China is a country with high incidence of gastric cancer, most of which are advanced gastric cancer, accounting for about half of the new cases in the world. Environmental factors play a crucial role in the occurrence and development of gastric cancer. Helicobacter pylori and Epstein Barr virus(EBV) infection have been confirmed as one of the important pathogenic factors of gastric cancer. With the development and application of molecular biology and sequencing technology, molecular typing based on patient genetic characteristics has been proposed to guide accurate treatment and predict prognosis. Surgery is the cornerstone of gastric cancer treatment. Laparoscopy has been developing rapidly in the past 20 years on account of its clinical application advantages such as minimally invasive and magnified visual field and refined anatomy, making it one of the standard treatment options for early gastric cancer, with its indications for the treatment of gastric cancer continuously expanding. The application of endoscopic treatment and reduction surgery for early gastric cancer further improves the quality of life of patients, and surgical treatment of gastric cancer tends to be precise and minimally invasive. The comprehensive treatment of surgery combined with radiotherapy and chemotherapy is a standard treatment of local advanced gastric cancer. The exploration of related drugs and treatment models is the current research hotspot, and the development and application of targeted therapy and immunotherapy provide more choices in this field. The treatment of advanced gastric cancer is focused on the exploration of chemotherapy, targeted therapy and immunotherapy. Some studies have shown good prospects and provided more opportunities for conversion therapy. This article will share the new developments in the field of gastric cancer research in 2018.
China ; epidemiology ; Combined Modality Therapy ; Epstein-Barr Virus Infections ; complications ; Helicobacter Infections ; complications ; Helicobacter pylori ; Herpesvirus 4, Human ; Humans ; Laparoscopy ; Prognosis ; Stomach Neoplasms ; epidemiology ; etiology ; pathology ; therapy

Gastric stump cancer (GSC) is a carcinoma arising from the remnant stomach following gastric surgery for benign or malignant disease, and is more common in men. The risk of morbidity has an obvious time dependence. GSC incidence is likely to rise with lengthening of the initial operation interval. The GSC time interval after malignant disease is significantly shorter than that of benign disease. GSC etiologies mainly include duodenogastric reflux and denervation of the gastric mucosa resulting in the change of the gastric environment after gastrectomy and the Helicobacter pylori infection. Due to atypical clinical symptoms, GSC is always identified at an advanced stage and the long-term survival rate is low. An optimal endoscopic surveillance system is essential to improve early detection rates. Treatments in GSC and primary gastric cancer are the same and include resection of the lesion and radical lymph node dissection. R0 resection is an important prognostic factor. Here we review previous reports with respect to epidemiological characteristics, etiology, clinical symptoms, treatment, and prognosis of GSC.
Gastrectomy ; Gastric Stump ; pathology ; surgery ; Helicobacter Infections ; complications ; Humans ; Lymph Node Excision ; Male ; Stomach Neoplasms ; surgery

BACKGROUND/AIMS: The interaction between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori remains controversial. We retrospectively investigated whether H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users. METHODS: From January 2010 to December 2013, a total of 245 long-term NSAID (including low-dose aspirin) users who had undergone an esophagogastroduodenoscopy and had been evaluated for H. pylori infection were enrolled at Okayama University Hospital and Tsuyama Chuo Hospital. The degree of gastric mucosal injury was assessed according to the modified Lanza score (MLS). Severe gastric mucosal injury was defined as an MLS > or =4. Univariate and multivariate logistic regression analyses were performed. RESULTS: In the univariate analysis, age > or =75 years (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.3 to 4.2), H. pylori-positivity (OR, 2.0; 95% CI, 1.2 to 3.5), and the concomitant use of proton pump inhibitors (PPIs) (OR, 0.48; 95% CI, 0.26 to 0.86) were significantly associated with severe gastric mucosal injury. The multivariate analysis was adjusted by age and sex and demonstrated that H. pylori-positivity (OR, 1.8; 95% CI, 1.0 to 3.3) and the concomitant use of PPIs (OR, 0.53; 95% CI, 0.28 to 0.99) significantly contributed to severe gastric mucosal injury. CONCLUSIONS: H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.
Aged ; Anti-Inflammatory Agents, Non-Steroidal/*adverse effects ; Case-Control Studies ; *Disease Progression ; Endoscopy, Digestive System ; Female ; Gastric Mucosa/*drug effects/*microbiology ; Helicobacter Infections/*complications/microbiology/pathology ; *Helicobacter pylori/drug effects ; Humans ; Logistic Models ; Male ; Middle Aged ; Odds Ratio ; Proton Pump Inhibitors/adverse effects ; Retrospective Studies

