(RxWiki News) Pancreatic ductal adenocarcinoma is the worst, and unfortunately, the most common form of pancreatic cancer. Researchers are getting a grip on what makes this cancer so aggressive.
Molecular signals, called cytokines, help create the environment that encourages further cellular transformation from a damaged cell to a cancerous cell.
These molecules cause local inflammation, and in some cases the cancerous cells produce cytokines to redirect blood vessel growth to feed the tumor.
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A team of researchers from The University of Texas MD Anderson Cancer Center in Houston connected two important pieces of information about the molecular signaling involved in the transformation of a normal pancreas to a pancreatic ductal adenocarcinoma, fleshing out the framework of the disease process in an attempt to find a therapeutic target, succeeded in isolating interleukin-1apha (IL-1α) for further study.
Former studies have shown that the gene K-ras must be activated before the pancreatic cancer develops fully. Following K-ras activation, another molecular signal known as NF-κB is then activated through a series of molecular signals known as cytokines.
Most importantly, the cytokine known as interleukin one alpha (IL-1α) creates a feedback loop that sustains the cancer's uncontrolled growth. The researchers concluded that lowering amounts of interleukin-1apha (IL-1α) would break the cycle.
Cytokines, notably interleukins, have been used in the past to alter immune system sensitivity and the conclusion of the study found that targeting IL-1α may be a future area for pharmaceutical therapy in pancreatic cancer.
The studies found that the initiation of the Kras, NF-κB, IL-1α positive feedback loop was associated with the worst outcomes in pancreatic cancer. The study noted that genes for p62 and IKK2 were also implicated in the growth feedback loop.
“Kras is mutated in 80 to 95 percent of pancreatic ductal adenocarcinomas, and is the most frequent mutation among all cancers,” said senior author Paul Chiao, Ph.D., professor at MD Anderson.
“There have been many attempts to inhibit mutated Kras, but it’s an elusive target that so far has defied treatment,” Chiao went on to say. “So if we can’t hit Kras, maybe we can target one of its downstream genes. This research identifies some of those genes and suggests that interleukin-1apha (IL-1α) is a potential therapeutic target.”
The study was published in the journal Cancer Cell.
Research was funded by grants from the National Cancer Institute, as well as through MD Anderson’s Cancer Center Core Support Grant.
