Gabriel Piedrafita
Computational Systems Biologist
Ph.D. in Biochemistry & Molecular Biology
quantitative cell biology | mathematical modeling | clonal competition | precancer | genetic lineage tracing
I am a systems biologist working with an Atracción de Talento fellowship between the experimental Epithelial Carcinogenesis group and the Bioinformatics Unit at the CNIO. My research interest is in understanding cell behavior, clonal competition and evolution in normal and precancerous epithelial tissues. In particular, I develop data-driven mathematical models with the aim of addressing the cellular mechanisms that underpin normal tissue homeostasis and the evolutionary principles that apply to early tumorigenesis, where the role of mutant clonal competition in cancer initiation is still unclear.
My early research career developed in the origin-of-life field. During my PhD (Universidad Complutense Madrid, UCM, 2013) I designed and studied minimal models of protocells that are capable to display robust, self-maintaining dynamics, through complementary in vitro experiments and computational simulation work. My studies on prebiotic metabolism intensified during a postdoctoral stay at Ralser’s group (University of Cambridge, 2014-2016), all of which helped me gaining experience in theoretical modeling and cellular/molecular kinetics. In 2016 I joined Jones’ group at the Sanger Institute to study cell clone dynamics in mouse skin and esophageal epithelia. My cell fate models and clonal competition simulations are fed and refined by in vivo lineage tracing data from lab-mates using transgenic mouse models. In this way we have successfully shed light on the single mode of cell proliferation and on the preferential cell fate coordination that occur in normal tissue. We have similarly contributed to unveil the mechanism of expansion of certain mutant clones. In my new post at the CNIO (2019-) we aim to extend similar quantitative methodology to study cellular dynamics in slow-renewing tissues such as the bladder urothelium, to ultimately contribute to illuminate on mutant clonal competition during neoplastic transformation in these less-studied tissues.
