Cancer is the result of a system's breakdown that arises in a cell society when a single cell (due to a mutation or set of mutations) starts to display uncontrolled growth. The cooperation that maintains the integrity of a multicellular organism is thus disrupted. Further changes in the population generated by such abnormal cell can lead to malignant tumor growth, eventually killing the host. From an evolutionary point of view, tumor progression is a microevolution process in which tumors must overcome selection barriers imposed by the organism.

The fight against cancer has been of limited success. It is true that a number of cancers can get cured and that major advances have happened over the last 50 years in our understanding of timor progression and its origins. But the frequency of non cured tumours remains the same after all this years. Using evolutionary arguments, theoreticians have been arguing in the last decades that perhaps a new way of looking at the whole problem is needed. A new way that takes into account the Darwinian, ecological nature of the disease.

In our Lab we have been studying one particularly important aspect of cancer, namely its enormous levels of genomic instability, which are easily observable in most advanced tumours, particularly at the level of chromosomes, which appear duplicated, lost or broken in apparently disorganised patterns. Despite such degree of aneuploidy, cancer populations are capable of adapting and eventually expanding, killing the host. Are there limits to such degree of instability? How can we model this phenomenon? Since it has been shown that thresholds to cancer viability are indeed present, we have been proposing that therapeutic approaches might consider this aspect of cancer dynamics as a potential advantage.


Can a minimal replicating construct be identified as the embodiment of cancer?  R Solé,S.Valverde,C.Rodriguez-Caso and J. Sardanyes. Bioessays 38 (2014) 503-512

Catastrophic shifts and lethal thresholds in a propagating front model of unstable cancer progression.D Rodriguez Amor and R Solé, Phys Rev. (to appear)

Accelerated tumor invasion under non-isotropic cell dispersal in glioblastomas.J. Fort and R Solé. New J. Phys. 15 (2013) 055001

Phase transitions in cancer.R. Solé. In: New Challenges for Cancer Biomedicine. Springer (2012) pp.35-51.

Cancer stem cells as the engine of unstable tumour progression. R Sole, C Rodriguez-Caso, TS Deisboeck, J Saldanya. J. Theor. Biol. 253 (2008) 629-673.

An error catastrophe in cancer? R Sole and T Deisboeck. J. Theor. Biol. 228 (2004) 47-54

Phase transitions in unstable cancer cell populations. R Solé. Europ. J. Phys. 35 (2003) 117-123.

Metapopulation dynamics and spatial heterogeneity in cancer. I Gonzalez-Garcia, R Sole and J. Costa. PNAS 99 (2002) 13085-13089.