IJE Advance Access originally published online on September 20, 2006
International Journal of Epidemiology 2006 35(5):1165-1167; doi:10.1093/ije/dyl192
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author 2006; all rights reserved.
Commentary |
Commentary: Carcinogenesis as Darwinian evolution? Do the math!
Departments of Radiology and Applied Mathematics, University of Arizona, AZ, USA
E-mail: rgatenby@uph.org
| The first 10% of the full text of this article appears below. |
The transition from normal tissue to invasive cancer is a multistep, multipath process in which increasingly malignant cellular populations emerge over time13 generally coincident with accumulating genomic mutations. This is often described as somatic evolution4,5 because it appears formally analogous to Darwinian processes in nature. While this conceptual model is well accepted, the interactions of phenotypic properties with environmental selection forces that determine individual fitness and cellular proliferation remain ill-defined. Furthermore, the
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
G. C. Bagby and G. Meyers Bone Marrow Failure as a Risk Factor for Clonal Evolution: Prospects for Leukemia Prevention Hematology, January 1, 2007; 2007(1): 40 - 46. [Abstract] [Full Text] [PDF] |
||||
