title: Carcinogenesis: a cellular model for age-dependence.
abstract: BACKGROUND
  Certain characteristics of cancer remain invariant between populations, the age of peak risk, the age ranges of significant and insignificant risk, and the pattern of risk variation with age. We offer an explanation that is built by analogy on that for trisomy 21.
  
  
  METHODS
  We calculated the rate of change in risk with age for the most common cancers, death from all causes, trisomy 21/birth, and trisomy 21/1000 women.
  
  
  RESULTS
  Beyond some milestone age, the risk of death from all causes and trisomy 21/birth exhibit constant acceleration, while risk of cancer and trisomy 21/1000 women exhibit increasing deceleration.
  
  
  CONCLUSIONS
  With advancing age, the risk of abnormal cell division increases continuously but remains harmless until some tissue-specific milestone, e.g., depletion of stem cells, and is then damped by a continuous decline in rate of cell division.
authors.affiliation: Department of Biology, University of Hartford, West Hartford, CT 06117, USA.
authors.forename: Ashley
authors.initials: A
authors.lastname: Nejako
authors.forename: Beisa
authors.initials: B
authors.lastname: Aranton
authors.forename: Douglas
authors.initials: D
authors.lastname: Dix
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D002455:Cell Division; D004314:Down Syndrome / Q000453:epidemiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009369:Neoplasms / Q000453:epidemiology* / Q000209:etiology; D012307:Risk Factors; D013234:Stem Cells / Q000473:pathology / Q000502:physiology