Higher rates of esophageal cancer cases may be attributed to lifestyle factors such as: diet, obesity, alcohol and tobacco use.Moreover, the presence of oral <i>P. gingivalis</i> and <i>T. forsythia</i> has been found to be associated with an increased risk of esophageal cancer.Our review describes the role of <i>P. gingivalis</i> and <i>T. forsythia</i> in signaling pathways responsible for cancer development.It has been shown that <i>T. forsythia</i> may induce pro-inflammatory cytokines such as IL-1β and IL-6 by CD4 + T helper cells and TNF-α.Moreover, gingipain K produced by <i>P. gingivalis,</i> affects hosts immune system by degradation of immunoglobulins and complement system (C3 and C5 components).
We conducted a hospital-based case-control study to evaluate the genetic effects of functional single nucleotide polymorphisms (SNPs) in the interleukin 1 (IL1A and IL1B), IL1f7, IL3 and IL7Ra genes on the development of esophageal cancer.
Activation of NF-kappa B, increase of E2-EPF ubiquitin carrier protein and subsequent epithelial-mesenchymal transition might be the underlying mechanisms of the more aggressive tumor growth in IL-1 beta-positive esophageal cancer.
In conclusion, subjects with IL-1 beta -511TT genotype or IL-1 beta*T-IL-1RN*1 (T1) haplotype had lower risk for middle third tumor location of EC in a northern Indian population.