Prevention Of Gastric Cancer Research Articles

Prevalence of Gastric Precursor Lesions in Countries With Differential Gastric Cancer Burden: A Systematic Review and Meta-analysis

The prevalence of precursor lesions for gastric cancer (GC) and the differential burden between countries of varying GC risk is not well-understood. We conducted a systematic review and meta-analysis to estimate the global prevalence of precursor lesions. We estimated the prevalence of atrophic gastritis (AG), gastric intestinal metaplasia (IM), and dysplasia in regions with low, medium, and high GC incidence. Because IM is an advanced manifestation of AG, we assessed the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. Prevalence was sub-stratified by Helicobacter pylori infection, symptomatology, and period (<2000, 2000-2010, and >2010). Among the 582 articles that underwent full-text review, 166 studies met inclusion criteria. The global prevalence estimates of AG, IM, and dysplasia were 25.4%, 16.2%, and 2.0%, respectively, on the basis of 126 studies that reported the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. The prevalence of all precursor lesions was higher in high and medium compared with low GC incidence countries (P < .01). Prevalence of AG and IM was significantly higher among H pylori-infected individuals (P < .01) but not statistically different between symptomatic and asymptomatic individuals (P > .17). All precursors demonstrated a secular decrease in prevalence over time. Gastric precursor lesions have differences in prevalence in regions with differential GC incidence and are associated with H pylori infection. Because of the substantial prevalence of precursor lesions in both symptomatic and asymptomatic individuals, symptomatic evaluation may not be sufficient to identify individuals at risk. These estimates provide important insights for tailoring GC prevention strategies.

Gastric Cancer: Clinical Features, Screening, Diagnosis, Treatment, and Prevention.

The objective of this article is to highlight the clinical features, screening, diagnosis, treatment, and prevention of gastric cancer (GC). Early GC is often asymptomatic leading to frequent delays in diagnosis. Weight loss and persistent abdominal pain are the most common symptoms at initial diagnosis. The diagnosis of GC typically involves a combination of endoscopy, biopsy, and imaging studies. Endoscopic resection techniques are emerging as successful treatment options for early GC. Treatment options for advanced GC include surgery and chemotherapy. The first line chemotherapy for advanced GC consists of doublet therapy with a combination of platinum and fluoropyrimidines. Trastuzumab, a monoclonal antibody, is used in the treatment of human epidermal growth factor 2 positive GCs. Antiangiogenic agents and immunotherapy are also useful in the treatment of GC. Currently there are no GC screening guidelines in the United States, but they exist in other regions where there is increased prevalence of GC. Prevention strategies for GC include Helicobacter pylori eradication and adoption of a healthy diet consisting of fruits and vegetables.

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis.

Duodenogastric reflux (DGR) has been linked to the onset of gastric cancer (GC), although the precise mechanism is yet obscure. Herein, we aimed to investigate how refluxed bile acids (BAs) and macrophages are involved in gastric carcinogenesis. In both active human bile reflux gastritis and the murine DGR model, ubiquitin specific protease 50 (USP50) was dramatically raised, and macrophages were the principal leukocyte subset that upregulated USP50 expression. Enhancing USP50 expression amplified bile acid-induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and subsequent high-mobility group box protein 1 (HMGB1) release, while USP50 deficiency resulted in the reversed alteration. Mechanistically, USP50 interacted with and deubiquitinated apoptosis-associated speck-like protein containing CARD (ASC) to activate NLRP3 inflammasome. The release of HMGB1 contributes to gastric tumorigenesis by PI3K/AKT and MAPK/ERK pathways. These results may provide new insights into bile reflux-related gastric carcinogenesis and options for the prevention of DGR-associated GC.

Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence.

Due to rapid research expansion on dietary factors and development of cancer prevention guidelines, the field of dietary pattern and its relationship to cancer risk has gained more focus. Numerous epidemiology studies have reported associations between Gastric Cancer (GC) and both data-driven posteriori dietary pattern and priori dietary pattern defined by predetermined dietary indexes. As dietary patterns have evolved, a series of patterns based on biological markers has advanced, offering deeper insights into the relationship between diet and the risk of cancer. Although researches on dietary patterns and cancer risk are booming, there is limited body of literature focusing specifically on GC. In this study, we compare the similarities and differences among the specific components of dietary patterns and indices, summarize current state of knowledge regarding dietary patterns related to GC and illustrate their potential mechanisms for GC prevention. In conclusion, we offer suggestions for future research based on the emerging themes within this rapidly evolving field.

