000235:genetics; D006801:Humans; D009369:Neoplasms / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D009857:Oncogenes / Q000235:genetics; D013601:T-Lymphocytes / Q000473:pathology