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tricolil [at] chop.edu
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Location - People View
3rd Floor, Room 309G

3615 Civic Center Blvd
Philadelphia, PA 19104
United States

Lucas Tricoli, PhD
Lucas Tricoli
Research Associate Scientist II

Dr. Tricoli's research involves developing a new generation of lentiviral vectors that will prove to limit toxicity and improve activity of the ARSA enzyme, extending the efficacy of and eligibility for gene therapy in metachromatic leukodystrophy, a devastating childhood lysosomal storage disease.

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Bio

Dr. Tricoli' s research involves developing a new generation of lentiviral vectors that will prove to significantly limit toxicity and improve activity of the ARSA enzyme, extending the efficacy of and eligibility for gene therapy in metachromatic leukodystrophy (MLD), a devastating childhood lysosomal storage disease caused by disfunction of ARSA. His career has been dedicated to the study of disease mechanism, model development, and a bedside to bench and back modality of therapeutics to combat them. He spent five years of postdoctoral work in the field of oncology, primarily in prostate cancer and developed the basic cell, molecular, and base level clinical skills to approach major problems faced in prostate carcinogenesis. Mechanisms of therapeutic resistance and development of models to better understand them were at the forefront of his research focus. He added more advanced 3D primary cell culture techniques, which he pioneered, and miRNA analysis to these to expand the understanding in the field of prostate cancer.

He has broadened his research scope in the field of clinical therapeutic development and moved into gene therapy research. Dysfunction of ARSA enzyme has significant neurological impact on children, eventually leading to death. Lentiviral gene therapy of MLD could prove to ameliorate the effects of the disease leading to a viable long-term treatment strategy. His current scientific contributions involve developing a new generation of lentiviral vectors that will prove to significantly limit toxicity and improve ARSA activity extending the efficacy of and eligibility for gene therapy in MLD. He has currently succeeded in developing a vector which is effective in treatment of a MLD disease in a mouse model. The continued research is focused on expanding the knowledge of our vector' s efficacy to refine its potency and novelty leading to clinical trials for our gene therapy-based treatment.