Trends in Gastric Cancer Mortality in Montenegro, 1990–2018: Joinpoint Regression

Introduction: Gastric cancer (GC) remains a significant global public health problem, despite the decreasing trends in GC mortality rates in the last 5 decades. Our study aimed to examine the pattern of GC mortality in Montenegro between 1990 and 2018 and to contribute to the future by designing a national long-term strategy for the control and prevention of GC. Methods: Gastric cancer mortality data in Montenegro from 1990 to 2018 were collected. Mortality rates were age-standardized to the World Standard Population for estimating both the overall and gender-specific trends. The joinpoint regression model was used to assess GC mortality and identified significant changes in the linear time trend. Linear and Poisson regressions were also applied for additional trend analyses. Results: Joinpoint regression reveals a statistically significant decrease in the age-standardized rate for the overall level, on average by 1.4% per year (AAPC [95% IP] = −1.4 [−2.4 to −0.4]; p = 0.007), which was due to a decrease in the age-standardized rate in men with an average annual change of −1.8% (AAPC [95% IP] = −1.8 [−2.9 to −0.6]; p = 0.003), while in women the rates were stable (p = 0.565). The results for age groups indicate that a decline was registered at the overall level, and among men, as a consequence of the trend of decreasing age-specific rates for the age group 55–64 on average annually by 2% among men (AAPC [95% IP] = −2 [−3.8 to −0.1]; p = 0.035), and for the overall level (AAPC [95% IP] = −2 [−3.7 to −0.3]; p = 0.026). Conclusion: Our findings indicate a noteworthy decline in age-standardized overall GC mortality rates among men in Montenegro, while rates for women have remained constant. National strategies to further reduce mortality rates for GC are necessary.

Protocolo de evaluación de las lesiones premalignas gástricas

Gastric carcinogenesis is associated with Helicobacter pylori(H. pylori) infection and occurs through histologic gastric cancer precursor lesions (GCPL). This protocol will discuss intestinal gastric cancer. It does not cover prevention of diffuse and cardia gastric cancer, neuroendocrine tumors, or hereditary syndromes. The most significant factors that cause an increased risk of gastric cancer are family history of the disease and the presence of GCPL. The two strategies evaluated to reduce the incidence and/or mortality of gastric cancer are eradication of H. pylori and monitoring and/or endoscopic treatments.

Not all carotenoids can reduce the risk of gastric cancer: a systematic review with meta-analysis

BackgroundGastric cancer is characterized by high invasiveness, heterogeneity, and late diagnosis, leading to high incidence and mortality rates. It is a significant public health concern globally. Early prevention is crucial in reducing the occurrence of gastric cancer, and dietary prevention, particularly focusing on carotenoids, has been considered a convenient and effective approach. However, the association between carotenoid intake and gastric cancer incidence remains controversial.MethodsA systematic search was conducted in PubMed, Ovid Embase, Web of Science, and Cochrane databases from inception to January 5, 2023. Two reviewers independently screened search results, extracted relevant data, and evaluated study quality. Statistical analysis was performed using the "metan" command in STATA 16 software. Random-effects or fixed-effects models were chosen based on the magnitude of heterogeneity among studies.ResultsThis study included a total of 35 publications, consisting of 23 case–control studies and 12 cohort studies. Meta-analysis of case–control studies showed that alpha-carotene (OR = 0.71, 95% CI: 0.55–0.92), beta-carotene (OR = 0.62, 95% CI: 0.53–0.72), and lutein (OR = 0.82, 95% CI: 0.69–0.97) significantly reduced the risk of gastric cancer, while beta-cryptoxanthin (OR = 0.88, 95% CI: 0.75–1.04) and lycopene (OR = 0.86, 95% CI: 0.73–1.00) showed no significant correlation. Meta-analysis of cohort studies indicated no significant associations between any of the five carotenoids and gastric cancer incidence (alpha-carotene: RR = 0.81, 95% CI: 0.54–1.23; beta-carotene: RR = 0.86, 95% CI: 0.64–1.16; beta-cryptoxanthin: RR = 0.86, 95% CI: 0.64–1.16; lutein: RR = 0.94, 95% CI: 0.69–1.29; lycopene: RR = 0.89, 95% CI: 0.69–1.14).ConclusionsThe relationship between carotenoids and gastric cancer incidence may vary depending on the type of study conducted. Considering that evidence from cohort studies is generally considered stronger than evidence from case–control studies, and high-quality randomized controlled trials show no significant association between carotenoids and gastric cancer incidence, current evidence does not support the supplementation of carotenoids for gastric cancer prevention. Further targeted research is needed to explore the association between the two.

