Chemoprevention of esophageal adenocarcinoma in a rat surgical model by a cysteinyl leukotriene receptor­1 antagonist.

Reflux of gastroduodenal contents into the esophagus leads to the development of esophagitis and inflammation-associated pathologies, such as Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). The role of the lipoxygenase (LOX) pathway in carcinogenesis has been recently reported; however, its involvement in esophageal carcinogenesis remains unclear. To address this, the present study investigated the potential of pranlukast, a cysteinyl leukotriene receptor-1 antagonist, to suppress the progression of BE and EAC in a rat duodenogastroesophageal reflux (DGER) model. Male Wistar rats that underwent DGER were divided into two groups. One group was fed commercial chow (control group), and the other was fed experimental chow containing pranlukast (pranlukast group). The rats were sacrificed at 10, 20, 30 and 40 weeks after surgery, and their esophagi were examined. Expression levels of 5-LOX, CD68, IL-8, VEGF and Ki-67 were investigated using immunohistochemistry, and apoptosis was analyzed using the TUNEL method. In the pranlukast group, esophagitis was milder, and the incidence of BE and EAC was significantly lower (P<0.05) compared with that in the control group at 40 weeks after surgery. The number of cells positive for IL-8 and VEGF were significantly lower in the pranlukast group compared with the control group. Proliferative activity was also lower in the pranlukast group compared with the control group (P<0.05). Pranlukast treatment increased apoptosis (P<0.05). Overall, Pranlukast suppressed esophageal carcinogenesis in a rat DGER model, decreasing inflammatory cytokines such as IL-8 and VEGF.

[A Case of Retroperitoneal Liposarcoma That Invaded and Filled the Jejunal Lumen].

A jejunal tumor was found with computed tomography in a 79-year-old man with a history of gastrectomy reconstructed with Billroth II method for gastric ulcers. The tumor with contrast effect extended into the afferent loop and invaded the retroperitoneum in the dorsal side. The tumor occupied the jejunal lumen in endoscopic examination. Malignant spindle cells were found in the biopsy specimen. An increase of MDM2 and CDK4 signals were observed in fluorescence in situ hybridization( FISH). Given the preoperative diagnosis of jejunal liposarcoma, we performed a resection of the tumor with partial jejunectomy and partial gastrectomy. In the pathological examination of the surgical specimen, the majority of the tumor was dedifferentiated sarcoma; relatively highly differentiated sarcoma cells were observed in the retroperitoneal lesion. Therefore, it was suspected that the retroperitoneal-derived liposarcoma had invaded the jejunal lumen.