• Pepsinogen
• gastric cancer
• sensitivity
• serologic biopsy
• specificity

• adenocarcinoma of esophagus
• cardia
• esophagogastric junction
• stomach
• stomach neoplasms

• Helicobacter pylori
• cardia gastric adenocarcinoma
• risk biomarkers

• Adenocarcinoma/epidemiology
• Adenocarcinoma/etiology
• Adenocarcinoma/genetics
• Cardia/pathology
• Gastroesophageal Reflux/complications
• Gastroesophageal Reflux/epidemiology
• Genetic Predisposition to Disease
• Health Behavior
• Helicobacter Infections/complications
• Helicobacter Infections/epidemiology
• Humans
• MicroRNAs
• RNA, Long Noncoding
• Risk Factors
• Stomach Neoplasms/epidemiology
• Stomach Neoplasms/etiology
• Stomach Neoplasms/genetics

• 958117 National Institute for Medical Research Development

• ASEAN countries
• Helicobacter pylori
• consensus

• Amoxicillin/administration & dosage
• Anti-Bacterial Agents/administration & dosage
• Bismuth/administration & dosage
• Clarithromycin/administration & dosage
• Consensus
• Drug Resistance, Bacterial
• Drug Therapy, Combination
• Fluoroquinolones/administration & dosage
• Follow-Up Studies
• Gastritis/diagnosis
• Gastritis/drug therapy
• Gastritis/epidemiology
• Gastritis/microbiology
• Helicobacter Infections
• Helicobacter pylori
• Humans
• Japan
• Metronidazole/administration & dosage
• Proton Pump Inhibitors/administration & dosage
• Taiwan
• Tetracycline/administration & dosage
• Thailand
• Treatment Outcome
• United States

• Aged
• Case-Control Studies
• Female
• Humans
• Incidence
• Logistic Models
• Male
• Middle Aged
• New Zealand/epidemiology
• Odds Ratio
• Risk Factors
• Stomach Neoplasms/epidemiology
• Stomach Neoplasms/etiology

• Health Research Council of New Zealand

• Family history
• Gastric cancer
• Meta-analysis
• Risk, Relatives

• Case-Control Studies
• Humans
• Risk Assessment
• Stomach Neoplasms/genetics

• Helicobacter pylori
• gastric cancer
• non-steroidal anti-inflammatory drugs
• peptic ulcer disease
• prevention
• screening
• vaccine

• Family history
• Helicobacter pylori
• Stomach neoplasms

• Biomarkers, Tumor/genetics
• Early Detection of Cancer/methods
• Endoscopy, Gastrointestinal
• Female
• Gene-Environment Interaction
• Genetic Predisposition to Disease
• Helicobacter Infections/complications
• Helicobacter Infections/microbiology
• Helicobacter pylori/genetics
• Helicobacter pylori/pathogenicity
• Heredity
• Humans
• Life Style
• Male
• Molecular Diagnostic Techniques
• Mutation
• Pedigree
• Phenotype
• Polymorphism, Single Nucleotide
• Predictive Value of Tests
• Prognosis
• Risk Assessment
• Risk Factors
• Stomach Neoplasms/genetics
• Stomach Neoplasms/microbiology
• Stomach Neoplasms/pathology
• Stomach Neoplasms/therapy