The association and clinicopathological significance of Integrin alphavbeta6 and Rac1 expression in gastric carcinoma.

The present study investigate the expression and correlation of ITGB6 and Rac1 proteins in gastric cancer tissues. By exploring the clinical significance and functions of these proteins, we aimed to gain further insights into the mechanisms underlying gastric cancer development. In this study, a total of 198 patients diagnosed with gastric cancer and who underwent gastrectomy between July 2010 to October 2012 were included. The median follow-up time was 52.00 months. To evaluate the factors influencing overall survival, Kaplan-Meier survival curve analysis and Cox regression analysis were conducted. Furthermore, an independent prognostic factor-based nomogram was constructed and validated to predict survival outcomes in gastric cancer patients. In addition, in vitro experiments including CCK8 and Transwell assays were conducted to explore the roles of ITGB6 and Rac1 in gastric cancer. The expression levels of ITGB6 and Rac1 in gastric cancerous and paraneoplastic tissues were detected by immunohistochemistry. The correlation and clinical significance of the two proteins were also investigated. ITGB6 expression showed significant associations with tumor size (P=0.030), pathological grading (P=0.013), location (P=0.031), N stage (P=0.002), and clinical stage (P=0.002). Additionally, we found that tumor size (P=0.013), tumor's anatomical location (P=0.031), N stage (P=0.002), clinical stage (P=0.035), and survival status (P<0.001) were significantly associated with the expression of Rac1. ITGB6 was moderately correlated with Rac1 (r=0.285, P<0.001). Both the Kaplan-Meier survival analysis and Cox regression model analysis demonstrated that the presence of positive expression of ITGB6 and Rac1 proteins served as independent prognostic factors for gastric cancer. These findings highlight the potential of ITGB6 and Rac1 as valuable markers for predicting the prognosis of gastric cancer patients (HR=2.212 P<0.001 and HR=2.073 P=0.001), with a significant poorer trend for 5-year survival (P<0.0001, respectively, the log-rank test). Additionally, subsequent in vitro experiments preliminarily demonstrated that ITGB6 and Rac1 promoted the proliferation, migration and invasion of gastric cancer cells, and ITGB6 may functions via targeting Rac1. ITGB6 and Rac1 are indicators of poor prognosis and tumor progression in gastric cancer patients. The potential signaling pathways associated with both may provide useful targets for the prevention and treatment of gastric cancer.

Current Status and Perspectives on the Use of Traditional Chinese Medicine in the Treatment of Gastric Cancer

In recent years, the potential of Traditional Chinese Medicine in preventing and treating gastric cancer has gained clear recognition. However, there is a lack of comprehensive analysis of the data on the involvement of Traditional Chinese Medicine in the prevention, diagnosis, and treatment of gastric cancer. Therefore, this article aims to organize and analyze relevant information to provide a reference for the use of Traditional Chinese Medicine in the prevention and treatment of gastric cancer.

MiR-520f-3p blocks MNNG-induced gastric precancerous lesions via the KLF7/NFκB pathway

Studying the regulatory mechanism of gastric disease progression to gastric cancer (GC) is essential. miR-520f expression is down-regulated in GC and inhibits the proliferation of gastric cancer cells, suggesting that it is associated with the development of GC, but whether it plays a role in the gastric precancerous lesion (GPL) is unclear. This study aimed to investigate the effect of miR-520f-3p in the N-methyl-N′-nitro-N-nitrosoguanidine (MNNG)-induced GPL model and to elucidate the role of its downstream target gene Kruppel-like factor 7 (KLF7) in it. The experimental results showed that miR-520f-3p expression was down-regulated in the MNNG-induced GES-1 cell model, and overexpression of miR-520f-3p reversed the effects of MNNG on cell migration, invasion and epithelial-mesenchymal transition (EMT) -related protein expression. Meanwhile, overexpression of KLF7 attenuated the effect of miR-520f-3p on GPL. In a mouse GPL model, it was observed that MNNG elicited inflammation and EMT processes in mouse gastric tissues through the KLF7/ Nuclear Factor Kappa B (NFκB) pathway, and silencing KLF7 alleviated MNNG-induced gastric epithelial cell injury and gastric atrophy symptoms. These results provide a new perspective for understanding the development of GPL, and the development of new therapies targeting miR-520f-3p and KLF7 may provide new ideas for the prevention and treatment of gastric cancer.

