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Protein Gives Clues to Pancreatic Cancer

When pp32 is gone, a tumor-spurring gene goes to work, researchers say


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FRIDAY, Oct. 19 (HealthDay News) -- Researchers say they've identified a protein that could play a key role in the development of pancreatic cancer.

According to a team at the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia, the protein -- called pp32 -- is a tumor-blocker than normally inhibits a cancer-causing gene called K-ras.

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However, pp32 is absent in the most aggressive form of pancreatic cancer, the researchers said. More research is required, but pp32 could eventually become a marker for this deadly form of pancreatic cancer and a potential drug target.

In laboratory experiments, the Jefferson team found that when pp32 is absent, mutations in the K-ras gene take over and turn cells cancerous. Adding pp32 to pancreatic cancer cells with K-ras mutations slowed the growth of the fast-growing cells. The researchers concluded that the loss of pp32 may be a key event in determining the aggressiveness of pancreatic cancer.

The study was published online in the journal Modern Pathology.

"If we are able to learn more about this molecule, this may be a potential target that we could turn on in aggressive types of pancreatic cancers," team leader Jonathan Brody, assistant professor of surgery, said in prepared statement. "In theory, if we could find a way to upregulate this molecule in these pancreatic cancers, we may be able to arrest these fast-growing cancer cells as we did in experiments in this study. As we understand its molecular interactions, we could also somehow find the things that regulate it and extend our molecular understanding of this devastating disease."

Previous research had also suggested a link between pp32 and prostate and breast cancer.

More information

The American Cancer Society has more about pancreatic cancer.



-- Robert Preidt

Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 10/19/2007

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SOURCE: Thomas Jefferson University, news release, October 2007


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