• (FGFR) fibroblast growth factor receptor
• FGF18
• cancer
• gene expression
• pathway

Explore the influence of family history of upper gastrointestinal (UGI) cancer on UGI cancer death, based on the Linxian Dysplasia Nutrition Intervention Trial (NIT) cohort.

Family history of UGI cancer was defined as at least one first-degree relative (parent, child, or sibling) had a history of esophageal or gastric cancer. Cancer death was carried out by ICD-10 code. Family history information was collected at baseline and cancer deaths were assessed at each annual follow-up. The COX proportional risk model was used to estimate the hazard ratio (HR) and 95% confidence interval (95% CI). We compared the positive family history group with the negative to determine the risk of family history on UGI cancer death. The effect of category of relatives, number of relatives with UGI cancer, and diagnosis age of relatives on the UGI death risk were further analyzed. Interaction and stratification analyses were done to see the subgroup effects. Sensitivity analyses were also conducted by exclusion of individuals who were followed up less than three years. We considered controlling of covariates including: gender, age (continuity), community, education level, number of siblings (continuity), BMI (continuity), smoking, alcohol use, fresh fruit intake, fresh vegetable intake, hot beverage intake, edible oil intake, meat intake, and moldy staple food intake. All food intake variables were converted into categorical variables.

From1985 to2015, we followed up total 3,318 individuals with 898 UGI cancer deaths (537 from ESCC, 77 from GNCC, and 284 from GCC). In a single factor analysis, family history of UGI cancer increased the risk of death of esophageal squamous cell carcinoma (ESCC) by 27% (HR=1.270, 95%CI1.072-1.504). No associations were observed in gastric cardia carcinoma (GCC) and gastric non-cardia carcinoma (GNCC). After adjusting for multi-factor, a family history of UGI cancer risk of death increased by 31.9% from ESCC (HR=1.319,95%CI:1.110-1.567). Subgroup analysis of different types of relatives with UGI cancers, UGI cancers in the mother (HR=1.457,95%CI:1.200-1.768), brother (HR=1.522,95%CI:1.117-2.073), and sister (HR=1.999,95%CI:1.419-2.817) were independent risk factors for ESCC death, while the father was not. In addition, 2 relatives with UGI cancer (HR=1.495, 95%, CI:1.110-2.013) and ≥3 relatives with UGI cancer (HR=2.836, 95%CI:1.842-4.367) significantly increased the risk of ESCC death, and the trend test was statistically significant (P<0.001). Relatives’ diagnostic age of 51-60 years (HR=1.322, 95%CI:1.046-1.672) and 41-50 years (HR=1.442, 95%CI:1.078-1.930) were the risk factors for ESCC death, with statistical significance in the trend test (P=0.010). No statistically significant result of the family history effect on the risk of death from GCC or GNCC was found. Sensitivity analysis of 80% of subjects, randomly selected, did not change the results.

A family history of UGI cancer may predict the risk of death from ESCC but not from GCC or GNCC. UGI cancer in the mother may predict the risk of death from ESCC, but not father, which indicates gender differences. Gender and smoking are the interaction items with family history in a similar extent. In the subgroup, the risk of ESCC death is more distinct by family history in younger, female, and better-lifestyle individuals, which indicates the unique role of genetic factors.

• Linxian Dysplasia Nutrition Intervention Trial
• esophageal squamous dysplasia
• family history
• lifestyle
• upper gastrointestinal cancer

