How nutrient uptake and utilization is altered in cancer, how the host systemic metabolic state can influence these alterations and in turn, get affected by tumor growth and metabolism, are major focus areas in our lab.

Altered metabolism is a hallmark of cancer. It is, however, not only driven by cell-autonomous genetic alterations in oncogenes and tumor suppressor genes, but also by the surrounding tissue microenvironment, as well as the systemic macroenvironment of the host. Evidence for a robust correlation between systemic metabolism and cancer incidence and progression has been accumulating for over a century. For instance, the anti-tumorigenic effects of dietary restriction have been recognized since the early 1900s. Moreover, recent epidemiological studies demonstrate a linear correlation between obesity, type 2 diabetes and mortality from cancers of a wide variety of tissues. Conversely, cancer-associated cachexia, or the organismal energy-wasting syndrome that degrades muscle and fat, can be detrimental to many cancer patients, negatively impacting their quality of life and shortening survival.

Using different models of lung and pancreatic cancer, our lab aims at identifying metabolic dependencies in tumors growing under distinct systemic metabolic states, with the goal of targeting them therapeutically in cancer patients, while minimizing toxicity in normal tissues.

In particular, our lab aims at understanding:

· How tumors survive and thrive in nutrient-limiting environments
· How tumor growth and metabolism can be affected by the systemic metabolic state of the host (e.g. dietary restriction, obesity, insulin resistance)
· How the host systemic metabolic state can, itself, get affected by tumor growth and metabolism (e.g. cancer-associated cachexia, or energy-wasting syndrome)