Aims: Data regarding expression of intestinal markers in hepatocellular carcinoma (HCC) are limited. We determined the clinicopathological associations of cytokeratin (CK)19, a progenitor liver epithelial cell marker as well as biliary epithelial marker, and intestinal immunohistochemical markers expression in HCC and assessed their prognostic value. Methods and results: Tissue sections and/or tissue microarrays (TMAs) from 202 known HCCs were immunostained using CK19, CK20, CDH17, CDX2 and SATB2 antibodies. Haematoxylin and eosin (H&E)-stained slides were reviewed for tumour grading. Clinical and oncological outcomes were retrieved. Associations of staining with clinicopathological features and survival outcomes were evaluated. CK19, CK20, CDH17, CDX2 and SATB2 were positive in 12.8, 5.4, 10.3, 8.6 and 59.9%, respectively. All but SATB2 were strongly associated with higher tumour grade and AFP levels > 400 ng/ml (P < 0.05). CK19positive HCC were more likely to express CDX2 (P = 0.001), CDH17 (P < 0.001) and/or CK20 (P = 0.012). CK20, CDX2 and CDH17 co-expression was seen in five cases (2.5%). CK19 and SATB2 positivity, tumour size ≥ 5 cm, background cirrhosis, AFP > 400 ng/ml and having no treatment were associated with decreased overall survival by log-rank test and univariable proportional hazards regression. However, in a multivariable model, CK19 and SATB2 positivity were not independent predictors of decreased survival while their association with known poor prognosticators in HCC was evident. Conclusions: HCC can express markers of intestinal differentiation. This phenotypical aberrancy correlates with variable clinicopathological parameters, some of which are independent predictors of poor survival.
Crohn's disease (CD), a form of idiopathic inflammatory bowel disease (IBD), has an estimated annual incidence of 3.1 to 20.2 per 100,000, and a prevalence of 201 per 100,000 in North America [1,2]. Based on its clinical behavior, CD is classified as B1 (non-stricturing, non-penetrating), B2 (stricturing) and B3 (penetrating) [3][4][5]. While most CD patients initially present as B1, they can have more than one phenotype, and clinical behavior may change over time [4]; i.e., a patient with B1 phenotype may develop strictures and or fistula during the disease course and subsequently be re-classified as having a B2 or B3 phenotype [6,7]. Eventually, about 70% of CD patients develop stenosis or fistula [7]. Stricture is the most common indication for surgery in CD [8].The progression of fibrosis and eventual stricture formation is a significant disease burden requiring escalation of medical treatment or surgical intervention in CD. Although many factors, such as genetic, epigenetic, serological, clinical, environmental, and endoscopic factors are postulated to portend an increased risk for fibrosis progression, its pathogenesis is relatively poorly understood [5,9,10]. Moreover, most of the pathological studies using formalin-fixed paraffin-embedded (FFPE) tissue are limited to morphological evaluation on routine hematoxylin and eosin (H&E)
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