Rosario Notaro

After his medical degree, Rosario Notaro trained in Hematology (Federico II University, Naples). In 1995 he moved to New York (USA) at the Memorial Sloan-Kettering Cancer Center and from 1999 he held the position of Assistant Professor of Medicine at the Weill Medical College of Cornell University. In 2001 he started his own laboratory at National Cancer Institute of Genoa. In 2007 he was appointed at the Core Research Laboratory of the Istituto Toscano Tumori (Florence). Throughout his career he has always combined scientific work and clinical work with the main goal of understanding human disease at the molecular level. His research has concentrated on the genetic basis of blood disorders paying a particular attention to anemias, bone marrow failure and clonal disorders. In 1999 he developed a novel approach to measure telomere length and he showed that hematopoietic stem cells lose telomere length after bone marrow transplantation concomitantly with their proliferation. He contributed to the characterization of the effects of G6PD deficiency through conventional targeted inactivation of the G6PD gene in mice. In addition, by using for the first time data from full genome sequencing projects, he defined the relationship between the evolution of the G6PD gene and the clinical severity of its mutations. Since the beginning of his career, Dr. Notaro has been puzzled by the clinical and the biological aspects of a rare and peculiar clonal hemolytic disorder: paroxysmal nocturnal haemoglobinuria (PNH). His group has provided evidences that in PNH patients are present auto-immune lymphocytes that, targeting the glycosylphosphatidylinositol anchor, destroy the normal hematopoiesis but spare PNH hematopoiesis explaining the paradoxical expansion of PNH clones. More recently, they have performed preclinical and clinical studies about complement inhibition for the targeted therapy of PNH. Finally, they are exploring the measurement of the frequency of mutated peripheral granulocytes (ƒ) as a surrogate marker of individual cancer risk.