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Researchers on the trail of a molecular pathway that may lead to lung cancer
  
By Birgit Hofmann-Reinert

Though lung cancer is the most common cause of cancer deaths in the United States, little is known about the exact molecular mechanisms that trigger airway epithelial cells to become cancerous. Since most people with early lung cancer do not have any symptoms, precancerous cells are often not detected until they have developed into cancer cells, with the result that 80 percent of patients die within a year. A team of researchers has now come one step closer to understanding the molecular pathway related to the development of lung cancer.

Generally, environmental pollutants and toxins—especially tobacco smoke—injure the lung's epithelial cells and trigger a change in cell differentiation. The cells gradually turn into precancerous, squamous cells and 'cornify' (form an interlocking barrier) against the persistent toxic exposures. These injured, squamous cells then change into cancerous ones, if their function is not properly regulated.

In a study published in the October 13, 2000 issue of The Journal of Biological Chemistry, the researchers describe the effects of a tumor-promoting toxin, phorbol ester, on a particular gene (SPRR1), whose expression is very closely associated with squamous cell differentiation. The findings suggest that the SPRR1 gene plays a role in the production of a protein involved in the cell's gradual 'cornification' against the toxic exposures.

"If we can understand these early precancerous cellular changes, we might be able to reverse them before it's too late," says Sekhar Reddy of The John Hopkins University School of Public Health in Baltimore, Maryland. "Or, if we can find a way to detect precancerous cells within a few months of their onset, we might be able to prevent the development of full-blown cancer, or provide effective treatment early on," he is quoted as saying.

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Vuong, H. et al. Phorbol ester-induced expression of airway squamous cell differentiation marker, SPRR1B, is regulated by protein kinase Cdelta/Ras/MEKK1/MKK1-dependent/AP-1 signal transduction pathway. J Biol Chem 275, 32250-32259 (October 13, 2000).
 

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