Academic journal article Journal of Environmental Health

Scientists Zeroing in on a Cellular Pathway to Lung Cancer

Academic journal article Journal of Environmental Health

Scientists Zeroing in on a Cellular Pathway to Lung Cancer

Article excerpt

In a major step toward understanding how air pollutants injure the lungs and trigger the cascade of molecular events leading to lung cancer, scientists at the Johns Hopkins School of Public Health have spelled out the molecular process whereby a tumor-promoting toxin, phorbol ester, can activate a gene called SPRR1. That gene is a building block of squamous cell differentiation, a precancerous lesion. The study appeared in the October 2000 issue of The Journal of Biological Chemistry.

Lung cancer is currently the leading cause of cancer death in the United States and other developed countries. About 80 percent of patients diagnosed with lung cancer die within 12 months because this type of cancer is silent in its early years and usually not detected until it has reached an advanced stage.

In previous studies, the Johns Hopkins researchers described how the lung's epithelial cells respond to a number of carcinogens and pro-carcinogens-including phorbol esters, retinoic-acid deprivation, and tobacco smoke--by changing into squamous cells. Although squamous cells are thought to be precancerous, they are initially a response to injury: They "cornify," or interlock, to form a tough extra barrier against toxic exposures. …

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