The Mechanism of CagA and VacA in Gastric Cancer under the Tumor Microenvironment and Vitro Factors

Gastric cancer is closely related to the stomach microbiota,especially Helicobacter pylori.Numerous reports and clinical studies have shown that microbial behavior in the stomach may lead to pathological changes in the gastrointestinal tract of the host,which ultimately leads to the production and development of gastric cancer.This review outlines the major pathogenic processes of Helicobacter pylori in the stomach,specifically focusing on Cag A,Vac A,inflammatory pathways and oxidative stress.In addition,we describe the effects of some non-Helicobacter pylori factors,such as other microbiota,alcohol,and tobacco,on the carcinogenesis induced by Helicobacter pylori.The effects of family history are also taken into account.We hope that understanding the stomach microbiota will make it possible to more easily prevent,detect and treat gastric cancer.

Microbiota:a Sword that Breaks Through Diabetes

Diabetes are a group of metabolic disorders characterized by persistent hyperglycemia that is a major public health problem.Middle-aged and elderly people are at the highest risk of type 2 diabetes,but younger cases are now being diagnosed with greater frequency.Numerous clinical studies have reported that the behavior of the intestinal microbiota may affect the development of metabolic disorders in humans,including obesity and diabetes.This review describes the relationship between the gut microbiota and diabetes,and discusses the possible mechanisms underlying their involvement in the development of type 1 diabetes,obesity,and type 2 diabetes.By better understanding the intestinal microbiota,it may become possible to treat diabetes and obesity by manipulating the gut microbes through probiotics and dietary changes,fecal microbiota transplantation,or surgical approaches.

Factors Associated with Postoperative Gallstone Formation in Gastric Cancer Patients: a Systematic Review and Meta-analysis

Objective In this meta-analysis,we analyzed the risk factors for gallstone formation after gastric cancer surgery.Methods Relevant studies published from 1990 to 2017 were retrieved from the PubMed,Embase,Medline,Web of Science,Cochrane Library,Springer Link,Chinese Biomedical Literature,and Wanfang databases.We performed a meta-analysis to determine the odds ratio and 95%confidence interval(95%CI).Results Nineteen studies were included in the meta-analysis:four randomized controlled trials(RCTs),10 case-control studies,and five cohort studies.The 19 studies included 32 to 16,045 patients.The pooled OR(95%CI)and P-values of the OR(95%CI)were 1.89(1.25,2.86)(P=0.003)for gastric resection,0.22(0.12,0.40)(P<0.00001)for vagus nerve retention,1.73(1.45,2.06)(P<0.00001)for digestive tract reconstruction,0.80(0.54,1.17)(P=0.25)for pylorus-preserving gastrectomy,0.59(0.33,1.04)(P=0.07)for the degree of lymph node dissection,1.98(0.50,7.86)(P=0.33)for D12 lymph node dissection,and 1.33(1.15,1.54)(P<0.0001)for diabetes.Conclusions Our findings indicate that partial gastrectomy,vagus nerve preservation,and physiological digestive tract reconstruction can reduce the incidence of gallstones after gastrectomy.Diabetes is a contributory factor to gallstone formation.There was no significant difference in the incidence of gallstones based on pylorus preservation/non-preservation,the degree of lymph node dissection,or D12 lymph node dissection.This is the first meta-analysis to comprehensively analyze the risk factors for gallstone formation after gastric cancer surgery.We investigated the risk associated with gastric resection,vagus nerve retention,digestive tract reconstruction,PPG,the degree of lymph node dissection,D12 lymph node dissection,and diabetes.

A Tool for the Treatment of Gastrointestinal Tumors: Micro- Ecological Immunotherapy

It has been proposed that the intestinal microbiota and gastrointestinal tumors are interdependent.Changes in the microbiota can cause dysfunction of the gastrointestinal tract,thereby promoting carcinogenic changes,leading to the occurrence of gastrointestinal tumors.Recent studies on intestinal microbiota have opened up a new area in intestinal micro-ecological immunotherapy.The intestinal microbiota is a double-edged sword.Gut microbes participate in carcinogenesis,but can also be used for immunotherapy.The intestinal microbiota is also regulated by the daily diet.Intestinal micro-ecological immunotherapy combines intestinal immune nutrition and intestinal ecological nutrition to make full use of the intestinal microbiota to strengthen nutritional support.Micro-ecological immunotherapy enhances the body’s immune function by providing energy,improving the functional state of tissues and organs,protecting the intestinal mucosal barrier and maintaining normal intestinal microbiota balance.This involves,to some extent,PD-1 and PD-L1.The microbiota is beneficial to improve the clinical efficacy of conventional anti-cancer therapy and to reduce the incidence of complications.At the same time,micro-ecological immunotherapy is itself active and effective in the perioperative treatment of tumors,which is of great significance for the prognosis of the patient.Gastrointestinal tumors are increasingly linked to intestinal microbiota,and various microbiota-related technologies and drugs have been developed.In the future,the intestinal microbiota may represent a screening marker for gastrointestinal tumors.In addition,clinicians may be able to prevent and treat cancers by changing the gene expression levels of certain microbiota,or by regulating the types of microbes present.

PSC-induced Galectin-1 Promotes the Malignant Behavior of Pancreatic Ductal Adenocarcinoma

Background Galectin-1 is aβ-galactoside-binding protein overexpressed in the pancreatic stellate cells(PSCs)of pancreatic ductal adenocarcinoma(PDAC),while its expression is typically low in pancreatic cancer cells(PCCs).The point at which galectin-1 expression in PCCs increases,and its association with PDAC progression,have been unclear.Methods Galectin-1 expression in PDAC and metastatic lymph nodes was investigated using an immunohistochemical assay.PANC-1 PCC cells were co-cultured with PSCs expressing different levels of galectin-1.Subsequently,galectin-1 was overexpressed in PANC-1 cells using recombinant lentiviruses,and their proliferation,invasion,anchorage-independent growth,and in vivo tumorigenicity were evaluated.Results There was intermediate galectin-1 expression in PCCs,and it was positively associated with galectin-1 expression in PSCs in the PDAC tissues.Galectin-1 was strongly expressed in the metastatic lymph nodes.In the co-culture,high galectin-1 expression in the PSCs increased the galectin-1 expression in the PANC-1 cells.The galectin-1 overexpression in the PANC-1 cells enhanced their clone formation ability,proliferation,and invasion,increased the expression of proliferating cell nuclear antigen(PCNA)and BCL-2,and decreased Bax expression,promoting the establishment and growth of tumors.Conclusion High galectin-1 expression in PSCs induces galectin-1 expression in PCCs and subsequently promotes the malignant biological behavior of PDAC.