Gastric intestinal metaplasia and gastric cancer prevention: Watchful waiting.

Gastric intestinal metaplasia (GIM), a common histologic finding, is associated with increased risk of gastric cancer, and GIM associated with Helicobacter pylori infection is classified as an environmental metaplastic atrophic gastritis. Patients may be asymptomatic or present with various dyspeptic symptoms. Autoimmune metaplastic atrophic gastritis is a less common but important cause of chronic gastritis. The Correa cascade describes the evolution of precancerous mucosal changes that lead to development of GIM, with differentiation of 2 histologic types of GIM (complete and incomplete) and the consequences of each type. The risk of progression to malignancy is higher with incomplete GIM. It is also higher for those who immigrate from regions with a high incidence of H pylori infection to areas where the incidence is low. Guidelines regarding endoscopic management of GIM vary by geographic region.

Network pharmacology and experimental verification: Unraveling Zhiwei Fuwei Pills's role and mechanism in angiogenesis of precancerous lesions of gastric cancer.

Precancerous lesions of gastric cancer (PLGC) are key pathological stages in the transformation of gastric "inflammation-cancer", and timely and effective intervention at this stage is of great importance in the prevention and treatment of gastric cancer. Zhiwei Fuwei Pills (ZWFW), as a traditional Chinese medicine formulation, has been proven to have good clinical efficacy in the treatment of PLGC, but its specific mechanism of action has not been fully explained. Thus, this study validated the efficacy and explored the potential mechanisms of ZWFW in treating PLGC by integrating network pharmacology analyses and experimental verification. The TCMSP database was used to obtain the active ingredients of ZWFW and their corresponding targets, and the GeneCards database was used to retrieve PLGC-related targets. The intersecting targets between ZWFW and PLGC were obtained through mapping, and protein-protein interaction (PPI) networks and "drug-active ingredient-target" networks were constructed by using Cytoscape software. The DAVID database was used for GO functional enrichment analysis and KEGG pathway enrichment analysis. AutoDockTools software was used for molecular docking of key active ingredients and key targets. In order to verify the analysis results of network pharmacology, TEM and H&E were used to observe the effects of different dosage groups of ZWFW on gastric mucosal microvasculature in PLGC rats. Subsequently, the ELISA, IF, IHC, RT-PCR and western blot were used to detected the expression levels of relevant targets in the tissues, so as to verify the potential mechanism of ZWFW in intervening PLGC. After the screening, 258 effective active ingredients and 325 targets were obtained, and 1294 disease-related targets were determined, resulting in 139 intersection targets through mapping. The KEGG enrichment results showed that PI3K/Akt and HIF-1 signaling pathway might play important roles in the treatment mechanism of PLGC. The molecular docking results showed that active ingredients of ZWFW all had a strong affinity and stable structure with key targets, including AKT1 and VEGF. In vivo experiments confirmed that ZWFW could improve gastric mucosal microvascular abnormalities in PLGC, effectively intervene in gastric mucosal pathological grading. Meanwhile, compared with the model group, this formulation could reduce the expression levels of PI3K, Akt, mTOR, HIF-1α, and VEGF in gastric mucosa, showing a dose-effect relationship. ZWFW can intervene in the neovascularization and pathological evolution of PLGC, and this mechanism of action may be achieved by inhibiting abnormal activation of the PI3K/Akt/mTOR/HIF-1α/VEGF signaling pathway.

Risk Prediction Models for Gastric Cancer: A Scoping Review.

