About our research
The Metabolic Cancer Reprogramming Group investigates how metabolic programs, nutrient fluxes, and metabolite-driven signaling pathways determine cancer cell fate, adaptive states, and therapeutic vulnerability. We aim to define the metabolic principles that enable tumors to progress, resist stress, remodel their microenvironment, and evade immune control.
By integrating mechanistic biology, quantitative metabolomics, functional genetics, and in vivo modeling, our objective is to map the regulatory circuits through which metabolism shapes tumor progression—from intracellular signaling circuits to whole-tumor dynamics. We translate these insights into actionable strategies that exploit metabolic dependencies to prevent progression, overcome resistance, and enhance treatment efficacy.
Our mission is to provide a mechanistic foundation for metabolism-driven precision oncology and to uncover therapeutic entry points that arise from the metabolic plasticity of cancer.
Head of Division "Metabolic Cancer Reprogramming"
Doctoral Researcher
Doctoral Researcher
Senior Technician
Postdoc
Technician
Our Most Recent Publications
Delemer, B. ; Florea, S.M. ; Decoudier, B. ; Boulagnon-Rombi, C. ; Karna, B. ; Pellegata, N.S. ; Buffet, A. ; Beckers, A. ; Petrossians, P. ; Daly, A.F.
Loss of heterozygosity and absence of MAX immunostaining in a prolactinoma associated with multiple endocrine neoplasia type 5 (MEN5).Dipol, T. ; Fortuna, A. ; Morsilli, O. ; Zecca, V. ; Singh, T. ; Palombelli, G. ; Mattei, F. ; Favero, V. ; Candelise, N. ; Maroccia, Z. ; Loizzo, A. ; Rimondini, R. ; Campana, G. ; Pellegata, N.S. ; Loizzo, S. ; Canese, R. ; Chiodini, I.
Mild chronic post-natal pain induces endocrine and metabolic alterations associated to enlargement in pituitary glands size in adult CD-1 male mice.Haider, A. ; Sundar, J. ; Beckers, A. ; Mohr, H. ; Kasajima, A. ; Pellegata, N.S. ; Petrossians, P. ; Daly, A.F.
Expanding the phenotype of multiple endocrine neoplasia type 5 (MEN5): Pituitary gigantism, myelolipoma and familial pheochromocytoma due to a germline pathogenic MAX variant.Contact Us