Stomach cancer has been strongly linked to chronic inflammation. Now, a new study, led by Columbia University scientists, has shed light on how inflammation contributes to the cancer of stomach.
The research team found that increased levels of a single proinflammatory cytokine, an immune system protein called interleukin-1 beta (IL-1B), can tart the progression towards stomach cancer.
"This study shows that accumulation of IL-1B, which is induced by infection with the bacterium Helicobacter pylori (H. pylori) in the gastrointestinal tract, is a significant contributor to the onset of stomach cancer," said lead author Timothy C. Wang, chief of the Division of Digestive and Liver Diseases and the Dorothy L. and Daniel H. Silberberg Professor of Medicine at Columbia University College of Physicians and Surgeons.
H. pylori is typically acquired in childhood through person to person transmission, and the bacterium lives within the stomach just above the stomach cells, where it induces a mild inflammatory response known as gastritis.
The study showed that IL-1B works by activating a type of white blood cell known as myeloid derived suppressor cells (MDSCs), which is believed to be strongly pro-inflammatory.
"Blocking IL-1B or the myeloid (MDSCs) cells may represent a potential strategy to prevent stomach cancer," said Wang.
The results are published journal Cancer Cell.