Scientists from the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center found that two genes, related to inflammation, may be major risk factors for developing lung cancer. "Our findings help explain how heavy smoking, for example, combines with a genetic predisposition to create a besieged environment within the lungs," said lead author Eric Engels, researcher at the Viral Epidemiology Branch of the NCI's Division of Cancer Epidemiology and Genetics. "Essentially, sustained inflammation alters the microenvironment of the lung tissue, damaging cells and altering DNA." The study discovered the mechanism by which damage to the lung through smoking triggers an over zealous inflammatory response by the immune system that can lead to lung cancer. The researchers studied 1,500 lung cancer patients and 1,700 controls and found that some variants or polymorphisms in the genes for interleukin (IL) 1A and 1B are found more frequently in patients with lung cancer. The findings of this study increase the understanding of how some people are predisposed to developing cancer and may lead to potential therapies.
Researchers at UT Southwestern Medical Center discovered a substance from the bark of the lapacho tree that has anti-cancer properties and could be useful for treating lung cancer. The researchers found that in non-small cell lung cancer, the substance beta-lapachone is metabolized by the enzyme NQO1 and results in cell death without damaging non-cancerous tissues which do not express NQO1. "Future therapies based on beta-lapachone and NQO1 interaction have the potential to play a major role in treating devastating drug-resistant cancers such as non-small cell lung cancer," said Erik Bey, lead author of the study and a postdoctoral researcher at the Harold C. Simmons Comprehensive Cancer Center. "This is the first step in developing chemotherapeutic agents that exploit the proteins needed for a number of cellular processes, such as DNA repair and programmed cell death."
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