Matteo Marchesini, PhD profile page

Matteo Marchesini, PhD, completed his doctoral studies in Oncology at the University of Perugia (Pelicci Lab), focusing on telomeric dysfunctions in normal and cancer cells (Marchesini et al., Oncogene 2015). During his postdoctoral training at MD Anderson Cancer Center (Simona Colla Lab), he expanded this research to hematologic diseases. Using the TERT/ER mouse model, his work demonstrated that telomere attrition leads to a myelodysplastic-like phenotype due to impaired differentiation of myeloid progenitor cells (Colla et al., Cancer Cell 2016).
At MDACC, Dr. Marchesini developed a strong interest in genomic abnormalities and translational research. He contributed to genetic screening of 1q21-amplified multiple myeloma (MM), identifying ILF2 as a vulnerability in therapy-resistant high-risk patients (Marchesini et al., Cancer Cell 2017; Thongon et al., Nature Communications 2024). He also led small-molecule screenings to identify inhibitors of dysfunctional transcription factors, including CAD204520 targeting mutated NOTCH1 in T-cell acute lymphoblastic leukemia (Marchesini et al., Cell Chemical Biology 2020) and histone deacetylase inhibitors to suppress aberrant EVI1/MECOM activity in acute myeloid leukemia with 3q26 abnormalities (Marchesini et al., Nature Communications 2024).
Currently at IRST, Dr. Marchesini focuses on early identification of high-risk patients through integration of clinical and multiomic data, while developing in vitro 3D systems to model high-risk MM for mechanistic studies and drug profiling. His career spans from basic science to translational and preclinical research, encompassing biochemical assays, genetic and phenotypic screenings, and in-silico approaches to uncover novel therapeutic strategies and understand molecular mechanisms in hematologic malignancies.