Tumor growth in pancreatic cancer patients may be slowed using glutamine. Glutamine is an amino acid, which is one of the building blocks of proteins. Although it is typically considered a non-essential amino acid (meaning the body may make it on its own), glutamine is technically a conditionally essential amino acid. The term “essential” means that it must be gotten through the diet, so this amino acid is—in certain circumstances—acquired via intake of food.

Glutamine, which is the most abundant amino acid in the human body, plays a role in cancer tumor growth; so depriving the cancer cells of glutamine may hold the key to slowing the spread of cancer of the pancreas, a study shows.

Study on pancreatic tumor growth and glutamine

At the Division of Genomic Stability and DNA Repair, Department of Radiation Oncology (part of the Dana-Farber Cancer Institute) in Boston, Massachusetts, a group of researchers and doctors, J Son, CA Lyssiotis, et al., have investigated just how the amino acid glutamine is involved with the KRAS-regulated metabolic pathway, which is part of the cause of tumor growth within the pancreas itself.

The researchers studied the metabolism of cancer cells and glutamine dependencies since, unlike normal cells, the cells within cancer tumors maintain their own type of metabolism. They said that “an increased use of the amino acid glutamine to fuel anabolic processes. Indeed, the spectrum of glutamine-dependent tumors and the mechanisms whereby glutamine supports cancer metabolism remain areas of active investigation.”

Because human pancreatic cells use a non-standard pathway, which identifies ductal adenocarcinoma (PDAC) cells, most cells use “glutamate dehydrogenase (GLUD1) to convert glutamine-derived glutamate.” What this means is that the PDAC cells “are strongly dependent … as glutamine deprivation or genetic inhibition of any enzyme in this pathway leads to [a] series of reactions [that] results in a pronounced suppression of PDAC growth in vitro and in vivo.”

The scientists established that because the glutamine metabolism is reprogrammed and “mediated by oncogenic KRAS, the signature genetic alteration in PDAC [represses] key metabolic enzymes in this pathway.”

With the PDAC pathway and pancreatic cells being dispensable, the glutamine in normal cells then becomes a possible new therapeutic approach in treating pancreatic tumors in humans. Hopefully more will be forthcoming on this new technique in the near future.