BACKGROUND/AIMS: Controversy exists regarding the characteristics of Helicobacter pylori infection-negative gastric cancer (HPIN-GC). The aim of this study was to evaluate clinicopathologic features of HPIN-GC compared to H. pylori infection-positive gastric cancer (HPIP-GC) using a comprehensive analysis that included genetic and environmental factors. METHODS: H. pylori infection status of 705 resectable gastric cancer patients was determined by the rapid urease test, testing for anti-H. pylori antibodies, histologic analysis and culture of gastric cancer tissue samples, and history of H. pylori eradication. HPIN-GC was defined as gastric cancer that was negative for H. pylori infection based on all five methods and that had no evidence of atrophy in histology or serology. RESULTS: The prevalence of HPIN-GC was 4% (28/705). No significant differences with respect to age, sex, smoking, drinking, family history of gastric cancer or obesity were observed between the two groups. HPIN-GC tumors were marginally more likely to involve the cardia (14.3% for HPIN-GC vs 5.3% for HPIP-GC, p=0.068). The Lauren classification, histology, and TNM stage did not differ according to H. pylori infection status. Microsatellite instability was not different between the two groups, but p53 overexpression in HPIN-GC was marginally higher than in HPIP-GC (56.0% for HPIN-GC vs 37.0% for HPIP-GC, p=0.055). CONCLUSIONS: The prevalence of HPIN-GC was extremely low, and its clinicopathologic characteristics were similar to HPIP-GC.
Antibodies, Bacterial/analysis ; Female ; Helicobacter Infections/*complications/epidemiology/microbiology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Prevalence ; Prospective Studies ; Republic of Korea/epidemiology ; Stomach Neoplasms/epidemiology/*microbiology/*pathology/surgery ; Urease/analysis

It is often difficult to differentiate gastric mucosa-associated lymphoid tissue (MALT) lymphoma from Helicobacter pylori-associated follicular gastritis, and thus, it becomes unclear how to manage these diseases. This study aimed to explore the management strategy for and the long-term outcomes of suspicious gastric MALT lymphoma detected by forceps biopsy during screening upper endoscopy. Between October 2003 and May 2013, consecutive subjects who were diagnosed with suspicious gastric MALT lymphomas by screening endoscopy in a health checkup program in Korea were retrospectively enrolled. Suspicious MALT lymphoma was defined as a Wotherspoon score of 3 or 4 upon pathological evaluation of the biopsy specimen. Of 105,164 subjects who underwent screening endoscopies, 49 patients with suspicious MALT lymphomas who underwent subsequent endoscopy were enrolled. Eight patients received a subsequent endoscopy without H. pylori eradication (subsequent endoscopy only group), and 41 patients received H. pylori eradication first followed by endoscopy (eradication first group). MALT lymphoma development was significantly lower in the eradication first group (2/41, 4.9%) than in the subsequent endoscopy only group (3/8, 37.5%, P = 0.026). Notably, among 35 patients with successful H. pylori eradication, there was only one MALT lymphoma patient (2.9%) in whom complete remission was achieved, and there was no recurrence during a median 45 months of endoscopic follow-up. H. pylori eradication with subsequent endoscopy would be a practical management option for suspicious MALT lymphoma detected in a forceps biopsy specimen obtained during screening upper endoscopy.
Adult ; Aged ; Anti-Bacterial Agents/therapeutic use ; Biopsy ; Female ; Follow-Up Studies ; Gastric Mucosa/*pathology ; Gastritis/diagnosis/etiology/microbiology ; Gastroscopy ; Helicobacter Infections/complications/*diagnosis/drug therapy ; Humans ; Lymphoma, B-Cell, Marginal Zone/complications/*diagnosis/pathology ; Male ; Middle Aged ; Republic of Korea ; Retrospective Studies

