Combined treatment of refractory benign stricture after esophageal endoscopic mucosal dissection: A case report.

BACKGROUND: Endoscopic submucosal dissection (ESD) post-procedure stricture is a relatively common long-term complication following ESD treatment. A range of approaches has been implemented for the treatment of post-procedural stricture using endoscopic techniques such as endoscopic dilation, self-expandable metallic stent insertion, local steroid injection in the esophagus, oral steroid administration, radial incision and cutting (RIC). The actual efficacy of these different therapeutic options is highly variable, and uniform international standards for the prevention or treatment of stricture. CASE SUMMARY: In this report, we describe the case of a 51-year-old male diagnosed with early esophageal cancer. To protect against esophageal stricture, the patient was administered oral steroids and underwent self-expandable metallic stent insertion for 45 d. Despite these interventions, stricture was detected at the lower edge of the stent following its removal. The patient remained refractory to multiple rounds of endoscopic bougie dilation treatment, and thus suffered from complex refractory benign esophageal stricture. As such, RIC combined with bougie dilation and steroid injection was employed to treat this patient more effectively, ultimately achieving satisfactory therapeutic efficacy. CONCLUSION: Combination of RIC, dilation, and steroid injection can be safely and effectively implemented to treat cases of post-ESD refractory esophageal stricture.

The tumor suppressor role of miR-155-5p in gastric cancer.

Gastric cancer (GC) is the fifth most common type of malignant tumor worldwide and the most common cause of cancer-associated mortality in China. Recent studies revealed that microRNAs (miRNAs) function in the pathogenesis of GC, and that miR-155-5p expression is downregulated in GC tissues. However, the function of miR-155-5p has not been fully identified. In the present study, it was demonstrated that overexpression of miR-155-5p inhibited GC-cell proliferation and promoted apoptosis, while downregulation of miR-155-5p promoted GC-cell proliferation and decreased the cisplatin sensitivity of GC cells. Mitogen-activated protein kinase kinase kinase 10 was demonstrated to be a potential target gene of miR-155-5p. In conclusion, an antitumor role of miR-155-5p in gastric cancer was suggested.