Recently, endoscopic screening systems have enabled the diagnosis of gastric cancer in the early stages. Early gastric cancer (EGC) is typically characterized by a shallow invasion depth and small size, which can hinder localization of EGC tumors during laparoscopic surgery. Here, we review nine recently reported tumor localization methods for the laparoscopic resection of EGCs. Preoperative dye or blood tattooing has the disadvantage of spreading. Preoperative 3-dimensional computed tomography reconstruction is not performed in real time during laparoscopic gastrectomy. Thus, they are considered to have a low accuracy. Intraoperative portable abdominal radiography and intraoperative laparoscopic ultrasonography methods can provide real-time feedback, but these methods require expertise, and it can be difficult to define the clips in some gastric regions. Despite a few limitations, intraoperative gastrofibroscopy provides real-time feedback with high accuracy. The detection system using an endoscopic magnetic marking clip, fluorescent clip, and radio-frequency identification detection system clip is considered highly accurate and provides real-time feedback; we expect a commercial version of this setup to be available in the near future. However, there is not yet an easy method for accurate real-time detection. We hope that improved devices will soon be developed and used in clinical settings.

• Early gastric cancers
• Intraoperative methods
• Laparoscopy
• Tumor localization

• Gastric Cancer
• IL-33/ST2 Axis
• M2 Macrophages
• SPEM/Intestinalized SPEM

• advance care
• anxiety
• depression
• gastric cancer

• Anxiety/epidemiology
• Anxiety/psychology
• China/epidemiology
• Depression/epidemiology
• Depression/psychology
• Endoscopy/methods
• Gastrectomy/adverse effects
• Gastrectomy/psychology
• Humans
• Quality of Life/psychology
• Randomized Controlled Trials as Topic
• Stomach/surgery
• Stomach Neoplasms/surgery

Gastric cancer (GC) is one of the most common malignant tumours with high mortality and metastasis rates. E2F3, miR-125a and DKK3 have been reported to be involved in various cancer types, but their detailed roles in GC have not been fully understood.

A QRT-PCR assay was used to examine the expression of E2F3, miR-125a and DKK3 in metastatic and nonmetastatic GC tissues. DKK3 plasmids, DKK3 shRNA, miR-125a mimic and miR-125a inhibitor were transfected into BGC823 cells to evaluate the biological functions of DKK3 and miR-125a. A scratch wound healing assay and Transwell assay were utilized to determine the migratory and invasive ability of BGC823 cells transfected with the DKK3 plasmids, DKK3 shRNA, miR-125a mimic and miR-125a inhibitor. Moreover, qRT-PCR and WB analysis were used to analyse the mRNA and protein expression levels of metastasis-related genes after proper transfection. The target relationship between miR-125a and the DKK3 mRNA 3′UTR was determined by a dual luciferase reporter assay, while the interaction between E2F3 and miR-125a was analysed by a ChIP assay.

The clinical data showed that the DKK3 expression level in metastatic GC samples was significantly less than that in nonmetastatic GC samples, whereas the E2F3 and miR-125a expression levels in metastatic GC samples were notably greater than those in nonmetastatic GC samples. Moreover, knockdown of DKK3 and overexpression of miR-125a markedly promoted the migratory and invasive abilities of GC cells. Additionally, the protein and mRNA expression levels of metastasis-related genes, including N-cadherin, Vimentin, MMP2 and MMP9, were markedly decreased in the DKK3 and miR-125a inhibitor groups compared to their control groups and markedly increased in the DKK3 shRNA and miR-125a groups compared with the control group. Finally, a dual luciferase reporter assay and ChIP assay showed that E2F3 binds to the miR-125a promoter and that the DKK3 mRNA 3′UTR is a direct target of miR-125a. Furthermore, analysis of Kaplan–Meier curves also confirmed the regulatory role of E2F3 on miR-125a. Additionally, BGC823 cells transfected with E2F3 plasmids and shRNA downregulated and upregulated the expression of DKK3, respectively.

Our results suggested that E2F3 might play a tumour-promoting role in the metastasis and progression of GC by regulating the miR-125a/DKK3 axis.