Intestinal metaplasia (IM) and dysplasia are precancerous lesions of gastric cancer (GC); however, the prevalence of IM and dysplasia in patients exhibiting single gastric ulcer (GU) and concomitant gastric and duodenal ulcer (CGDU) varies. In the present study consecutive patients who had undergone esophagogastroduodenal endoscopy were retrospectively screened, and those presenting with GU or CGDU were further evaluated for IM and dysplasia. Patients diagnosed with GC or lymphoma and patients with a history of anti-Helicobacter pylori, non-steroidal anti-inflammatory medicine (NSAIM), H₂-receptor antagonist or proton pump inhibitor therapy, were excluded from the present study. Of the 204,073 consecutively screened cases, 8,855 (4.3%) and 2,397 (1.2%) were diagnosed with GU and CGDU, respectively. A total of 1,722 GU and 233 CGDU patients were excluded; thus, 7,133 and 2,164 cases of GU and CGDU, respectively (n=9,297), were included in the present study. IM and dysplasia were observed in 1,348 (14.5%) and 210 (2.3%) patients, respectively. IM was more frequently identified in GU patients compared with CGDU patients (16.4 vs. 8.3%; odds ratio [OR], 2.158; 95% confidence interval [CI], 1.830–2.545; χ²=86.932; P<0.001); furthermore, GU patients exhibited significantly more frequent IM compared with CGDU patients at the gastric antrum (14.2 vs. 5.5%; OR, 2.818; 95% CI, 2.199–3.610; χ²=72.299; P<0.001), gastric incisura (24.0 vs. 14.1%; OR, 1.922; 95% CI, 1.502–2.432; χ²=30.402; P<0.001) and gastric corpus (12.6 vs. 3.3%; OR, 4.259; 95% CI, 1.030–17.609; χ²=4.736; P=0.026). Dysplasia was significantly more frequently identified in GU patients compared with CGDU patients (2.7 vs. 0.7%; OR, 4.027; 95% CI, 2.376–6.823; χ²=31.315; P<0.001), with GU patients exhibiting significantly more severe dysplasia at the gastric antrum (2.4 vs. 0.7%; OR, 3.339; 95% CI, 1.735–6.425; χ²=14.652; P<0.001) and the gastric incisura (2.9 vs. 0.7%; OR, 4.255; 95% CI, 1.694–10.689; χ²=11.229; P<0.001). Additionally, mild IM was more frequently identified in GU patients compared with CGDU patients (15.2 vs. 7.1%; OR, 2.353; 95% CI, 1.972–2.807; χ²=94.798; P<0.001) and dysplasia of a mild (1.7 vs. 0.6%; OR, 2.807; 95% CI, 1.580–4.987; χ²=13.519; P<0.001) or moderate/severe grade (1.1 vs. 0.09%; OR, 11.642; 95% CI, 2.857–47.439; χ²=18.896; P<0.001) was more frequent in GU patients compared with CGDU patients. IM and dysplasia were more frequently observed in GU compared with CGDU patients in the present study, which may be associated with an increased probability of developing GC.

• concomitant gastric and duodenal ulcers
• dysplasia
• gastric cancer
• gastric ulcer
• intestinal metaplasia

• helicobacter pylori
• immigrant
• peptic ulcer
• gastric adenocarcinoma
• dyspepsia

• Emigrants and Immigrants
• Evidence-Based Medicine/methods
• Helicobacter Infections/diagnosis
• Helicobacter Infections/ethnology
• Helicobacter pylori
• Humans
• Peptic Ulcer/diagnosis
• Peptic Ulcer/ethnology
• Population Surveillance/methods
• Stomach Neoplasms/diagnosis
• Stomach Neoplasms/ethnology
• United States/epidemiology

• K23 CA157929 NCI NIH HHS

There is a paucity of data on familial risk of developing esophageal adenocarcinoma, gastric cardia adenocarcinoma and distal gastric adenocarcinoma from population-based studies.

A population-based case–control study of newly diagnosed gastroesophageal adenocarcinoma was conducted in Los Angeles County. This analysis included data of case-patients whom we were able to interview directly (147 patients with esophageal adenocarcinoma, 182 with gastric cardia adenocarcinoma, and 285 with distal gastric adenocarcinoma) and 1,309 control participants. Multivariate polytomous logistic regression was used to estimate odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the three cancer types.

Risk of esophageal adenocarcinoma was positively associated with a family history of prostate cancer (OR = 2.84; 95% CI = 1.50-5.36) and a family history of hiatal hernia (OR = 2.04; 95% CI = 1.12-3.71). Risk of gastric cardia adenocarcinoma was strongly associated with a family history of esophageal cancer (OR = 5.18; 95% CI = 1.23-21.79) and a family history of hiatal hernia (OR = 2.31; 95% CI = 1.37-3.91). Risk of distal gastric adenocarcinoma was positively associated with a family history of gastric cancer (OR = 2.15; 95% CI = 1.18-3.91), particularly early-onset (before age 50) gastric cancer (OR = 2.82; 95% CI = 1.11-7.15).

This study provides evidence that family history of hiatal hernia is a risk factor for esophageal adenocarcinoma and gastric cardia adenocarcinoma and that cancer in specific sites is associated with risk of esophageal adenocarcinoma, gastric cardia adenocarcinoma, and distal gastric adenocarcinoma. It is important to determine the extent to which shared environmental and genetic factors explain these familial associations.

Few studies to date have evaluated gastric cancer(GC)-related malignant neoplasm family history (MN-FH), and their findings have been largely inconsistent. The aim of this study is to evaluate the prevalence of MN-FH and its relation to the clinicopathologic features of GC.

