ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) is a lethal tumor with a high mortality rate. The distinction between PDAC and chronic pancreatitis is sometimes challenging on routine histopathological examination, highlighting the need to identify biomarkers that can facilitate this distinction. This retrospective study was conducted to evaluate the diagnostic utility of nuclear receptor co-activator 3 (NCOA3), Maspin and Von Hippel-Lindau protein (VHL) immunostaining in PDAC. Eighty cases of PDAC, 46 cases of chronic pancreatitis and 53 normal pancreatic tissue were immunohistochemically assessed using NCOA3, Maspin and VHL antibodies on sections from a tissue microarray. NCOA3, Maspin and VHL were positive in 90 %, 100 % and 35 %, of PDAC cases respectively, whereas NCOA3, Maspin and VHL expressions were positive in 3.8 %, 0 and 100 % of normal pancreatic tissue and in 15.2 %, 21.7 % and 97.8 % of chronic pancreatitis cases respectively. Significant differences were observed between PDAC and other groups regarding NCOA3, Maspin and VHL expression (p < 0.001). The H scores of NCOA3, Maspin and VHL could significantly distinguish between PDAC and normal cases with high sensitivity (90 %, 100 % and 98.75 % respectively) and specificity (100 %, 100 % and 96.23 % respectively). Similar findings were found in the distinction between PDAC and chronic pancreatitis (Sensitivity: 90 %, 95.25 % and 98.75 %; specificity: 100 %, 100 % and 93.48 % for NCOA3, Maspin and VHL respectively). In conclusion, NCOA3 and Maspin were found to be significantly expressed in PDAC compared to non-tumorous tissue while VHL was significantly expressed in non-tumorous tissue. A panel of NCOA3, Maspin and VHL could potentially distinguish PDAC from non-tumorous pancreatic tissue.
ABSTRACT
Liver transplantation is the selected treatment for patients with advanced liver disease and cirrhosis, mostly as a complication of hepatitis C virus (HCV). Recurrent HCV and acute cellular rejection (ACR) of the graft are the most common causes of graft failure. The distinction between the 2 conditions is essential because they are managed differently. In some cases, the clinical and histopathologic features may overlap between recurrent hepatitis C and ACR, making differentiation difficult. The aim of this study was to investigate the role of C4d, CD68, and nuclear factor kappa-B (NF-κB) in the differentiation between ACR and recurrent HCV in the post-liver-transplant biopsy using immunohistochemistry. C4d expression in endothelial cells of portal or central veins (P=0.001) and the number of macrophages highlighted by CD68 (P=0.02) were in favor of ACR, whereas NF-κB expression by hepatocytes was in favor of recurrent hepatitis C. Vascular injury demonstrated by endothelial expression of C4d and prominent macrophage infiltration identified by CD68 expression were the distinguishing criteria for ACR and representing humoral and cellular-mediated immunity as evoking factors for graft injury. The upregulation of NF-κB in the hepatocytes of recurrent hepatitis C could be an immune response to infection or it may be induced by HCV itself.
