(RxWiki News) Cancer can be thought of as a series of tiny molecular mistakes adding up until the situation is out of control. New research has detailed the specifics of the process occurring in pancreatic cancer.
Stanford University's School of Medicine has used molecular analysis to examine 70 different samples of pancreatic cancer to find the specific patterns of genetic abnormalities that cause the disease.
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While initial analysis in the past had not found any obvious links, specialized statistical software showed that over a third of the samples contained a mutation, deletion or rearrangement in one of five subunits of a family of proteins known as SWI/SNF.
This is significant because the SWI/SNF complex is involved in the regulation of the DNA replication, a key component necessary for cancer to go wild and begin dividing rapidly.
Restoring function of these damaged genes in a laboratory experiment by the same team caused the pancreatic cancer cells to stop growing.
"This is really strong genetic evidence that this complex plays a role in pancreatic cancer," said senior author Jonathan Pollack, M.D., Ph.D., from Stanford University, "and it suggests the influence of the SWI/SNF complex is on par with that of other well-known tumor suppressors, such as p53."
"Our intention was to identify new genes involved in pancreatic cancer," said Dr. Pollack. "The discovery that SWI/SNF plays a role was exciting because we never would have found it any other way. It really validates the use of genome-wide analysis."
While genetic based therapies are complex, further development of the principles in this research could lead to more treatments for this very difficult cancer.
Results were published in the Proceedings of the National Academy of Sciences.
No relevant financial relationships were disclosed by the researchers.