Gastric cancer is a significant contributor to the global cancer burden. Risk prediction models aim to estimate future risk based on current and past information, and can be utilized for risk stratification in population screening programs for gastric cancer. This review aims to explore the research design of existing models, as well as the methods, variables, and performance of model construction. Six databases were searched through to November 4, 2023 to identify appropriate studies. PRISMA extension for scoping reviews and the Arksey and O'Malley framework were followed. Data sources included PubMed, Embase, Web of Science, CNKI, Wanfang, and VIP, focusing on gastric cancer risk prediction model studies. A total of 29 articles met the inclusion criteria, from which 28 original risk prediction models were identified that met the analysis criteria. The risk prediction model is screened, and the data extracted includes research characteristics, prediction variables selection, model construction methods and evaluation indicators. The area under the curve (AUC) of the models ranged from 0.560 to 0.989, while the C-statistics varied between 0.684 and 0.940. The number of predictor variables is mainly concentrated between 5 to 11. The top 5 most frequently included variables were age, helicobacter pylori (Hp), precancerous lesion, pepsinogen (PG), sex, and smoking. Age and Hp were the most consistently included variables. This review enhances understanding of current gastric cancer risk prediction research and its future directions. The findings provide a strong scientific basis and technical support for developing more accurate gastric cancer risk models. We expect that these conclusions will point the way for future research and clinical practice in this area to assist in the early prevention and treatment of gastric cancer.

Regulation of regulatory T cells and tumor-associated macrophages in gastric cancer tumor microenvironment.

Despite advancements in the methods for prevention and early diagnosis of gastric cancer (GC), GC continues to be the fifth in incidence among major cancers and the third most common cause of cancer-related death. The therapeutic effects of surgery and drug treatment are still unsatisfied and show notable differences according to the tumor microenvironment (TME) of GC. Through screening Pubmed, Embase, and Web of Science, we identified and summarized the content of recent studies that focus on the investigation of Helicobacter pylori (Hp) infection, regulatory T cells (Tregs), and tumor-associated macrophages (TAMs) in the TME of GC. Furthermore, we searched and outlined the clinical research progress of various targeted drugs in GC treatment including CTLA-4, PD-1\PD-L1, and VEGF/VEGFR. In this review, the findings indicate that Hp infection causes local inflammation and leads to immunosuppressive environment. High Tregs infiltration in the TME of GC is associated with increased induction and recruitment; the exact function of infiltrated Tregs in GC was also affected by phenotypes and immunosuppressive molecules. TAMs promote the development and metastasis of tumors, the induction, recruitment, and function of TAMs in the TME of gastric cancer are also regulated by various factors. Discussing the distinct tumor immune microenvironment (TIME) of GC can deepen our understanding on the mechanism of cancer immune evasion, invasion, and metastasis, help us to reduce the incidence of GC, and guide the innovation of new therapeutic targets for GC eventually.

Efficacy evaluation of upper gastrointestinal endoscopy screening for secondary prevention of gastric cancer using the standardized detection ratio during a medical check-up in Japan.

We used standardized detection ratio to evaluate the quality of nasal upper gastrointestinal endoscopy screening for the secondary prevention of gastric cancer, and examined the gastric cancer risk in the era of total Helicobacter pylori (H. pylori) eradication. We performed 21,931 upper gastrointestinal endoscopies, 77 subjects were diagnosed with gastric cancer. Of these, 28 had gastric cancer after H. pylori eradication, 47 had gastric cancer with H. pylori-positive or others, and 2 had H. pylori-negative gastric cancer. The Standardized detection ratios for men and women were 5.33 and 4.82, respectively. Multivariable logistic regression analyses performed exclusively on first endoscopy subjects, excluding H. pylori-negative gastric cancer, revealed that smoking was a risk factor for developing gastric cancer (adjusted odds ratio, 3.31; 95% confidence interval, 1.65-6.64; p = 0.001). A statistically significant interaction was found between daily alcohol consumpption and H. pylori eradication on gastric cancer development (p = 0.005). In conclusion, relatively high standardized detection ratio values suggest that an appropriate endoscopic diagnosis of gastric cancer should be performed during a medical check-up. Smoking is a risk factor for developing gastric cancer, and continued alcohol consumption suggests a possible risk for developing gastric cancer after H. pylori eradication.

Risk Factors of Gastric Cancer and Lifestyle Modification for Prevention.