• E2F3/miR-125a/DKK3 regulatory axis
• Gastric cancer (GC)
• Metastasis and progression of tumours

• Gastric cancer
• Invasion
• KLF4
• MicroRNA-106a
• Smad7

• Animals
• Carcinogenesis/genetics
• Cell Line, Tumor
• Cell Movement/genetics
• Cell Proliferation/genetics
• Gene Expression Regulation, Neoplastic/genetics
• Humans
• Kruppel-Like Factor 4
• Kruppel-Like Transcription Factors/genetics
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs/genetics
• Smad7 Protein/genetics
• Stomach Neoplasms/genetics
• Transcription Factors/metabolism

• DNA double-strand break
• gastric cancer
• p21
• pepsinogen
• stomach
• γ-H2AX

• N-of-1 trials
• chemotherapy-induced leukopenia
• gastric cancer
• traditional Chinese medicine (TCM)

Gastric cancer, as a malignant epithelial tumor, is a major health threat leading to poor overall survival and death. It is usually diagnosed at an advanced stage due to asymptomatic or only nonspecific early symptoms. The present study demonstrated that gankyrin contributes to the early malignant transformation of gastric cancer and can be selected to predict the risk of gastric cancer in those patients harboring the precancerous lesions (dysplasia and intestinal metaplasia). In addition, a new insight into gastric cancer was provided, which stated that gankyrin alleviates oxidative stress via mTORC1 pathway activation. It can potentiate the mTORC1 by PGK1-AKT signaling that promotes the tumor process, and this phenomenon is not completely consistent with the previous report describing colorectal cancer.

• Latcripin 1
• Lentinula edodes
• apoptosis
• autophagy
• gastric cancer
• metastasis

• Apoptosis/drug effects
• Autophagy/drug effects
• Cell Line, Tumor
• Cell Movement/drug effects
• Cell Proliferation/drug effects
• Cell Survival/drug effects
• Fungal Proteins/pharmacology
• Humans
• Neoplasm Invasiveness
• Neoplasm Metastasis
• Phosphatidylinositol 3-Kinases/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• S Phase/drug effects
• Shiitake Mushrooms/chemistry
• Signal Transduction/drug effects
• Stomach Neoplasms/pathology
• TOR Serine-Threonine Kinases/metabolism
• Wound Healing/drug effects

• H. pylori
• aryl hydrocarbon receptor
• aryl hydrocarbon receptor repressor
• gastric cancer

• TRPM2
• autophagy
• cell proliferation
• chemotherapy
• gastric cancer
• mitochondria
• transient receptor potential channels (TRP channels)

The prevalence of Helicobacter pylori gastritis has been declining, whereas H. pylori-negative gastritis has become more common. We evaluated chronic gastritis in children with regard to H. pylori status and celiac disease (CD).

Demographic, clinical, endoscopic, and histologic features of children who underwent elective esophagogastroduodenoscopy were reviewed retrospectively. Gastric biopsies from the antrum and corpus of the stomach were graded using the Updated Sydney System. H. pylori presence was defined by hematoxylin and eosin, Giemsa, or immunohistochemical staining and urease testing.

A total of 184 children (61.9% female) met the study criteria with a mean age of 10 years. A total of 122 (66.3%) patients had chronic gastritis; 74 (60.7%) were H. pylori-negative. Children with H. pylori-negative gastritis were younger (p=0.003), were less likely to present with abdominal pain (p=0.02), and were mostly of non-Arabic origin (p=0.011). Nodular gastritis was found to be less prevalent in H. pylori-negative gastritis (6.8%) compared with H. pylori-positive gastritis (35.4%, p<0.001). The grade of mononuclear infiltrates and neutrophil density was more severe in the H. pylori-positive group (p<0.001). Pan-gastritis and lymphoid follicles were associated most commonly with H. pylori. Although less typical, lymphoid follicles were demonstrated in 51.3% of H. pylori-negative patients. The presence or absence of CD was not associated with histologic findings in H. pylori-negative gastritis.

Our findings suggest that lymphoid follicles are a feature of H. pylori-negative gastritis in children independent of their CD status.

