The Telegraph
Since 1st March, 1999
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Smoker hope in vitamin A

Washington, Feb. 5 (Reuters): A cousin of vitamin A may be able to repair some of the genetic damage done by smoking and perhaps even prevent lung cancer, US researchers have said.

They hope their research will help them find ways to prevent lung cancer in former smokers, who have a high risk of the disease even years after they quit.

“The drug we used acts to reverse a genetic abnormality associated with development of lung cancer,” said Jonathan Kurie of the University of Texas M.D. Anderson Cancer Center, who led the study.

They do not believe the drug they used will be a final product — it causes too many side-effects such as rashes. But their study showed there was hope and pointed researchers down the road toward better compounds.

“The work is a proof of concept, suggesting that compounds like this may prove to have a protective effect against development of precancerous lesions,” Kurie said. Such lesions can become cancerous tumours.

Researchers have been studying antioxidants, compounds that prevent and in some cases reverse genetic damage, as a possible route to preventing or treating a range of cancers. Some of the most common antioxidants are vitamins such as vitamins A.

Studies have not shown taking megadoses of these vitamins can help smokers — and one study showed it may hurt. Taking vitamins at home is probably no solution, either, said Kurie.

“You have to take too high a dose and have to be under a doctor’s supervision for that,” he said. So Kurie’s team tried a cousin of vitamin A known as 9-cis-retinoic acid.

Writing in yesterday’s issue of the Journal of the National Cancer Institute, Kurie and colleagues said the compound seemed to fix some of the DNA damage seen in former smokers. They focused on the RAR-beta gene. They studied 226 patients who had stopped smoking for at least a year.

One-third of them were given 9-cis-retinoic acid, one-third got a related compound called 13-cis-retinoic acid, which has shown promise against other cancers, and a third group got a placebo or dummy pill.

Tissue samples taken from their lungs showed clear damage in many of the patients before treatment. Before treatment, 69 per cent of the patients had good, working versions of the RAR-beta gene. Afterward, the only real change was seen in those who got 9-cis-retinoic acid — 76 per cent of them had working versions of the gene.

Kurie said his team now wants to test related compounds that may be safer. “We are starting to talk to Ligand Pharmaceuticals about Targretin,” he said. This drug has a similar mechanism and has shown promise in a range of cancers. “It is probably better tolerated than 9-cis-retinoic acid,” Kurie said.

His team is also testing Celebrex, a second-generation version of drugs such as ibuprofen and aspirin. Marketed by Pfizer and Pharmacia, Celebrex, and possibly related drugs, may prevent the development of cancer by stopping tumors from growing blood vessels to feed themselves.

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