title: Apoptosis and carcinogenesis.
abstract: Apoptosis has long been known to be effected through a common sequence of structural changes, despite the wide variety of initiating stimuli. These common structural events appear to depend upon activation of a set of enzymes (caspases) which direct a strongly conserved, terminal effector pathway. The regulation of this pathway, and in particular its coupling to DNA damage, appears to be critical in maintaining at low levels the number of mutated cells within tissues. The frequency with which tumours (experimental and human) bear deficiency in p53 or MSH-2 repair function may indicate the importance of these proteins in coupling DNA damage to apoptosis.
authors.affiliation: Department of Pathology, University of Edinburgh Medical School, UK.
authors.forename: A H
authors.initials: AH
authors.lastname: Wyllie
authors.forename: C O
authors.initials: CO
authors.lastname: Bellamy
authors.forename: V J
authors.initials: VJ
authors.lastname: Bubb
authors.forename: A R
authors.initials: AR
authors.lastname: Clarke
authors.forename: S
authors.initials: S
authors.lastname: Corbet
authors.forename: L
authors.initials: L
authors.lastname: Curtis
authors.forename: D J
authors.initials: DJ
authors.lastname: Harrison
authors.forename: M L
authors.initials: ML
authors.lastname: Hooper
authors.forename: N
authors.initials: N
authors.lastname: Toft
authors.forename: S
authors.initials: S
authors.lastname: Webb
authors.forename: C C
authors.initials: CC
authors.lastname: Bird
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics / Q000473:pathology*; D009374:Neoplasms, Experimental / Q000209:etiology / Q000235:genetics / Q000473:pathology