We are committed to elucidating the complex metabolic pathways that drive disease pathogenesis, with the ultimate goal of identifying innovative therapeutic targets.
Project 1: From Fat to Fight: Modulating Bone Marrow Adipocyte Metabolism in Leukemia through Caloric and Feeding Patterns
Obesity is a well-established risk factor for poor treatment outcomes in acute lymphoblastic leukemia (ALL), associated with higher rates of relapse, increased measurable residual disease, and reduced overall survival. With obesity rates climbing across all age groups, the clinical burden of obesity-related leukemia is projected to increase, underscoring the urgent need for mechanistic insight and targeted therapeutic strategies tailored to this high-risk population.
Despite strong epidemiological evidence linking obesity to leukemia outcomes, the biological underpinnings remain poorly understood—particularly the contribution of adipose tissue within the leukemia microenvironment. Bone marrow adipocytes possess specialized secretory profiles and direct proximity to leukemia cells, making them ideal candidates to mediate obesity-induced metabolic support for leukemia. Our work takes a novel approach by investigating how dietary interventions reshape BMA metabolism and alter leukemia outcomes. Beyond ALL, the insights gained may extend to other hematologic malignancies positioning this research at the cutting edge of cancer metabolism and microenvironment-focused therapy.
Project 2: Modulating Energy Metabolism to Limit Tumor Progression
Brown adipose tissue (BAT) is a type of fat tissue primarily involved in thermogenesis, which is the process of generating heat. Several studies have suggested that brown fat activation may have implications for cancer progression, although the exact nature of this relationship is still not fully understood. Metabolic effects including glucose and lipid metabolism, hormonal factors, inflammation and immunity and angiogenesis are key factors that are modulated by brown fat activation. This project aims to constrain tumor growth by targeting adipose tissue metabolism and promoting the greatest amount of energy expenditure.
Project 3: Exploring the Regulation of Gαq Signaling in Key Metabolic Processes and Energy Homeostasis
The increase in obesity worldwide has led to rising health care costs and a surge in the prevalence of type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), heart disease, and many cancers. Activation of mitochondrial respiration provides thermogenic fat the capacity to dissipate chemical energy as heat and offers tremendous potential to combat obesity. However, the molecular mechanisms controlling mitochondrial thermogenic respiration are not fully understood. Gαq signaling plays a crucial role in regulating key metabolic processes and maintaining energy homeostasis in cells. Gαq is a member of the G protein family, which acts as a molecular switch to transmit signals from cell surface receptors to intracellular effectors. This project aims at delineating the mechanisms underlying the role of Gαq signaling pathway in regulating whole-body metabolism.
Rahbani Lab 