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Target for Lung Cancer Chemoprevention Identified

April 2, 2011
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• Endobronchial dysplasia can be modified pharmacologically.
• Effect on endobronchial dysplasia was seen in former smokers.
• Full study details to be presented at AACR press conference.

ORLANDO, Fla. — Scientists have identified a biomarker for measuring the success of lung cancer chemoprevention, an emerging frontier in the fight against this disease that has long been stymied by a lack of measureable outcomes. These study results were presented at the AACR 102nd Annual Meeting 2011, held April 2-6.

Paul Bunn, M.D., executive director of the International Association for the Study of Lung Cancer and the James Dudley endowed professor of lung cancer research at the University of Colorado Cancer Center at the University of Colorado School of Medicine, said measurements of endobronchial dysplasia, abnormal cell development that can lead to lung cancer, could predict how well a chemoprevention agent is working.

Bunn presented updated results of a study that tested the effect of oral iloprost on the improvement on endobronchial dysplasia in 152 former smokers. As smoking cessation messages take hold and quit rates increase, former smokers are still at greater risk for lung cancer than the general population.

“We told people to quit smoking and they did, but half of our lung cancer cases in the United States are coming from people who are former smokers,” he said. “We need to work on ways to repair their lungs through chemoprevention.”

Bunn analyzed the effect of iloprost among those who had endobronchial dysplasia at enrollment, and found a significant difference in prevalence of endobronchial dysplasia. Moreover, when they analyzed the effect of iloprost on Ki-67, a measure of cell proliferation, the difference was not significant.

This is an important advancement for the chemoprevention field, Bunn said, because it shows that they can test agents, like iloprost, and measure the effect on endobronchial dysplasia as an outcome. Chemoprevention is a goal for cancer researchers, and many of them liken the idea to heart disease prevention with statins, a major public health advance of the past 50 years.

“The challenge is there has been no real equivalent to cholesterol with cancer. This study shows that endobronchial dysplasia could play that role,” he said.

This abstract was presented at an AACR press conference on Saturday, April 2 at 10:00 a.m. ET in room W313 of the Orange County Convention Center.

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The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, the AACR is the world’s oldest and largest professional organization dedicated to advancing cancer research. The membership includes 33,000 basic, translational and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 90 other countries. The AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants, research fellowships and career development awards. The AACR Annual Meeting attracts more than 18,000 participants who share the latest discoveries and developments in the field. Special conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment and patient care. Including Cancer Discovery, the AACR publishes seven major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; Cancer Epidemiology, Biomarkers & Prevention; and Cancer Prevention Research. AACR journals represented 20 percent of the market share of total citations in 2009. The AACR also publishes CR, a magazine for cancer survivors and their families, patient advocates, physicians and scientists.

Media Contact:
Jeremy Moore
(267) 646-0557
Jeremy.Moore@aacr.org
In Orlando, April 2-6:
(407) 685-4001

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