Lung cancer is the second most commonly diagnosed cancer among American men and women. The American Cancer Society estimates about 221,130 new cases of lung cancer will be diagnosed in the U.S. this year. The most common type is non-small cell lung cancer, accounting for 85 to 90 percent of cases.
The cancer is the leading cause of cancer death in this country and is expected to kill 156,940 Americans this year. Roughly 87 percent of lung cancer deaths are attributed to smoking. The longer a person smokes and the more cigarettes smoked/day, the greater the risk.
Researchers estimate about 19 percent of Americans are current cigarette smokers. Cigarette smoke consists of vapor and particulate matter that contains more than 4,000 different compounds. At least five of those compounds are known carcinogens. When a smoker inhales, those compounds and other toxic agents enter the lungs, where they are absorbed into the bloodstream and carried throughout the body.
Laura Hays, Ph.D., Cancer Biologist with Oregon Health and Science University in Portland, OR, says while smoking is the leading cause of lung cancer, not everyone who smokes gets the cancer. Lung cancer is associated with a significant amount of chromosome damage. Hays explains that damage appears to be related to a deficiency of a protein, called Fanconi Anemia Complementation Group D2 (FANCD2).
FANCD2 is like a doctor to the cell. It normally protects the cell from DNA damage. Overexpression of FANCD2 helps protect cells from the toxic chemicals in cigarette smoke. On the other hand, people with a deficiency of FANCD2 have a higher risk of chromosome damage after exposure to toxic compounds.
Investigating the Role of Tobacco Smoke
Hays and her colleagues wanted to try to better understand the damage process in cigarette smoking and how FANCD2 may play a role. The researchers used a special machine to collect cigarette smoke. James Pankow, Ph.D., Chemist at Portland State University, explains that the machine "inhales" the tobacco and collects the vapor and particulates in a special bag. The collected material is then liquefied and added to a culture plate lined with healthy (nonsmoking) human tracheal cells to simulate the effects of cigarettes. The researchers discovered that FANCD2 disappears from the airway cells in as little as six hours after exposure to the contents in tobacco smoke.
Hays says the next step in the research is to determine which particular chemicals in the tobacco are destroying the FANCD2 protein. Investigators say the finding may also help them to one day determine which patients are most susceptible to developing lung cancer.
Research compiled and edited by Barbara J. Fister
American Cancer Society, http://www.cancer.org
National Cancer Institute, http://www.cancer.gov