An international study, led by Dr. Santiago Ramón y Cajal, head of the Pathological Anatomy Service of the Vall d'Hebron Hospital and head of the group for http://es.vhir.org/portal1/grup-equip.asp?s=recerca&contentid=186726 research in Translational Molecular Pathology of the Vall d'Hebron Research Institute (VHIR) presents a new approach in current cancer biology to increase the efficiency in the diagnosis and treatment of this disease.The heterogeneity of cancer goes beyond existing Genomic Theory, which defends the cancer as a clone cell that collects different molecular alterations. Dr. Ramón y Cajal proposes to focus on cancer as a set of clones that cooperate with each other and with micro-environmental factors. For this reason, he calls it ecomolecular disease and a neoplastic consortium. Thus, "the cancer works as an ecosystem, where molecular cooperation between several types of cells and the microenvironment present a consortium in which tumour and stromal cells collaborate," describes Dr. Ramón y Cajal.And it is that "the concept of cancer goes beyond genomic alterations in the cells, it has to be understood that there is communication by factors between tumour clones that favour their proliferation and invasion and factors secreted by the stroma that favour the tumour formation. The identification of these factors of cooperation open new therapeutic perspectives to hamper the development of metastasis," he stresses.Cancer can be considered an emerging, complex and dynamic entity where the final result of invasiveness and metastasis is greater than the sum of individual clones. Something like what happens with our TV pixels: they don't rebel anything if they are not seen together to discovered the meaning of the image. And the image (or the success of the tumour) not only depends on the consortium of clonal populations, but on the molecular changes that the clonal community has suffered and the environment in which it is located.The failure in clinical therapiesThe most current treatments focus on the inhibition of specific genetic alterations detected in diagnostic biopsies. Alterations that may be activated in other areas of the tumour or the progression in metastasis are not considered. In this way, to carry out therapies for genetic variations detected in a limited sampling can cause the promotion of other cellular areas (clones) or the activation of routes that had not been identified.How to move towards the detection and the personalized treatments?Dr. Ramón y Cajal proposes two major approaches. First, to identify the factors involved in cell communication and with cells of the microenvironment through exosomes. The blocking of such collaboration could inhibit the development of metastasis.In second place, and given the great intratumuoral heterogeneity and redundancy of molecular alterations, in addition to different signalling circuits varying according to cell type, the study of new inhibitors based on circuits and specific intracellular biochemical connections must be addressed, using models based on systems biology that integrate all available information. Through the mapping and dissection of the consortium at the molecular level, and using mathematical models that contain the molecular alterations described in a particular patient, all routes and networks involved in tumorigenesis will be characterized, generating more efficient and specific information of carcinogenic types and targets. "Through the knowledge of these interconnected routes, can be detected which factors should be inhibited so they really have a therapeutic effect, in the context of each patient's tumour. We need to optimize each route to see the most effective node, to take into account what will move when you touch a piece and if it is not done by systems biology, it is impossible to predict," adds Dr. Ramón y Cajal. All this in a context of tissue and according to cell types: the biological significance and response to treatment on the basis cannot be extrapolated to the simple detection of mutations (e.g., mutated BRAF inhibitors work well on melanomas but have an opposite effect on tumours of the colon). The more characterized the oncogenic networks and the critical nodes of the tumour are, the easier it will be to understand what steps are needed to reorient the route of diversification and to identify the best therapeutic targets.In the making of this study published in the journal http://www.sciencedirect.com/science/article/pii/S0304419X17300525?via%3Dihub BBA Review on Cancer participated Vall d'Hebron Research Institute (VHIR), the Center for Biomedical Research in Cancer Network (CIBERONC), the Lady Davis Institute (Monreal, Canada), Department of Oncology - Pathology Science for Life Laboratory (Sweden) and the Cancer Research Institute of the Department of Oncology at the Alberta University (Canada).