A total of 104 hospitalized patients with primary gastric adenocarcinoma was prospectively analyzed from 2008 to 2009. Positive MN-FH was defined as MN-affected first- and second-degree relatives of the current GC cases. The relation between prevalence of positive MN-FH and clinicopathologic features in the current GC patients was assessed using the Chi-square test with Cramer’s V coefficient.

Thirty-seven (35.6%) of the GC patients had positive MN-FH, with 42 associated tumors in first- and second-degree relatives. Twenty-six (61.9%) of the associated tumors were located in the digestive system, including the esophagus (26.2%), stomach (23.8%), liver (9.5%) and colon (2.4%). Lung cancers were the most prevalent non-digestive system-associated tumors (9.5%). Correlation analysis revealed no significant relations with prevalence of MN-FH and any of the clinicopathologic features (all, P > 0.05), including sex (V = 0.044), age (V = 0.060) and histological subtypes (V = 0.109).

More than one-third of the GC patients in our hospital had positive MN-FH. The most frequent forms of MN-FH were esophageal cancer and GC. The prevalence of positive MN-FH was not correlated to any of the clinicopathologic features, including sex, age and histological subtypes in the study population of GC patients.

• Helicobacter Infections/diagnosis
• Helicobacter Infections/therapy
• Helicobacter pylori
• Humans

AIM: To examine the association between parity and gastric cancer (the cases are almost all premenopausal women) risk in a cohort of young parous women.

METHODS: The study cohort consisted of all women with a record of a first and singleton childbirth in the Birth Register between 1978 and 1987. We tracked each woman from the time of her first childbirth to December 31, 2008. Their vital status was ascertained by linking records to the computerized mortality database. Cox proportional hazard regression models were used to estimate hazard ratios of death from gastric cancer associated with parity.

RESULTS: There were 1090 gastric cancer deaths (85.87% of them were premenopausal) during 33 686 828 person-years of follow-up. The mortality rate of gastric cancer was 3.24 cases per 100 000 person-years. A trend of increasing risk of gastric cancer was seen with increasing parity. The adjusted hazard ratio was 1.24 [confidence interval (95% CI): 1.02-1.50] for women who had borne two to three children, and 1.32 (95% CI: 1.01-1.72) for women with four or more births, when compared with women who had given birth to only one child.

CONCLUSION: These results suggest that higher parity may increase the risk of death from gastric cancer among premenopausal women.

• Gastric cancer
• Parity
• Mortality
• Cohort study

AIM: To elucidate etiologic associations between Helicobacter pylori (H pylori), lifestyle, environmental factors and gastric cardiac adenocarcinoma (GCA) among men.

METHODS: A hospital-based case-control study was conducted in Taiwan from 2000 to 2009. All cases were newly confirmed as primary GCA. Five controls were selected matching with age, sex, and admission date to each case. Participants were informed of potential risk factors with a structured questionnaire by trained interviewers during hospitalization and provided a blood sample for the determination of H pylori infection. Odds ratio (OR) and 95% confidence interval (95% CI) were used to evaluate risk, and a multivariate conditional logistic regression model was performed.

RESULTS: All participants recruited for this study were men, consisting of 41 cases and 205 controls. Results of the univariate analysis showed that significant factors associated with the etiology of GCA included H pylori (OR = 2.69, 95% CI = 1.30-5.53), cigarette smoking (OR = 2.28, 95% CI = 1.05-4.96), working or exercising after meals (OR = 3.26, 95% CI = 1.31-8.11), salted food (OR = 2.51, 95%CI = 1.08-6.11), fresh vegetables (OR = 0.28, 95% CI = 0.09-0.80), fruits (OR = 0.19, 95% CI = 0.04-0.89), and rice as principal food (OR = 0.53, 95% CI = 0.30-0.85). Multivariate conditional logistic regression models indicated that a significantly elevated risk of contracting GCA was associated with working or exercising after meals (OR = 3.18, 95% CI = 1.23-9.36) and H pylori infection (OR = 2.93, 95% CI = 1.42-6.01). In contrast, the consumption of fresh vegetables (OR = 0.22, 95% CI = 0.06-0.83), fruits (OR = 0.28, 95% CI = 0.09-0.79) and rice as principal food (OR = 0.48, 95% CI = 0.24-0.93) remained as significant beneficial factor associated with GCA.

