Ugo Cavallaro
[email protected] | |
Telephone | +39 02 9437 5165 |
Location |
Building 13
Floor 3rd Via Adamello 16, Milano |
Member of
I have a broad background in cell biology, biochemistry and molecular oncology. As a junior scientist, I focused on the biological mechanisms that underlie the role of cell adhesion molecules in cancer cells. Upon establishing my own group, I built on that knowledge to investigate the cellular and molecular events that drive ovarian cancer. The projects that I have conducted so far as PI or co-investigator provided not only the basis and the rationale for the ongoing research, but also a series of clinically relevant experimental models. Over the last years, my group collected a repository of viable tissue from ovarian cancer and healthy normal ovary and fallopian tube. We also have a repository of primary cell cultures and of patient-derived xenografts.
The recent achievements of my lab included profiling the proteome and the phosphoproteome of primary ovarian cancer cells vs. their normal counterpart, which resulted in the discovery of the CDK7/POLR2A pathway as a novel driver in ovarian cancer. We were also the first to report the novel role of CD73 in ovarian cancer stem cells and the possibility to design CD73-based cancer stem cell-targeted therapy. My group is also interested in tumor/microenvironment interactions, with particular emphasis on the vasculature. We identified L1CAM as a master regulator of cancer vessel morphology and function, and have recently discovered a novel, soluble L1CAM isoform with angiogenic activity involved in ovarian cancer vascularization.
Most Relevant Publications
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CD73 Regulates Stemness and Epithelial-Mesenchymal Transition in Ovarian Cancer-Initiating Cells.
Stem Cell Reports, 2018
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Phosphoproteomics of Primary Cells Reveals Druggable Kinase Signatures in Ovarian Cancer.
Cell Rep, 2017
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Endothelial deficiency of L1 reduces tumor angiogenesis and promotes vessel normalization.
J Clin Invest, 2014
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L1CAM promotes ovarian cancer stemness and tumor initiation via FGFR1/SRC/STAT3 signaling.
Exp Clin Cancer Res, 2021