Article in Seminars in Cancer Biology · April 2008 doi: 10. 1016/j semcancer

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Theories of carcinogenesis: An emerging perspective

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Seminars in Cancer Biology · April 2008

DOI: 10.1016/j.semcancer.2008.03.012 · Source: PubMed

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THEORIES of CARCINOGENESIS: An Emerging Perspective

Carlos Sonnenschein and Ana M. Soto

Tufts University School of Medicine, Department of Anatomy and Cellular Biology, 136 Harrison

Ave, Boston MA 02111

Abstract

Four decades ago Leslie Foulds remarked that “Experimental analysis has produced an alarming

mass of empirical facts without providing an adequate language for their communication or effective

concepts for their synthesis.” Examining the relevance of the data avalanche we all generate and are

subjected to in the context of the premises and predictions of the current cancer theories may help

resolve this paradox. This goal is becoming increasingly relevant given the looming attempts to

rigorously model and parameterize crucial events in carcinogenesis (microenvironmental conditions,

cellular proliferation and motility), which will require the adoption of reliable premises on which to

base those efforts. This choice must be made a priori, as premises are not testable, and data are not

free of the theoretical frame used to gather them. In this review we provide a critical analysis of the

two main currents in cancer research, one centered at the cellular level of biological organization,

the somatic mutation theory, which conceptualizes carcinogenesis as a problem of cell proliferation

control, and the other centered at the tissue level, the tissue organization filed theory, which considers

carcinogenesis a process akin to organogenesis gone awry.

Keywords

microenvironment; stroma; proliferation; stroma-epithelium interactions; tissue organization field

theory

Carcinogenesis continues to be a highly controversial subject despite the incessant stream of

publications aimed at explaining it. It would be sensible to find an answer to this paradox, i.e.,

increased accumulation of data and no commensurate clarification of this important biomedical

problem. Examining the relevance of the data avalanche in the context of the premises and

predictions of the current cancer theories may help resolve this paradox. This goal is becoming

increasingly relevant given the looming attempts to rigorously model and parameterize crucial

events in carcinogenesis (microenvironmental conditions, cellular proliferation and motility),

which will require the adoption of reliable premises on which to base those efforts [1]; and in

this issue).

To avoid unnecessary confusions regarding the theories of carcinogenesis and the premises

that underlie them, it will be useful to identify the different types of human cancers that exist.

First, there are those that are inherited through the germline of the carriers; they represent about

5% of the total incidence of human cancers. There is consensus about the mutational origin of

Corresponding Authors: Carlos Sonnenschein MD/ Ana M. Soto MD, Phone: [phone] 636 6954, Fax: [phone], Emails:

[e-mail]/ [e-mail].