RT Journal Article
SR Electronic
T1 Carcinogenesis: A Cellular Model for Age-dependence
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 1385
OP 1389
VO 25
IS 2B
A1 NEJAKO, ASHLEY
A1 ARANTON, BEISA
A1 DIX, DOUGLAS
YR 2005
UL http://ar.iiarjournals.org/content/25/2B/1385.abstract
AB 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. Materials and 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. Conclusion: 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. Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved