010422 Study Sheds Light on Carcinogen in Beef, Chicken

New York - A new study sheds light on exactly how a carcinogen found in well-done cooked beef and chicken can damage cells in the body. By looking closely at the process, the researchers hope to get a better handle on exactly how such carcinogens in the diet may lead to cancer--and thus help prevent the disease.

The carcinogen, known as PhIP, apparently causes cells to end up with too few or two many chromosomes, which are major chunks of DNA that can be lost or gained when a cell divides and the genetic material is divvied up incorrectly.

This situation -- known as chromosomal instability -- is one factor that can increase the risk of cancer, according to the report in the online early edition of the Proceedings of the National Academy of Sciences.

In contrast, a second carcinogen known as MNNG causes mutations in the repair genes, or those responsible for fixing mistakes that arise in the genetic code, but not in the chromosomes themselves. This condition, known as microsatellite instability, can lead to a build-up of mutations that result in cancer.

MNNG is produced by the colon during digestion and known to cause cancer in rats. Cells in the digestive tract are constantly exposed to carcinogens like MNNG and PhlP, which is abundant in the Western diet.

“The experimental data reported here strongly support the hypothesis that carcinogen exposure determines the type of instability in these cancers,” the authors conclude. “These data provide potential clues to one of the remaining unsolved problems in cancer research, namely, the relationship between dietary factors and the genetic abnormalities that drive the development of tumors.”

Different cancer-causing chemicals use distinctly different methods to start normal cells down the pathway leading to cancer, and understanding these methods could lead to improved treatments, according to the researchers.

“Cancer is a genetic disease,” Dr. Christoph Lengauer from Johns Hopkins Oncology Center in Baltimore, Maryland, said. “However, these genetic abnormalities are often caused by the environment, our diet, and other external factors.”

In the study, Lengauer and associates examined the genetic changes in cells exposed to PhIP and MNNG in the laboratory.

“We have known for a long time that environmental carcinogens cause direct damage to genes,” according to Dr. Jarle Breivik from University of Oslo at the Norwegian Radium Hospital in Oslo, Norway.

“These new findings indicate that environmental factors also shape the entire genetic evolution of cancer cells, and by investigating such relationships we should be able to pinpoint the causes of cancer more accurately,” Breivik said.

“I believe that these findings strongly indicate that there will be dramatic alterations in the way we think about cancer therapy,” added Breivik, who is the author of an editorial accompanying the study. “Most of all, we will see a much more differentiated practice, where therapeutic regimens are designed from the genetic profile of the patient and the individual tumor.”

SOURCE: Proceedings of the National Academy of Sciences Early Edition April 2001.

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