Pancreatic cancer, notorious for its low survival rates and unique metabolic attributes, might be on the verge of meeting a novel adversary.
Scientists from Sanford Burnham Prebys bring forth an inventive approach, focusing on manipulating the nutrient reliance of the cancer cells, and thus, interfering with their fuel source to potentially halt their proliferation and spread.
This innovative method, outlined in Nature Cancer, has already been piloted in early-stage lung cancer trials but shows promising specificity for pancreatic cancer due to its peculiar reliance on the nutrient glutamine.
Pancreatic Cancer: A Silent Killer with Unique Traits
Despite accounting for a mere 3% of all cancers, pancreatic cancer casts a somber shadow with one of the lowest survival rates among its counterparts.
Cosimo Commisso, Ph.D., highlighted the urgent necessity for new treatments, given that survival rates over the past decade have only marginally improved, plateauing around 10%.
A key characteristic of pancreatic tumors is their encasement within dense connective tissue, essentially isolating them and hindering their oxygen supply.
This has driven the development of distinctive metabolic properties, a potential Achilles’ heel which the scientists aim to exploit.
Glutamine: A Critical Fuel Source for Pancreatic Tumors
One standout metabolic peculiarity of pancreatic cancer lies in its pronounced dependency on glutamine for energy, growth, and survival.
While past scientific endeavors aimed to obstruct access to glutamine, actualizing this approach has proved to be intricate.
Enter DON, a molecule bearing structural likeness to glutamine but devoid of its nutrient properties.
The research team, through mouse studies, discovered that DON notably decelerated pancreatic tumor growth and thwarted their metastasis.
Combating Nutritional Backup Plans of Cancer Cells
Despite the disruption in glutamine usage via DON, pancreatic cancer cells possess the ability to pivot and harness other nutrients, such as asparagine, for their perpetuation.
Thus, researchers amalgamated DON with an existing cancer treatment that obstructs asparagine metabolism.
This tandem treatment exhibited a synergistic effect, curbing the metastasis of pancreatic tumors to distant organs like the liver and lungs.
Commisso explained, “With DON, the cancer cells can’t use glutamine, but they can start to depend on other nutrients as a backup, including asparagine.
We thought that if we could stop them from using glutamine and asparagine, the tumors would run out of options.”
A Beacon of Hope: Advancing Toward Clinical Exploration
While the dual-nutrient-deprivation strategy is pioneering, DON has already entered the clinical trial arena for lung cancer, providing an existing framework that could potentially be adapted and expedited for pancreatic cancer trials.
Commisso expressed optimism about this groundbreaking approach, which could reframe the therapeutic landscape for pancreatic cancer, stating that “a lot of the preclinical work needed to rationalize it is already happening.”
The combination of treatments is stepping into uncharted territories, potentially becoming a pivotal game-changer in the battle against pancreatic cancer by not merely striking at the tumor but strategically incapacitating its ability to adapt and survive under nutrient deprivation.
Future investigations and clinical trials will determine the efficacy, viability, and potential to become a staple in pancreatic cancer treatment regimens.
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For more information about cancer prevention, please see recent studies about nutrient in fish that can be a poison for cancer, and results showing this daily vitamin is critical to cancer prevention.
The research findings can be found in Nature Cancer.
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