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Clues to Cell Death Could Fight Disease

Insights might produce treatments to kill off cancer cells, experts say

FRIDAY, Sept. 21 (HealthDay News) -- New information about a process called unplanned cell death, or necrosis, could help in the fight against heart disease, cancer, stroke and other life-threatening conditions, scientists say.

Necrosis is not the same as apoptosis -- natural, healthy programmed cell death. Necrosis is an unplanned cell death caused by outside factors, such as traumatic injury or infection.

It was long believed that the process of necrosis was chaotic and irreversible, note researchers at the University of Pittsburgh School of Medicine. But their new study suggests the process may actually be triggered as part of a regulated response to stress by a powerful protein called SRP-6. This protein can also potentially halt cell necrosis, the researchers explained.

It may be possible to harness SRP-6 to direct certain cells -- such as those in cancerous tumors -- to die off, or to save other kinds of cells, such as the degenerating neural cells that cause Alzheimer's and Parkinson's diseases.

The study appears in the Sept. 21 issue of Cell.

"For years, we believed that cell death related to a catastrophic insult such as stroke or heart attack that deprives tissue of oxygen couldn't really be treated, so we focused on strategies to prevent further damage by restoring blood flow as quickly as possible with clot busters and surgery," study senior author Dr. Gary A. Silverman, chief of newborn medicine in the department of pediatrics, said in a prepared statement.

"But our research indicates that necrosis can be interrupted and possibly repaired, even after the injury process is well underway. This insight has exciting implications for the management of heart disease, stroke and neurological illness," he said.

More information

For more on the life of the cell, head to the City University of New York.

-- Robert Preidt

SOURCE: University of Pittsburgh Schools of the Health Sciences, news release, Sept. 20, 2007

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