Trail Overexpression Inversely Correlates with Histological Differentiation in Intestinal-Type Sinonasal Adenocarcinoma. (7th October 2013)

• Record Type: Journal Article
• Authors: Re, M.; Santarelli, A.; Mascitti, M.; Bambini, F.; Lo Muzio, L.; Zizzi, A.; Rubini, C.
• Other Names: Pawlik Timothy M. Academic Editor.
• Is Part Of: International journal of surgical oncology. Volume 2013(2013)
• Publication Date: 2013-10-07
• Subjects: Surgery -- Periodicals; Oncology -- Periodicals; Cancer -- Surgery -- Periodicals; Neoplasms -- surgery; Medical Oncology; Neoplasms; General Surgery; Cancer -- Surgery; Oncology; Surgery; Periodicals; Periodicals; 616.994059
• DOI: 10.1155/2013/203873
• Languages: English
• ISSNs: 2090-1402

Abstract

Abstract : 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.