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SPINK1 can be used to differentiate between a WD-HCC and a HGDN with high diagnostic validity.

Background: Pancreatic ductal adenocarcinoma (PDAC) had a poor prognosis and surgical resection remains the only potentially curative treatment. The aim of the study was to identify the outcome and risk factors affecting survival after pancreaticoduodenectomy (PD) for PDAC.Methods: The patients who underwent PD for PDAC from 2007 to 2015 were retrospectively studied. Cox regression test for multivariate analysis was used for evaluation of prognostic factors for survival.Results: Ninety-four patients underwent PD for PDAC, 20 patients (21.3%) had major postoperative complications. The perioperative mortality was 4.3%. The 1-, 3-, and 5-years survival rates were 74.5%, 38.7%, 23.4, respectively. In univariate analysis the risk factors for survival were; presence of co-morbidity (P=0.03), high preoperative carbohydrate antigen (CA)19-9 > 400U/ml (P=0.02), advanced tumor stage (P=0.03), large tumor diameter >3cm (P=0.01), poorly differentiated tumor (P= 0.02), involved resection margin (P=0.04), and positive lymph nodes in pathology after surgery (P=0.03). In multivariate analysis the independent risk factors for survival were; high preoperative CA 19-9 (P=0.042), tumor size >3cm (P=0.038), poorly differentiated tumor in histopathology (P=0.045).Conclusions: High tumor marker CA19-9, tumor size, and grade are significant risk factors for poor survival after resection of PDAC and should be taken into account in the selection of patients for surgery to improve the outcome.

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Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy in adults. Several studies have classified HCC into molecular subtypes aiming at detecting aggressive subtypes. The aim of the present study was to investigate the role of p53, β-catenin, CD133, and Ki-67 in subclassification of HCC into different aggressive subtypes and the correlation between those markers and the clinicopathologic characteristics of HCC patients. This retrospective study was conducted on paraffin-embedded blocks of 114 HCC specimens. Tissue microarray was constructed and immunostaining for p53, β-catenin, CD133, and Ki-67 was performed and HCC score was formulated. P53 expression was associated with old age (P=0.028), large tumor size (P=0.019), poorly differentiated HCC (P=0.012), hepatitis B virus (HBV) positivity (P=0.032), and hepatitis C virus (HCV) negativity (P =0.046). β-catenin expression was associated with small sized tumors (P=0.005), HBV negativity (P=0.027), early-staged tumors (P=0.029), and prolonged recurrence-free survival (P=0.045). High percentage of CD133 expression was associated with old patients (P=0.035) and HBV positivity (P= 0.045). Ki-67 expression was associated with large tumor size (P= 0.049), vascular invasion (P= 0.05), old age (P=0.035), and previous treatment of HCV by direct acting antiviral agents (P=0.005). Cases with high HCC score showed significant association with old patients (P=0.002), previous treatment of HCV by direct acting antiviral agents (P<0.001), large tumor size (P<0.001), and poorly differentiated tumors (P= 0.009). The proposed HCC score can divide HCC patients into subtypes necessitating tailoring of treatment strategy according to this proposed score to target and optimally treat the aggressive subtypes. This score needs to be further validated on large number of patients with longer follow-up period.

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