Laparoscopic Paraesophageal Hernia Repair With Nissen Fundoplication in a Patient With Ancient Schwannoma of the Gastroesophageal Junction.

Schwannomas are mostly benign tumors that originate from Schwann cells and are rarely seen in the gastrointestinal tract. Our patient is a 65-year-old female who was found to have a 1.5 cm lesion at the gastroesophageal junction, which was clipped and excised on endoscopy. Histologic examination demonstrated an ancient schwannoma. Two years afterward, she presented to our clinic for a large type III paraesophageal hernia. We took her to the operating room for a laparoscopic paraesophageal hernia repair and Nissen fundoplication. We performed an upper endoscopy during the case and found no recurrence of the ancient schwannoma. The case progressed well without complications. She was discharged on postoperative day 1 after tolerating a pureed diet and reported no issues in follow-up. In summary, we demonstrate a successful surgical outcome in a patient who had undergone resection of this rare tumor 2 years prior to her surgery.

Enhancer of zeste homolog 2 (EZH2) regulates adipocyte lipid metabolism independent of adipogenic differentiation: Role of apolipoprotein E.

Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27. However, inhibition of EZH2 induced lipid accumulation in certain cancer and hepatocyte cell lines. To address this discrepancy, we investigated the role of EZH2 in adipogenic differentiation and lipid metabolism using primary human and mouse preadipocytes and adipose-specific EZH2 knockout (KO) mice. We found that the EZH2-selective inhibitor GSK126 induced lipid accumulation in human adipocytes, without altering adipocyte differentiation marker gene expression. Moreover, adipocyte-specific EZH2 KO mice, generated by crossing EZH2 floxed mice with adiponectin-Cre mice, displayed significantly increased body weight, adipose tissue mass, and adipocyte cell size and reduced very low-density lipoprotein (VLDL) levels, as compared with littermate controls. These phenotypic alterations could not be explained by differences in feeding behavior, locomotor activity, metabolic energy expenditure, or adipose lipolysis. In addition, human adipocytes treated with either GSK126 or vehicle exhibited comparable rates of glucose-stimulated triglyceride accumulation and fatty acid uptake. Mechanistically, lipid accumulation induced by GSK126 in adipocytes was lipoprotein-dependent, and EZH2 inhibition or gene deletion promoted lipoprotein-dependent lipid uptake in vitro concomitant with up-regulated apolipoprotein E (ApoE) gene expression. Deletion of ApoE blocked the effects of GSK126 to promote lipoprotein-dependent lipid uptake in murine adipocytes. Collectively, these results indicate that EZH2 inhibition promotes lipoprotein-dependent lipid accumulation via inducing ApoE expression in adipocytes, suggesting a novel mechanism of lipid regulation by EZH2.