Nada Y. Kalaany

Abstract Cachexia or body wasting is a significant contributing factor to the morbidity and mortality of pancreatic cancer. Despite an unmet need, its metabolic underpinnings remain poorly understood. Here, we characterize a mouse model that recaptures the longitudinal progression of human cachexia during pancreatic cancer development.

Main text First Cell Metabolism publication: Arany et al., Transcriptional coactivator PGC-1 alpha controls the energy state and contractile function of cardiac muscle, April 2005. In 2004, I was an undifferentiated cardiology fellow looking for a research topic. My focus on cancer during my PhD seemed disconnected from my newfound clinical interest. I looked for where the “puck was going to be” in cardiovascular (CV) research (channeling the great hockey player Wayne Gretzky).

Inhibiting glutamine metabolism has thus far been clinically challenging. Two studies in preclinical mouse models now report that, in contrast to the failure of glutaminase inhibitors, broad suppression of glutamine metabolism with glutamine analogs delivered to tumors results in reduced pancreatic cancer growth, with targetable resistance mechanisms. Glutamine is the most abundant amino acid in the mammalian body.