Dr. Ogidigo will investigate how obesity affects lung cancer progression using a diet-induced obesity mouse model. She will focus on understanding how obesity-driven metabolic and chromatin changes influence lung tumor biology, and test incretin mimetics (metabolism-targeting drugs such as GLP1 agonists) as potential treatments to slow tumor growth in obesity models of lung cancer. By identifying obesity-specific molecular mechanisms and therapeutic targets, she aims to develop more effective, personalized treatment strategies for lung cancer patients with obesity or metabolic dysfunction.
- Research Summary
This project investigates how obesity and overweight influences lung cancer progression by using a diet-induced obesity (DIO) mouse model. I will assess tumor growth through imaging and analyze transcriptomic, metabolomic, and epigenetic changes linked to overnutrition or obesity. A key focus is understanding how obesity-driven metabolic and chromatin alterations affect lung tumor biology. The study also tests incretin mimetics—metabolism-targeting drugs—for their potential to slow tumor growth in obese or overweight models. By uncovering obesity-specific molecular mechanisms and therapeutic vulnerabilities, this work aims to inform more effective, personalized treatment strategies for lung cancer patients with obesity and associated metabolic dysfunctions.
- Technical Abstract
The overall goal of this project is to improve the quality of life for lung cancer patients. Lung cancer is lethal and accounts for ~20% of all cancer-related mortality in the United States. Lung cancer, a leading cause of cancer-related mortality worldwide, poses significant challenges due to limited therapeutic options and poor survival rates, particularly in the context of obesity.
To address these complexities, this study will utilize a diet-induced obesity (DIO) mouse model along with dietary interventions to investigate the impact of obesity and overnutrition on lung tumorigenesis. We will monitor tumor growth using imaging techniques and conduct transcriptomic and metabolomic profiling to characterize the functional consequences of the obese phenotype at various stages of tumor progression. Furthermore, we will explore the epigenetic landscape of overnutrition and obesity-associated lung cancer by generating a comprehensive genome-wide map of histone modifications and chromatin accessibility. In addition, we will evaluate the therapeutic role of metabolism-related agents in obesity-related lung cancer. Using the DIO mouse model, we will assess the efficacy of monotherapy therapy with incretin mimetic or combination therapy with immune inhibitor in attenuating overnutrition lung cancer progression.
This research will provide unprecedented insights into the molecular mechanisms underlying obesity-associated lung cancer and identify novel therapeutic strategies to improve patient outcomes. The successful completion of this project will offer valuable insights into the interplay between obesity, metabolism, and epigenetics in lung cancer progression. By targeting metabolic and epigenetic vulnerabilities, this research has the potential to advance our understanding of lung cancer biology and pave the way for the development of more effective and improved therapeutic interventions. Ultimately, this work aims to address the unmet need for targeted therapeutic strategies to combat lung cancer and enhance patient outcomes.