News from CEXS-UPF
"How can the networks that make up the tumour cells maintain a tumour?" was the initial question posed by Sergi Valverde, Carlos Rodríguez-Caso and Josep Sardanyés (members of the Complex Systems Lab led by Ricard Solé, ICREA professor at DCEXS, the Institute of Evolutionary Biology (UPF-CSIC) and the Santa Fe Institute) in a study published in the journal Bioassays on April 9th, which merited comment by Andrew Moore, editor-in-chief of the journal.
Most tumours have genomic instability due to gains and losses of genes, chromosome breakage, mutations, etc., and although these changes are lethal for normal cells, they are not for tumour cells.
Tumour cell networks are able to live with these alterations, which also seem essential for these cells to evolve and adapt. "In many ways, tumour populations were shown to share many essential features with microbial populations," suggest the authors of the paper.
Ricard Solé observes that "a few years ago, we launched the hypothesis that the rate of genomic instability must have a limit, beyond which the cancer would not be viable. We suspect that tumours spontaneously develop near this threshold. This is what we call error catastrophe".
In the paper published in Bioassays, the authors show evidence of the existence of this "catastrophe" while examining different scenarios to study it, from genomics to computational modelling.
Reference:Ricard V. Solé, Sergi Valverde, Carlos Rodríguez-Caso i Josep Sardanyés (2014), "Can a minimal replicating construct be identified as the embodiment of cancer?", Bioassays, 36, 35 (5), 503-512. DOI 10.1002/bies.201300098