A recent study by researchers at the Stanford School of Medicine indicates that a protein complex called SWI/SNF could play a previously unsuspected role in slowing the growth of pancreatic cancer cells.

 

The study, which was published on Monday in the Proceedings of the National Academy of Sciences, used samples of 70 different pancreatic cancers, which were provided by the Sol Goldman Pancreatic Cancer Research Center at the Johns Hopkins University School of Medicine. In one-third of these 70 cases, at one subunit of the multiunit SWI/SNF protein complex was either deleted, mutated or rearranged.

 

Forty-eight of the cancer cases used in the study were primary samples from human patients, then implanted into immune-deficient mice. The other 22 cases were grown in the laboratory.

 

Using a technique called array comparative genomic hybridization (CGH), which involves using a single-stranded DNA to seek and bind to its mirror image, researchers were able to pinpoint all the disparities in the genome between normal and cancerous pancreatic epithelial cells. Researchers discovered that genes for individual subunits of SWI/SNF were altered 5 to 10 percent of the time.

 

According to the study, the link between the mutations in the SWI/SNF protein complex and pancreatic cancer had not been encountered in the past because these genetic differences are spread amongst the five different subunits of the protein complex. Researchers said it was not until the data was considered together that they realized more than a third of the cancer samples contained a deletion, mutation or rearrangement in at least one of the five subunits in the protein complex.

 

“This is really strong genetic evidence that this complex plays a role in pancreatic cancer,” said Jonathan Pollack, associate professor of pathology and senior author of the research, in a press release by the School of the Medicine. “It suggests the influence of the SWI/SNF complex is on par with that of other well-known tumor suppressors, such as p53.”

 

Upon this discovery, researchers then experimented by engineering the pancreatic cancer cell to re-express the altered subunit. They found that the artificial expression slowed the growth of the cancer cells — and even caused them to enter permanent suspended state instead of dividing wildly.

 

According to the press release, the researchers now plan on working to identify which particular genes are responsible for the growth of pancreatic cells by experimenting with the expression of genes on the SWI/SNF subunits.

 

Graduate student Hunter Shain is the first author of the study. Other contributors include graduate student Craig Giacomini and former pathology resident Karen Matsukuma.

 

— Melody Wong