The science behind why cancer tumors grow or do not grow within any particular human body is tricky; but medical scientists now think that they have an answer to why glutamine may be involved in the growth of pancreatic tumors.
Glutamine, also known as L-glutamine is the most abundant amino acid in the body. Amino acids can be “essential” (meaning you must get it from your diet) or “non-essential” (meaning your body makes these aminos). Glutamine is not necessarily an essential amino acid, but it may be considered essential in certain circumstances, but is classified typically as nonessential.
In Boston, Massachusetts it is a group of just such scientists and doctors, J Son, CA Lyssiotis, et al., at the Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, which is part of the Dana-Farber Cancer Institute, who have done some research on this very topic of glutamine amino acid and how it relates to the KRAS-regulated metabolic pathway that causes pancreatic tumor growth.
Some tumors rely on glutamine and mechanisms that support cancer metabolism
Cancer cells have their own kind of metabolism, which are unlike normal cells. According to the study by the team of professionals and specialists in Boston, these cancer cell metabolic glutamine dependencies includes “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.”
They report that where most cells use a “glutamate dehydrogenase (GLUD1) to convert glutamine-derived glutamate” human pancreatic cells, specifically, use a non-canonical pathway that identifies ductal adenocarcinoma (PDAC) cells, which are needed for tumor growth. After that it starts getting complicated!
The bottom line 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. Furthermore, we establish that the reprogramming of glutamine metabolism is mediated by oncogenic KRAS, the signature genetic alteration in PDAC [to repress] key metabolic enzymes in this pathway.”
All of this means that pancreatic cells and the PDAC pathway is dispensable, so that normal cells may actually provide the key to producing some unique therapeutic approaches to treat these tumors. Knowing that glutamine is involved in the pancreatic cell metabolism, as compared to normal cells, may lead the way to new discoveries for treating pancreatic cancer.
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