Nada Y. Kalaany, PhD

Over half of lung cancer patients experience extreme and rapid weight loss at advanced disease stages. This devastating condition of fat and muscle wasting, called cachexia, is thought to be irreversible and contributes to a decline in the patients' quality of life and death from the disease. Despite urgent need, little is known about the metabolic causes of cancer-associated cachexia. Moreover, prevention or therapy for this condition is still lacking. We will use mouse models of lung cancer to explore the idea that insulin resistance could contribute to this wasting condition. In this scenario, blood sugar (glucose) is no longer stored as fat or used by muscles, while the liver continuously supplies glucose to lung tumors for their use and growth. We hope to identify metabolic changes in lung cancer-associated cachexia and help the development of clinical strategies to prevent and/or treat lung cancer patients at different disease stages.

Update:

Our findings in mice with cachexia confirmed our hypothesis that insulin resistance can contribute to this wasting condition. Blood sugar (glucose) is no longer stored as fat or used by muscles, while the liver continuously supplies glucose to lung tumors for their use and growth. We have been able to gain a deeper understanding of the metabolic basis of body wasting in lung cancer, which results in significant frailty, increased morbidity, and the inability to receive proper cancer therapy to improve survival.