89 Beaumont Avenue
HSRF 216
Burlington, VT 05405
United States
- Ph.D., University of Vermont/Maastricht University, Vermont
- M.S., Medical Sciences, University of Calgary, Canada
- B.S., Pharmaceutical Sciences, Alexandria University, Egypt
Department of Pathology and Laboratory Medicine
University of Vermont Cancer Center
Areas of expertise
- Redox Biology and Protein S Glutathionylation
Expertise in redox regulated signaling pathways, glutathione metabolism, and the regulatory role of protein S glutathionylation in lung disease and cancer - Lung Cancer Biology and Therapeutic Resistance
Focus on identifying redox‑sensitive mechanisms governing lung adenocarcinoma progression, metabolic vulnerabilities, and chemotherapy resistance, including the discovery of redox‑dependent regulation of OTUB1 and system xc⁻ - Fibrosis, Inflammation and Airway Disease Mechanisms
Extensive experience in epithelial cell biology, fibrosis mechanisms, and multi omics approaches to uncover drivers of asthma, pulmonary fibrosis, and inflammation induced remodeling
BIO
My research program centers on defining how redox perturbations drive lung cancer progression, therapeutic resistance, and inflammatory lung disease. By uncovering how oxidative modifications such as protein S glutathionylation regulate signaling pathways, metabolic reprogramming, and epithelial cell behavior, my long-term goal is to identify redox dependent vulnerabilities that can be targeted to improve outcomes for patients with lung adenocarcinoma and chronic inflammatory lung disorders. Ultimately, my work aims to translate discoveries in redox chemistry and glutathione biology into new therapeutic strategies that overcome drug resistance and halt disease progression.
To achieve this goal, my work integrates biochemical, molecular, and multi omics approaches—including proteomics, metabolomics, and transcriptomics—to map oxidative signaling networks in epithelial cells and tumors. We leverage genetically engineered mouse models, patient derived samples, precision cut lung slices and advanced organoid systems to dissect redox regulated pathways in vivo and ex vivo. My recent work identified S glutathionylation of the deubiquitinase OTUB1 as a key mechanism that stabilizes the cystine transporter subunit SLC7A11, thereby promoting glutathione synthesis and chemotherapy resistance in lung adenocarcinoma. In parallel, we investigate redox regulated drivers of fibrosis, inflammation, and metabolic remodeling, uncovering mechanisms that span from TRPV1 mediated pain signaling to glutathione dependent regulation of extracellular matrix proteins. These integrated strategies allow us to define redox controlled therapeutic targets with high translational potential.
Publications
Bio
My research program centers on defining how redox perturbations drive lung cancer progression, therapeutic resistance, and inflammatory lung disease. By uncovering how oxidative modifications such as protein S glutathionylation regulate signaling pathways, metabolic reprogramming, and epithelial cell behavior, my long-term goal is to identify redox dependent vulnerabilities that can be targeted to improve outcomes for patients with lung adenocarcinoma and chronic inflammatory lung disorders. Ultimately, my work aims to translate discoveries in redox chemistry and glutathione biology into new therapeutic strategies that overcome drug resistance and halt disease progression.
To achieve this goal, my work integrates biochemical, molecular, and multi omics approaches—including proteomics, metabolomics, and transcriptomics—to map oxidative signaling networks in epithelial cells and tumors. We leverage genetically engineered mouse models, patient derived samples, precision cut lung slices and advanced organoid systems to dissect redox regulated pathways in vivo and ex vivo. My recent work identified S glutathionylation of the deubiquitinase OTUB1 as a key mechanism that stabilizes the cystine transporter subunit SLC7A11, thereby promoting glutathione synthesis and chemotherapy resistance in lung adenocarcinoma. In parallel, we investigate redox regulated drivers of fibrosis, inflammation, and metabolic remodeling, uncovering mechanisms that span from TRPV1 mediated pain signaling to glutathione dependent regulation of extracellular matrix proteins. These integrated strategies allow us to define redox controlled therapeutic targets with high translational potential.