Altered expression of COX-2 and TNF-a in patients with hepatocellular carcinoma

• Published in: Revista española de enfermedades digestivas Vol. 111; no. 5; p. 364
• Main Authors: de Freitas Alves, Andressa, Baldissera, Vanessa Dido, Chiela, Eduardo Cremonese Filippi, Cerski, Carlos Thadeu Schmidt, Fontes, Paulo Roberto Ott, Fernandes, Marilda da Cruz, Porawski, Marilene, Giovenardi, Marcia
• Format: Journal Article
• Language: English; Spanish
• Published: Sociedad Espanola de Patologia Digestivas 01-05-2019
• ISSN: 1130-0108
• DOI: 10.17235/reed.2019.5898/2018

Background and aim: hepatocellular carcinoma is a type of cancer related with inflammation, as 90% of cases develop in a chronic inflammation condition. Excess inflammation can affect tissue homeostasis. Cytokines and inflammatory mediators are immunological components that can influence the functioning of cells and tissues. In addition, the estrogen receptor appears to play an important role in hepatocarcinogenesis. The aim of the study was to evaluate the expression of inflammatory markers and ER in patients with hepatocellular carcinoma. Methods: data from 143 patients of ISCMPA were analyzed. Immunohistochemistry was performed of cyclooxygenase-2 enzyme (COX-2), nuclear factor kappa B (NF-[kappa]B), tumor necrosis factor alpha (TNF-[alpha]) and ER in paraffin-embedded hepatic tissue. The percentage of the stained area, intensity of staining and of the number of ER positive nuclei were evaluated using the ImageJ 1.50 software. Results and conclusion: there was a significant difference between the groups in terms of the percentage of marked area (p = 0.040) for COX-2 and the intensity of staining of TNF-[alpha] (p = 0.030). No significant differences were observed in any of other parameters evaluated. In conclusion, COX2 and TNF-[alpha] are possible markers that should be further studied to determine their immunohistochemical profile and role in HCC development. Key words: Hepatocelular carcinoma. Immunohistochemistry. Inflammation. Ciclooxigenase-2. Tumor necrosis factor-alpha. Nuclear kappa B factor.