Experience

Axxam

• Italy
• Biotechnology Research
• 100 - 200 Employee

• Cell Biology Scientist

  • Apr 2021 - Present



MD Anderson Cancer Center

• United States
• Hospitals and Health Care
• 700 & Above Employee

• Senior Postdoctoral Fellow

  • Aug 2016 - Sep 2021

  Leading a group of 3 passionate PhD students.Uncovered a novel and potentially druggable target induced by short inflammatory events on a genetically engineered mouse model of pancreatic cancer and subsequently characterized on tissue-derived 3D organoids (currently under revision at Science).Independently designing and managing part of a project focused on the identification and validation of druggable targets in pancreatic cancer, leveraging orthogonal approaches on mouse models and tissue-derived 3D and 2D cell culture (currently in press in Cancer Research).Contributed as experimental designer to the characterization of Gemcitabine-resistant clonal subpopulations of human pancreatic cancer cells (Cell Report, 2019).Contributed as experimental designer and imaging expert on a collaborative project aiming to identify functional vulnerabilities in SMARCB1-deficient tumors (Cancer Cell, 2019). Finding led to the approval of a phase II clinical trial for an innovative therapeutic approach to treat malignancies characterized by SMARCB1-deficiency (NIH: NCT03587662).Contributed as experimental designer to the generation of an in vivo genetic platform to rapidly generate somatic mosaic genetically engineered immune-competent mouse models of renal tumors, recapitulating the genomic and phenotypic features of human malignancies.Recently submitted a patent with 3 colleagues on a new platform for screening compounds able to counteract on-going pancreatitis-derived inflammation and prevent tumorigenesis.



Università degli Studi di Firenze

• Higher Education
• 700 & Above Employee

• PHD Student

  • Nov 2012 - Aug 2016

  My Ph.D. training was mainly focused on the study of the structure, conformational stability, folding and aggregation processes of Profilin-1 and its mutants associated with Amyotrophic Lateral Sclerosis.While characterizing the refolding steps from the urea-induced unfolded state of the wild type protein with the intrinsic fluorescence and the circular dichroism assays, I also purified four pathologic mutant variants and evaluated their folding dynamics. Our results indicated that all four variants have an aggregation propensity higher than that of the wild-type; in particular, the C71G mutation was found to induce the most dramatic change in aggregation and the generation of fibrils with high density intermolecular β-sheet structures. Moreover, we demonstrated a strong correlation between such increased aggregation propensity and structural changes of the folded state.

• postgraduate internship

  • Sep 2010 - Dec 2012

  In the last part of my master degree I joined a project which aimed to explore the effects of Salarin-C, an anticancer macrolide extracted from the Fascaplysinopsis sponge, on Chronic Myeloid Leukemia (CML) stabilized cell lines K562 and KCL22 both in normoxia and hypoxia condition. Our results indicated a treatment-induced mitotic cycle arrest, apoptosis and DNA damage in both cell lines. Moreover, Salarin C also concentration-dependently inhibited the maintenance of stem cell potential in cultures in low oxygen of either CML cell lines or primary cells. Surprisingly, the drug also concentration-dependently enforced the maintenance of BCR/Abl signaling in low oxygen, an effect which was paralleled by the rescue of sensitivity of stem cell potential to imatinib-mesylate treatment. These results suggested a potential use of Salarin C for the suppression of CML cells refractory to tyrosine kinase inhibitors.