Trail overexpression inversely correlates with histological differentiation in intestinal-type sinonasal adenocarcinoma

Int J Surg Oncol. 2013;2013:203873. doi: 10.1155/2013/203873. Epub 2013 Oct 7.


Introduction: Despite their histological resemblance to colorectal adenocarcinoma, there is some information about the molecular events involved in the pathogenesis of intestinal-type sinonasal adenocarcinomas (ITACs). To evaluate the possible role of TNF-related apoptosis-inducing ligand (TRAIL) gene defects in ITAC, by investigating the immunohistochemical expression of TRAIL gene product in a group of ethmoidal ITACs associated with occupational exposure.

Material and methods: Retrospective study on 23 patients with pathological diagnosis of primary ethmoidal ITAC. Representative formalin-fixed, paraffin-embedded block from each case was selected for immunohistochemical studies using the antibody against TRAIL. Clinicopathological data were also correlated with the staining results.

Results: The immunohistochemical examination demonstrated that poorly differentiated cases showed a higher percentage of TRAIL expressing cells compared to well-differentiated cases. No correlation was found with other clinicopathological parameters, including T, stage and relapses.

Conclusion: The relationship between upregulation of TRAIL and poorly differentiated ethmoidal adenocarcinomas suggests that the mutation of this gene, in combination with additional genetic events, could play a role in the pathogenesis of ITAC.

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology*
  • Aged
  • Ethmoid Sinus / metabolism
  • Ethmoid Sinus / pathology*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Occupational Diseases / metabolism
  • Occupational Diseases / pathology*
  • Occupational Exposure / adverse effects
  • Paranasal Sinus Neoplasms / metabolism
  • Paranasal Sinus Neoplasms / pathology*
  • Retrospective Studies
  • TNF-Related Apoptosis-Inducing Ligand / metabolism*


  • TNF-Related Apoptosis-Inducing Ligand