Elevated hepatocyte paraffin 1 and neprilysin expression in hepatocellular carcinoma are correlated with longer survival.

Hepatocyte paraffin 1 (Hep Par 1) and neprilysin (CD10) are well-known markers of hepatocellular carcinoma (HCC). To assess their potential prognostic role, we conducted a retrospective analysis of 97 formalin-fixed and paraffin-embedded HCC from patients treated by surgery with curative intent, using standard immunohistochemical procedures and semiquantitative analysis. Strong Hep Par 1 expression and canalicular CD10 staining pattern were significantly correlated with smaller tumor size (p=0.

Monoallelic methylation of the APC promoter is altered in normal gastric mucosa associated with neoplastic lesions.

Adenomatous polyposis coli (APC) promoter hypermethylation has been reported frequently in normal gastric mucosa, but it remained to be clarified whether this occurs in every individual. In this study, methylation of the APC promoter was analyzed in histologically normal-appearing gastric mucosa samples by methylation-sensitive single-strand conformation analysis and by a methylation-sensitive dot blot assay. Epithelial cell samples were collected by microdissection from tissue sections.

Mucosal ablation with photodynamic therapy in the esophagus: optimization of light dosimetry in the sheep model.

Background: Photodynamic therapy is an attractive technique for mucosal ablation in patients with superficial squamous cell carcinoma of the esophagus, or high-grade dysplasia or early stage adenocarcinoma arising in Barrett's esophagus. Although illumination with green light is assumed to be safe, choice of the light has been empirical in clinical studies; light dose is often reduced to avoid potential complications. The present study assessed the safety of green and blue lights during photodynamic therapy in the esophagus by progressively administrating increasing doses in an attempt to standardize the dose and determine a safe upper limit.

p16 inactivation by methylation of the CDKN2A promoter occurs early during neoplastic progression in Barrett's esophagus.

Background & Aims: The potential role of p16 inactivation by CDKN2A/p16 promoter hypermethylation and/or loss of heterozygosity (LOH) of the CDKN2A gene was investigated in neoplastic progression of Barrett's esophagus.

Methods: CDKN2A promoter hypermethylation was studied by methylation sensitive single-strand conformation analysis and sequencing using bisulfite modified DNA in Barrett's esophageal adenocarcinomas, premalignant lesions, and normal squamous esophageal epithelium. All of the lesions of interest were sampled by microdissection from paraffin-embedded fixed tissue sections.

Beta-catenin expression and its association with prognostic factors in adenocarcinoma developed in Barrett esophagus.

The majority of the adenocarcinomas arising in Barrett esophagus manifest clinically at an advanced stage and have a poor prognosis. As a result of this poor prognosis, much attention has been directed toward the exploration of markers for neoplastic progression in Barrett esophagus. The objective of the present study was to determine the expression of beta-catenin by immunohistochemical analysis in 70 adenocarcinomas developed in Barrett esophagus and to examine its relationship to various prognostic factors currently in use.