CONCLUSION: Working or exercising after meals and H pylori infection increase the risk of GCA, but higher intakes of rice, fresh vegetables and fruits reduce the risk.

• Gastric cardiac adenocarcinoma
• Helicobacter pylori
• Diet
• Obesity
• Gastroesophageal reflux disease
• Cigarette smoking
• Family history

Both environmental and genetic factors have a role in the aetiology of gastric cancer. The nature of the genetic factors has not been well-studied and, outside of a few rare cancer syndromes, the genes involved have not been identified. Having a first-degree relative with gastric cancer is a consistent risk factor for gastric cancer, although the magnitude of the odds ratio (OR) associated with a positive family history varies with the ethnic group and with the geographic region. In published case–control studies, the odds ratio varies from approximately 2 to 10, depending on the country. Unlike other common adult cancers, the risk of gastric cancer in migrants is similar to that of the population of origin and does not approach that of the host population in the first generation post-migration. It is hoped that molecular studies, including genomewide association studies (GWAS), will illuminate the genetic factors underlying this important association.

Family history (FH) by different relative types and risk of upper gastrointestinal (UGI) cancers has been only rarely reported; the data on UGI cancer survival are sparse.

600 esophageal squamous cell carcinoma (ESCC) cases, 598 gastric cardia adenocarcinoma cases, and 316 gastric non-cardia adenocarcinoma cases, and 1514 age-, gender-, and neighborhood-matched controls were asked for FH in first degree relatives and non-blood relatives. Odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regressions, and hazard ratios (HRs) from Cox proportional hazard regressions were estimated.

Increased ESCC risk was associated with FH of any cancer (OR = 1.72, 95% CI = 1.39–2.12), FH of any UGI cancer (OR = 2.28, 95%CI = 1.77–2.95) and FH of esophageal cancer (OR = 2.84, 95%CI = 2.09–3.86), but not FH of non-UGI cancer. Individuals with two or more affected first-degree relatives had 10-fold increased ESCC risk. FH of gastric cardia cancer was associated with an increased risk of all three cancers. Cancer in non-blood relatives was not associated with risk of any UGI cancer. FH of UGI cancer was associated with a poorer survival rate among younger ESCC cases (HR = 1.82, 95%CI = 1.01–3.29).

These data provide strong evidence that shared susceptibility is involved in esophageal carcinogenesis and also suggest a role in prognosis.

AIM: To compare the gastric cancer (GC) patients by their family history with gastric and non-GC.

METHODS: Positive family histories within second-degree relatives and clinicopathological features were obtained for 256 patients.

RESULTS: Of the 256 probands, 112 (76 male, 36 female) were incorporated into familial GC (FGC) group: at least two GC members; 144 (98 male, 46 female) were included in the non-FGC group (relatives only affected with non-GCs). Of 399 tumors in relatives (181 from FGC against 212 from non-FGC), GC was the most frequent, followed by esophageal, hepatocellular, and colorectal cancer. Nasopharyngeal cancer was next to lung cancer but prior to breast and urogenital cancers. Most affected members aggregated within first-degree relatives (FGC: 66 siblings, 48 fathers, 31 mothers, four offspring; non-FGC: 56 fathers, 55 siblings, 43 mothers, and 15 offspring). The ratio of males to females in affected first-degree relatives was usually higher in male probands. Paternal history of GC was a slight risk for GC in males (OR = 1.19, 95% CI: 0.53-2.69), while risk of GC by maternal history of non-GCs was increased in females (OR = 0.46, 95% CI: 0.22-0.97). Diffuse-GC was the major histological type in all subgroups. Difference in tumor sites between the two groups was derived from an excess of upper sites in non-FGC female probands.

CONCLUSION: Distribution of associated non-GCs in a family history of GC may vary with geographic areas. GC may have different genetic and/or environmental etiology in different families, and a certain subtype may be inherited in a female-influenced fashion.

• Gastric cancer
• Family history
• Familial gastric cancer
• Familial predisposition
• Female-influenced fashion

• Adult
• Aged
• Aged, 80 and over
• Cardia
• Duodenal Ulcer/complications
• Female
• Follow-Up Studies
• Gastrectomy
• Humans
• Male
• Middle Aged
• Peptic Ulcer/complications
• Peptic Ulcer/surgery
• Retrospective Studies
• Stomach Neoplasms/etiology
• Stomach Ulcer/complications
• Vagotomy