A photo of Nicolas Nassar.

Member, Division of Experimental Hematology & Cancer Biology

Associate Professor, UC Department of Pediatrics

513-636-6597

513-636-3549

Biography & Affiliation

Biography

My areas of research interest include drug development and signaling with focus on small GTPases. My research is both basic and translational.

My research efforts encompass several methodologies, including protein crystallography, biophysical and biochemical studies, cellular functional assays, and ultimately, identifying small molecule compounds that bind to and modulate GTPase signaling in in vivo models of cancer.

Rac GTPases are key regulators of cell growth. By reorganizing the actin cytoskeleton in response to extracellular cues, Rac GTPases play a key role in cancer cell metastasis. My lab's goal is to understand the regulation of Rac and its role in cancer. More specifically, my work aims to find ways to inhibit its hyperactivation in leukemia.

One of my lab’s groundbreaking discoveries is the identification of a small molecule inhibitor of Vav3, a Rac activator. Our research aims to unravel the mechanism of action of the Vav3-inhibitor. In addition, our small molecule technology has been submitted to the US Patent Office.

My research has been published in PLoS ONE, Leukemia, JCI Insight, and Oncogene: Including Oncogene Reviews. I have been a researcher for more than 20 years and began working at Cincinnati Children’s in 2010.

Academic Affiliation

Associate Professor, UC Department of Pediatrics

Divisions

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases



Blog Posts

Education

PhD: University Joseph Fourier, Grenoble,France, 1992.

Postdoc: Max Plank Institut, Dortmund, Germany, 1996.

Research Associate: Cornell University, Ithaca, NY, 2000.

Assistant Professor: Stony Brook University, NY, 2006.

Research Assistant Professor: Stony Brook University, Stony Brook, NY, 2010.

Publications

Selected Publication

IODVA1, a guanidinobenzimidazole derivative, targets Rac activity and Ras-driven cancer models. Gasilina, A; Premnauth, G; Gurjar, P; Biesiada, J; Hegde, S; Milewski, D; Ma, G; Kalin, TV; Merino, E; Meller, J; et al. PLoS ONE. 2020; 15:e0229801-e0229801.

Rational identification of a Cdc42 inhibitor presents a new regimen for long-term hematopoietic stem cell mobilization. Liu, W; Du, W; Shang, X; Wang, L; Evelyn, C; Florian, MC; Ryan, MA; Rayes, A; Zhao, X; Setchell, K; et al. Leukemia. 2019; 33:749-761.

Real-time genomic profiling of histiocytoses identifies early-kinase domain BRAF alterations while improving treatment outcomes. Lee, LH; Gasilina, A; Roychoudhury, J; McCormack, FX; Pressey, J; Grimley, MS; Lorsbach, R; Ali, S; Bailey, M; Stephens, P; et al. JCI insight. 2017; 2.

UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO. Goyama, S; Schibler, J; Gasilina, A; Shrestha, M; Lin, S; Link, KA; Chen, J; Whitman, SP; Bloomfield, CD; Nicolet, D; et al. Leukemia. 2016; 30:728-739.

Breast cancer-associated missense mutants of the PALB2 WD40 domain, which directly binds RAD51C, RAD51 and BRCA2, disrupt DNA repair. Park, J; Singh, TR; Nassar, N; Zhang, F; Freund, M; Hanenberg, H; Meetei, AR; Andreassen, PR. Oncogene: Including Oncogene Reviews. 2014; 33:4803-4812.