The surgical management of gastroesophageal reflux disease has evolved significantly with the increased understanding of the physiology of the reflux barrier. Initially, emphasis was on reduction of hiatal hernias and crural closure. With persistence of reflux symptoms, along with the development of esophageal manometry and the discovery of a high-pressure zone, focus evolved to surgical augmentation of the lower esophageal sphincter, including reconstruction of the angle of His, ensuring sufficient intra-abdominal esophageal length, fundoplication, and magnetic sphincter augmentation. More recently, the role of crural closure in antireflux and hiatal hernia repair has again received renewed attention due to the persistence of postoperative complications and recurrences. Rather than simply preventing transthoracic herniation of the fundoplication as was originally thought, crural closure has been documented to have a critical role in re-establishing intra-abdominal esophageal length and maintaining the pressure of LES. The application of mesh provides more options for strengthening crural closure. In this review, this article will discuss the evolution of surgical techniques for gastroesophageal reflux disease over the past century, aiming to better guide the surgical treatment and clinical research of gastroesophageal reflux disease.

Gastric cancer is one of the most common malignancies worldwide. The capacity for invasion and metastasis, as well as high heterogeneity, are the main reasons that gastric cancer patients lose the opportunity for surgery and have a poor prognosis. Despite the rapid advancement of molecular targeted therapies, such as HER2 and immune checkpoint inhibitors, survival of gastric cancer patients is still unsatisfactory because the understanding of the mechanism of gastric cancer progression is still incomplete. Recently, genomic research has critically deepened our knowledge of which gene products are dysregulated in invasive gastric cancer. Furthermore, the study of the interaction of gastric cancer cells with the tumor microenvironment has emerged as a principal subject in driving invasion and metastasis. These results are expected to provide a profound knowledge of how biological molecules are implicated in gastric cancer development. This review will summarize the advances in our current understanding of the molecular mechanism of gastric cancer invasion. Compared to conventional therapy using protease or molecular inhibitors alone, multi-therapy targeting invasion plasticity may seem to be an assuring direction for the progression of novel strategies.