Context.— The liver is frequently affected by Epstein-Barr virus (EBV) infection, but involvement is commonly subclinical and self-limited. Severe and potentially fatal EBV hepatitis has also been occasionally reported in immunocompromised patients and, even more rarely, in immunocompetent individuals. Objective.— To provide a review of the clinicopathologic findings of EBV hepatitis, with a focus on microscopic features and ancillary testing with a brief discussion of the differential diagnosis. Data Sources.— Analysis of the pertinent literature (PubMed) and clinical practice experience based on institutional materials. Conclusions.— Characteristic microscopic findings in EBV hepatitis include a diffuse lymphocytic sinusoidal infiltrate in a “string of beads” pattern, expansion of portal tracts by a predominantly lymphocytic infiltrate, and intact lobular architecture. In situ hybridization of EBV-encoded RNA is a helpful ancillary test. Correlation of clinical history, laboratory findings, and histopathologic features is essential to distinguish EBV hepatitis from autoimmune liver diseases, transplant rejection, lymphomas, and drug-induced liver injury.

Loss of KDM6A promotes pancreatic cancer progression and metastasis and delays pancreatic tissue recovery from pancreatitis. Mechanistically, a noncanonical p38-dependent activin A pathway likely mediates KDM6A function.BACKGROUND & AIMS: Inactivating mutations of KDM6A, a histone demethylase, were frequently found in pancreatic ductal adenocarcinoma (PDAC). We investigated the role of KDM6A in PDAC development. METHODS:We performed a pancreatic tissue microarray analysis of KDM6A Q8

Epigenetic regulation is emerging as a critical mechanism for pancreatic ductal adenocarcinoma (PDA) development. Histone methylation is an important regulatory mechanism, altering chromatin structure and promoter accessibility and causing aberrant gene expression. NSD1 and SETD2 genes encoding two histone H3K36 methyltransferases, are mutated or altered in 8-10% of PDA cases. However, whether there is altered protein expression of NSD1 or SETD2 in PDA and its precursors, and whether they have diagnostic or prognostic utility is unknown.

Aims Distinguishing true oesophageal Candida infections from oral contaminants is a common diagnostic issue. Historically, histological features believed to indicate true infection included epithelial invasion by pseudohyphae and intraepithelial neutrophils. Whether or not these features correlate with endoscopic lesions, symptoms and response to therapy has never been tested in a large cohort. The aim of this study was to determine whether specific histological features correlate with clinical and endoscopic findings when Candida is found in oesophageal biopsies. Methods and results We reviewed 271 biopsies in which Candida was detected. Cases were evaluated for the presence of desquamated epithelial cells, location/type of fungal forms, neutrophils, and ulceration. Medical records were reviewed for clinical history, endoscopic lesions, and response to antifungal therapy. Statistical analysis was used to determine whether any histological features significantly correlated with clinical variables. There were 120 males and 151 females with a mean age of 42 years. Fifty‐nine per cent had symptoms referable to the oesophagus, particularly dysphagia (36%). Most (73%) patients had abnormal endoscopic findings, with plaques, ulcers, or macroscopic evidence of oesophagitis. Seventy‐one per cent of patients with documented antifungal therapy showed symptomatic improvement. Overall, there was no statistically significant correlation between any histological feature and presenting symptoms, endoscopic findings, or response to therapy. Importantly, the lack of pseudohyphae, demonstrable invasion of intact epithelium or neutrophilic infiltrates did not exclude clinically significant infection. Conclusions We conclude that detection of Candida in oesophageal biopsies is always potentially clinically significant. Treatment decisions should be made on the basis of an integration of clinical, endoscopic and histological findings.

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