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Research Strengthens Link Between Smoking, Pancreatic Cancer

Mar. 11, 2007 — Researchers at Michigan State University have added yet another piece to the puzzle that links cigarette smoking with cancer of the pancreas, one of the deadliest forms of cancer.


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In research published in the recent issue of the International Journal of Cancer, MSU’s James Trosko and colleagues zeroed in on the mechanism by which a healthy cell turns cancerous.

Specifically, they found that the chemicals produced by the burning of tobacco products – polycyclic aromatic hydrocarbons, or PAHs – interfere with communication between the body’s cells. More importantly, the work showed that some of these chemicals don’t necessarily initiate the cancer, but rather contribute to the promotion of it.

“These PAH chemicals are related to the multistage, multimechanism process of carcinogenesis, not by mutating the stem cell, but by triggering the stem cell that’s been previously mutated to proliferate,” said Trosko, a professor of pediatrics and human development. “This finding has major implications, including the possibility that dietary intervention might interrupt or even reverse the promotion of pancreatic cancers.”

Until now, most scientists thought that specific PAHs produced by burning tobacco mutated genes which, in turn, triggered the cancer mechanism.

“We take issue with this interpretation,” Trosko said. “We don’t believe that the PAH chemicals cause mutations which then lead to cancer.”

Pancreatic cancer is one of the more deadly forms of cancer, with an average survival rate of only about a year. It’s projected that more than 37,000 Americans will be diagnosed with pancreatic cancer in 2007.

Trosko noted that PAHs are formed when any substance containing certain proteins is burned, including foods.

“PAHs are all over,” he said. “When you grill a steak or a hamburger, for example, you get exactly the same class of chemicals.”

This research is the culmination of nearly 30 years of work in Trosko’s lab. It was in 1979 that Trosko, colleagues and students demonstrated that tumor-promoting chemicals interfered with a cell’s ability to communicate with other cells. Later, this group isolated adult human pancreatic stem cells from human pancreatic tissue.

Subsequent published findings indicated that these stem cells appeared to be targets for cancer.

“Since we had the system here in our lab, we decided to see if PAHs would act as a tumor promoter,” he said. “And sure enough they did.”

The good news is that people who quit smoking can dramatically improve their chances of avoiding cancers.

“If these chemicals act like cancer promoters and not initiators,” Trosko said, “then quitting smoking can assist in interrupting the process.”

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The above story is reprinted from materials provided by Michigan State University.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


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