• Helicobacter pylori
• child
• gastritis
• lymphoid follicles

• Helicobacter pylori
• eradication
• levofloxacin
• resistance

• Cell migration
• Cell invasion
• DMEM, Dulbecco's Modified Eagles's Medium
• DMSO, Dimethyl sulfoxide
• ECM, Extracellular matrix
• FBS, fetal bovine serum
• GTPs, Green tea polyphenols extract
• Green tea polyphenols
• LPS, Lipopolysaccharide
• MKN-28 gastric cancer cells
• MMP-, Matrix metalloproteinase
• Matrix Metalloproteinase-2 (MMP-2)
• Matrix Metalloproteinase-9 (MMP-9)
• PBS, Phosphate-buffer saline
• ROS, Reactive Oxygen Species
• TNF-α, Tumor necrosis factor α

AIM: To assess the value of combined detection of serum pepsinogen (PG) and MG-Antigen7-Ag (MG7-Ag) in the diagnosis of precancerous lesions of gastric cancer (PLGC).

METHODS: The study included 102 patients with digestive tract symptoms who sought medical treatment at Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital. According to endoscopic and pathological results, the patients were divided into two groups, 65 patients with PLGC and 37 with benign lesions. Additionally, 30 healthy volunteers were included in a normal control group. These three groups were subjected to PGⅠ, PGⅡ, PGR and MG7-Ag detection tests. Using endoscopic and pathology results as a standard, the correlation of PG and MG7-Ag with gastric lesions was determined.

RESULTS: Compared with the normal control group and benign gastric lesion group, serum PGⅠ and PGR levels were significantly reduced (P < 0.05), and PGⅡ and MG7-Ag levels were significantly increased (P < 0.05) in the PLGC group. The sensitivity of combined detection of serum PG and MG7-Ag in the diagnosis of PLGC was 92.3%, which was significantly higher than those of single tumor marker (TM) detection; and the specificity was 90.0%, which was not significantly different from those of single TM detection.

CONCLUSION: The combined detection of PG and MG7-Ag in the diagnosis of PLGC has high sensitivity, good specificity, and can be used as a good index for screening of PLGC.

• PLGC
• Pepsinogen
• MG7-Ag

• Chemotherapy
• Gastric cancer
• Immunotherapy
• Targeted therapy

Magnifying endoscopy with narrow-band imaging (ME-NBI) is a novel, image-enhanced endoscopic technique for differentiating gastrointestinal neoplasms and potentially enabling pathological diagnosis.

The aim of this analysis was to assess the diagnostic performance of ME-NBI for gastric neoplasms.

We performed a systematic search of the PubMed, EMbase, Web of Science, and Cochrane Library databases for relevant studies. Meta-DiSc (version 1.4) and STATA (version 11.0) software were used for the data analysis. Random effects models were used to assess diagnostic efficacy. Heterogeneity was tested by the Q statistic and I² statistic. Meta-regression was used to analyze the sources of heterogeneity.

A total of 10 studies, with 2151 lesions, were included. The pooled characteristics of these studies were as follows: sensitivity 0.85 (95% confidence interval [CI]: 0.81–0.89), specificity 0.96 (95% confidence interval [CI]: 0.95–0.97), and area under the curve (AUC) 0.9647. In the subgroup analysis, which compared the diagnostic efficacy of ME-NBI and white light imaging (WLI), the pooled sensitivity and specificity of ME-NBI were 0.87 (95% CI: 0.80–0.92) and 0.93 (95% CI: 0.90–0.95), respectively, and the area under the curve (AUC) was 0.9556. In contrast, the pooled sensitivity and specificity of WLI were 0.61 (95% CI: 0.53–0.69) and 0.65 (95% CI: 0.60–0.69), respectively, and the area under the curve (AUC) was 0.6772.

ME-NBI presents a high diagnostic value for gastric neoplasms and has a high specificity.