Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Most cancers occur with the same characteristic pattern of incidence. The simplicity of this pattern is in contrast to the perceived complexity of carcinogenesis. Therefore, age-onset statistics represent a tempting set of data and have provoked many bold but often misguided conclusions concerning the physiopathological mechanisms of cancer. Half a century has passed since the original multistage theory of Armitage and Doll. Although their basic notion of a healthy cell becoming malignant in several rate-limiting steps is still accepted, prevailing wisdom about the nature and number of these steps has never settled into a consensus. Why have we been unable to elucidate the quantitative dependence of cancer incidence on the molecular processes that feature in its aetiology? In this review we aim to provide answers for this question.

Original publication

DOI

10.1016/S1470-2045(07)70343-1

Type

Journal article

Journal

Lancet Oncol

Publication Date

11/2007

Volume

8

Pages

1030 - 1038

Keywords

Age Factors, Disease Progression, Humans, Incidence, Models, Statistical, Neoplasms, Risk Factors