BACKGROUND/AIMS: Helicobacter pylori cytotoxin-associated gene A (CagA) has been suggested to be involved in the inactivation of Runt-related transcription factor 3 (RUNX3), a known gastric carcinoma tumor suppressor gene. It remains unclear how H. pylori CagA initiates or maintains RUNX3 promoter methylation and inactivates its protein expression in gastric carcinoma. METHODS: RUNX3 promoter methylation status, RUNX3 expression, and H. pylori CagA were investigated in 76 sample pairs of gastric carcinoma tissue. The patients' medical records were reviewed. The association between RUNX3 methylation or loss of RUNX3 expression and clinicopathologic variables according to H. pylori CagA status were investigated. RESULTS: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation did not show association with lymphatic invasion, venous invasion, and TNM stages. However RUNX3 methylation was observed more frequently in poorly differentiated adenocarcinoma and signet ring cell carcinoma (77.8% vs. 20.0%, p=0.023) in early stage. In gastric carcinoma patients with H. pylori CagA-positive infection, loss of RUNX3 expression did not show association with lymphatic invasion, venous invasion, and TNM stages. However loss of RUNX3 expression was observed more frequently in early gastric carcinoma than in advanced gastric carcinoma (84.2% vs. 75.0%, p=0.51), but this difference was not significant. CONCLUSIONS: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation or loss of RUNX3 expression did not show correlation with lymphovascular invasion and TNM stages. In early gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation was observed more in poorly differentiated adenocarcinoma and signet ring cell carcinoma.
Adult ; Aged ; Aged, 80 and over ; Antigens, Bacterial/*metabolism ; Bacterial Proteins/*metabolism ; Cell Line, Tumor ; Core Binding Factor Alpha 3 Subunit/genetics/*metabolism ; Female ; *Gene Expression Regulation, Neoplastic ; Helicobacter Infections/complications/microbiology ; Helicobacter pylori/isolation & purification/*metabolism ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Male ; Methylation ; Middle Aged ; Neoplasm Staging ; Promoter Regions, Genetic ; Retrospective Studies ; Stomach Neoplasms/complications/microbiology/*pathology

Helicobacter pylori can cause variety of upper gastrointestinal disorders such as peptic ulcer, mucosa associated lymphoid tissue (MALT)-lymphoma, and gastric cancer. The prevalence of H. pylori infection has significantly decreased in Korea since 1998 owing to active eradication of H. pylori. Along with its decrease, the prevalence of peptic ulcer has also decreased. However, the mean age of gastric ulcer increased and this is considered to be due to increase in NSAID prescription. Gastric cancer is one of the leading causes of cancer deaths in Korea and Japan, and IARC/WHO has classified H. pylori as class one carcinogen of gastric cancer. Despite the decreasing prevalence of H. pylori infection, the total number of gastric cancer in Korea has continuously increased from 2006 to 2011. Nevertheless, the 5 year survival rate of gastric cancer patients significantly increased from 42.8% in 1993 to 67% in 2010. This increase in survival rate seems to be mainly due to early detection of gastric cancer and endoscopic mucosal dissection treatment. Based on these findings, the prevalence of peptic ulcer is expected to decrease even more with H. pylori eradication therapy and NSAID will become the main cause of peptic ulcer. Although the prevalence of gastric cancer has not changed along with decreased the prevalence of H. pylori, gastric cancer is expected to decrease in the long run with the help of eradication therapy and endoscopic treatment of precancerous lesions.
Anti-Bacterial Agents/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Gastrointestinal Diseases/complications/*epidemiology ; Helicobacter Infections/complications/drug therapy/epidemiology ; Humans ; Lymphoma, B-Cell, Marginal Zone/epidemiology ; Peptic Ulcer/epidemiology/etiology ; Prevalence ; Stomach Neoplasms/etiology/mortality/pathology

