Dr. Eugenio Montini started his scientific career in 1995 in the field of human molecular and medical genetics at the Telethon Institute of Genetics and Medicine (TIGEM, Milan, Italy). Later he worked as postdoctoral fellow in the laboratory of Dr. Markus Grompe (Oregon Health Science University, Portland, USA) in the field of liver gene therapy and liver regeneration and characterized the therapeutic potential and the genomic integration events of Sleeping Beauty transposons and showed for the first time that adeno associated vectors integrate in the genome of hepatocytes in vivo. In December 2003, he joined Luigi Naldini’s laboratory at the San Raffaele Telethon Institute for Gene Therapy (SR-Tiget, Milan, Italy) to investigate the oncogenic potential of self-inactivating Lentiviral Vector (SIN-LV) integration in vivo and to identify the factors that modulate the genotoxicity of integrating vectors in general.

He is now a tenured group leader of a research unit and head of the Vector Integration Core in SR-Tiget. His main scientific contributions include the demonstration that SIN-LV vectors have a superior safety profile over gamma-retroviral vectors, which has resulted in the adoption of SIN-LVs as the preferred platform for therapeutic gene delivery internationally. He has also successfully used integration site analysis to perform clonal tracking and cell lineage specification and differentiation in preclinical models and clinical trials; utilized novel ad hoc designed LV vectors to uncover novel cellular oncogenes and novel pathways involved in drug resistance in several human cancers; discovered that HIV insertions targeting BACH2 and STAT5B in humans lead to the expansion of regulatory T cell clones as the result of selective advantage conferred by these insertions; developed liquid biopsy integration site sequencing (LiBIS-seq), a polymerase chain reaction technique optimized to quantitatively retrieve vector integration sites from cell-free DNA released into the bloodstream by dying cells residing in several tissues; discovered that oncogene-induced senescence in hematopoietic progenitors features myeloid restricted hematopoiesis, chronic inflammation and histiocytosis in a humanized model.