Enterocina

Theoretical Biology and Medical Modelling
Commentary

BioMed Central

Open Access

Cancer initiation and progression: an unsimplifiable complexity
Fabio Grizzi*1,5, Antonio Di Ieva2, Carlo Russo1, Eldo E Frezza3,4, Everardo Cobos4,5, Pier Carlo Muzzio6,7 and Maurizio Chiriva-Internati4,5
Address: 1Laboratories of Quantitative Medicine, Istituto Clinico Humanitas IRCCS, Via Manzoni 56,20089 Rozzano, Milan, Italy, 2Department of Neurosurgery, Istituto Clinico Humanitas IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy, 3Department of Surgery, Texas Tech University Health Sciences Center and Southwest Cancer Treatment and Research Center, Lubbock, Texas 79430, USA, 4Department of Microbiology & Immunology, Texas Tech University Health Sciences Center and Southwest Cancer Treatmentand Research Center, Lubbock, Texas 79430, USA, 5Division of Hematology & Oncology, Texas Tech University Health Sciences Center and Southwest Cancer Treatment and Research Center, Lubbock, Texas 79430, USA, 6Department of Medical-Diagnostic Sciences and Special Therapies, University of Padua, Via Giustiniani 2, 35128 Padua, Italy and 7Istituto Oncologico Veneto IRCCS, Ospedale Busonera – ViaGattamelata 64, Padua, Italy Email: Fabio Grizzi* - fabio.grizzi@humanitas.it; Antonio Di Ieva - fabio.grizzi@humanitas.it; Carlo Russo - fabio.grizzi@humanitas.it; Eldo E Frezza - fabio.grizzi@humanitas.it; Everardo Cobos - fabio.grizzi@humanitas.it; Pier Carlo Muzzio - pcmuzzio@unipd.it; Maurizio Chiriva-Internati - maurizio.chiriva@ttuhsc.edu * Corresponding author

Published: 17 October 2006Theoretical Biology and Medical Modelling 2006, 3:37 doi:10.1186/1742-4682-3-37

Received: 09 June 2006 Accepted: 17 October 2006

This article is available from: http://www.tbiomed.com/content/3/1/37 © 2006 Grizzi et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License(http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract
Background: Cancer remains one of the most complex diseases affecting humans and, despite the impressive advances that have been made in molecular and cell biology, how cancer cells progress through carcinogenesis and acquire their metastatic ability is stillwidely debated. Conclusion: There is no doubt that human carcinogenesis is a dynamic process that depends on a large number of variables and is regulated at multiple spatial and temporal scales. Viewing cancer as a system that is dynamically complex in time and space will, however, probably reveal more about its underlying behavioural characteristics. It is encouraging that mathematicians,biologists and clinicians continue to contribute together towards a common quantitative understanding of cancer complexity. This way of thinking may further help to clarify concepts, interpret new and old experimental data, indicate alternative experiments and categorize the acquired knowledge on the basis of the similarities and/or shared behaviours of very different tumours.

Background
There is nodoubt that cancer operates at the different levels of the hierarchical organization making up a human, and evolves through an assortment of states (or possible pattern configurations) and a number of transitions between two successive states [1,2]. According to the reductionist view of cancer, expressed in myriads of molecular biology-based investigations, all the information necessary for a cellto transform itself into a neoplastic cell can be attributed to changes at the genomic

level. This "certainty" is based on the fact that the genome carries all of the information related to any cell process, and that any cellular transformation is due to a specific genomic change. Although this approach has offered and remains a fundamental means of generating knowledge [3-7], the accumulated...