Gum disease bacteria linked to esophageal cancer
IN A NEW study, researchers propose for the first time that Porphyromonas gingivalis - the bacterium behind gum disease - could be a risk factor for esophageal cancer. The researchers, from the University of Louisville (UofL), KY, and Henan University of Science and Technology in Luoyang, China, report their findings in the journal Infectious Agents and Cancer. According to the Centers for Disease Control and Prevention (CDC), every year, around 15,000 people in the US are diagnosed with esophageal cancer - a cancer that starts in the esophagus or gullet, the muscular tube that moves food from the throat into the stomach.
The lining of the esophagus is made of two kinds of cell, which is why there are two main types of esophageal cancer: esophageal adenocarcinoma and esophageal squamous cell carcinoma (ESCC). ESCC is more common in developing countries. Known risk factors for esophageal cancer include chemical exposure, diet, heredity and age - all factors already common to many other cancers. The cancer is hard to diagnose in the early stages. For many patients, the cancer develops rapidly after diagnosis and the prognosis is not good.
For their study, the team tested tissue from 100 patients with ESCC and 30 patients who did not have the disease (the controls). They tested samples taken from three types of esophageal tissue: cancerous tissue, non-cancerous tissue adjacent to cancerous tissue and normal tissue from the controls. Co-senior author Huizhi Wang, assistant professor of oral immunology and infectious diseases at the UofL School of Dentistry, says: “These findings provide the first direct evidence that infection could be a novel risk factor for ESCC, and may also serve as a prognostic biomarker for this type of cancer.” He notes that if these findings are confirmed, then it could mean that eradication of a common oral bacterium could help reduce the significant number of people who develop ESCC.
To detect P. gingivalis in the tissue samples, the researchers measured expression of lysinegingipain, an enzyme unique to the bacterium. They also looked for DNA traces of the bacterial cell. They found levels of both the enzyme and the bacterial DNA were significantly higher in the cancerous tissue of ESCC patients than in surrounding tissue or tissue of normal controls. The team found that levels of P. gingivalis measures were in line with levels of other measures, such as extent of cancer cell differentiation, metastasis (extent of spread) and overall survival rate.
Speculating on possible explanations, Prof. Wang offers two. Either ESCC cells are a “preferred niche” for the bacterium to thrive in, or infection with the bacterium somehow spurs the development of the cancer. If the reason is that the cancer cells offer the bacterium a niche, then simple antibiotics could be a way forward for treatment. Another approach could be to use genetic technology to target the bacterium and ultimately eliminate the cancer cells.