No abstract available.
Adenocarcinoma/*diagnosis/pathology ; Adult ; Gastroscopy ; Helicobacter Infections/complications/diagnosis ; Helicobacter pylori ; Humans ; Male ; Stomach Neoplasms/*diagnosis/pathology

BACKGROUND/AIMS: Helicobacter pylori infection is linked to the development of gastric cancer. H. pylori-associated gastric inflammation is considered to be the first important step in the histogenesis of such neoplasia. However, studies that compare proteome of gastric mucosa infected with or without H. pylori are lacking. METHODS: We employed proteomics analysis on the endoscopic biopsy specimens of gastric mucosa obtained from two groups (30 cases): healthy subjects without H. pylori infection (15 cases), and gastritis patients with H. pylori infection (15 cases). The pooled proteins obtained from gastric mucosa infected with or without H. pylori were separated by two-dimensional gel electrophoresis and analyzed by a computer-aided program. The altered protein expressions were then identified by mass spectrometry and validated by Western blotting and immunohistochemistry. RESULTS: On mass spectrometry using MALDI TOF(TM) Analyzer, the up-regulation of Keratin 1, ezrin, adenosine triphosphate (ATP) synthase subunit alpha mitochondrial isoform c, Keratin type I cytoskeletal 19, and Keratin type I cytoskeletal 9 were identified; in contrast, 71 kd heat shock cognate protein, ATP synthase subunit alpha mitochondrial precursor, and annexin IV were down-regulated. Among them, membrane cytoskeleton linker ezrin was validated using Western blot and immunohistochemistry. CONCLUSIONS: Expression of ezrin was significantly different between the gastric mucosa with and without H. pylori infection. Therefore, ezrin could be considered a promising potential molecular marker for detecting H. pylori infection in gastric mucosa.
Blotting, Western ; Cytoskeletal Proteins/metabolism ; Down-Regulation ; Electrophoresis, Gel, Two-Dimensional ; Female ; Gastric Mucosa/*metabolism/microbiology ; Gastritis/complications/metabolism/pathology ; Gastroscopy ; Helicobacter Infections/complications/metabolism/*pathology ; *Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Proteome/*analysis ; *Proteomics ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Up-Regulation

OBJECTIVETo determine serum pepsinogen levels in patients with liver cirrhosis and investigate the functions of the gastric mucosa in these patients with concurrent portal hypertensive gastropathy (PHG).

METHODSFifty-one patients with liver cirrhosis and 22 healthy controls were studied by gastroscopy. The hepatic function of the patients with or without PHG were evaluated with Child-Pugh grade. Helicobacter pylori infection was detected using rapid urease test or exhalation of carbon 13. The serum pepsinogen I and II levels were tested by latex-enhanced immunoturbidimetry to calculate the PGI/PGII ratio (PGR).

RESULTSIn cirrhotic patients, the levels of serum PGI and PGR were lower than those in the healthy controls. The patients without PHG had a serum PGI level of 49.48+23.86 µg/L, significantly lower than that in PHG patients (74.85+30.27 µg/L, P=0.000). The levels of serum PG II in patients with H.pylori infection was significantly higher that in patients free of H.pylori infection (P=0.003).

CONCLUSIONThe serum level of PGI decreases obviously in patients with hepatic cirrhosis and PHG, who can have damages of the gastric mucosa lamina propria and reduced secretory function of the gastric mucosa. H.pylori infection may affect the level of PGII. There is no significant correlation between serum PG level and liver function, but to a certain extent, serum PG level especially PGI can reflect the function of gastric mucosa in patients of liver cirrhosis.

Adult ; Case-Control Studies ; Female ; Gastric Mucosa ; pathology ; Helicobacter Infections ; Humans ; Hypertension, Portal ; complications ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Pepsinogen A ; blood ; Stomach Diseases ; blood ; etiology ; microbiology