Gastric cancer has been consistently decreasing worldwide, whereas cardia gastric cancer is on the rise. This indicates that the exposure rates to epidemiological causes are changing. In this study, we aim to review the risk factors for gastric cancer with respect to cardia and non-cardia types. One of the most significant risk factors for gastric cancer is Helicobacter pylori infection. H. pylori infection is known as a risk factor for non-cardia gastric cancer, and there have been results indicating that H. pylori infection is not associated with cardia gastric cancer. However, in the East Asian region, there is epidemiological evidence suggesting that H. pylori infection might be a risk factor for cardia gastric cancer. Smoking and alcohol consumption are known risk factors for gastric cancer, regardless of anatomical location. Obesity is considered a factor in the development of cardia gastric cancer. However, further research is needed to understand the specific relationship with non-cardia gastric cancer. The consumption of high-salt and processed meat is more distinctly associated with non-cardia gastric cancer than in cardia gastric cancer. In addition to these factors, exposure to chemicals and radiation are considered risk factors for gastric cancer. Primary prevention of gastric cancer involves eliminating or avoiding risk factors such as H. pylori eradication and adopting a healthy lifestyle, including quitting smoking, reducing alcohol consumption, maintaining a healthy weight, and having a low-salt diet.

HNF4A-Bridging the Gap Between Intestinal Metaplasia and Gastric Cancer.

Intestinal metaplasia (IM) of gastric epithelium has traditionally been regarded as an irreversible stage in the process of the Correa cascade. Exploring the potential molecular mechanism of IM is significant for effective gastric cancer prevention. The GSE78523 dataset, obtained from the Gene Expression Omnibus (GEO) database, was analyzed using RStudio software to identify the differently expressed genes (DEGs) between IM tissues and normal gastric epithelial tissues. Subsequently, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, Gene Set Enrichment Analysis (GESA), and protein-protein interaction (PPI) analysis were used to find potential genes. Additionally, the screened genes were analyzed for clinical, immunological, and genetic correlation aspects using single gene clinical correlation analysis (UALCAN), Tumor-Immune System Interactions Database (TISIDB), and validated through western blot experiments. Enrichment analysis showed that the lipid metabolic pathway was significantly associated with IM tissues and the apolipoprotein B (APOB) gene was identified in the subsequent analysis. Experiment results and correlation analysis showed that the expression of APOB was higher in IM tissues than in normal tissues. This elevated expression of APOB was also found to be associated with the expression levels of hepatocyte nuclear factor 4A (HNF4A) gene. HNF4A was also found to be associated with immune cell infiltration to gastric cancer and was linked to the prognosis of gastric cancer patients. Moreover, HNF4A was also highly expressed in both IM tissues and gastric cancer cells. Our findings indicate that HNF4A regulates the microenvironment of lipid metabolism in IM tissues by targeting APOB. Higher expression of HNF4A tends to lead to a worse prognosis in gastric cancer patients implying it may serve as a predictive indicator for the progression from IM to gastric cancer.

Research Progress on Eradicating Helicobacter pylori to Prevent Gastric Cancer

Gastric cancer is a malignant tumor that originates in the gastric mucosal epithelium. It mainly occurs in people over 50 years old. With the increasing work pressure, Helicobacter pylori infection, and other factors, gastric cancer patients are also getting younger. Gastric cancer has no obvious symptoms in its early stages. Therefore, gastric cancer patients are often diagnosed at the middle and late stages of the disease. The prognosis and survival rate of gastric patients are not ideal. Therefore, prevention should be taken for people who are at risk of getting gastric cancer. Helicobacter pylori is a significant cause of the occurrence and development of gastric cancer. The bacterium produces various virulence factors, triggering the Correa cascade reaction, ultimately culminating in the development of gastric cancer. Clinically, it is believed that eradication of Helicobacter pylori can reverse precancerous lesions of the stomach and therefore prevent gastric cancer, but it has not been confirmed yet. This article explores explicitly the research progress on eradicating Helicobacter pylori in the context of gastric cancer prevention.

Trends in gastric cancer incidence and mortality in Asia and association analysis with human development index, 1990-2019

ObjectivesTo describe the epidemiological time trends and gender, age and regional differences of gastric cancer in Asia during 1990–2019, and to analyze the association between the human development index (HDI) and the statistical indicators of the burden of disease. MethodsDescribing trends in age-standardized incidence rates (ASIR) and age-standardized mortality rate (ASMR) in Asia from 1990 to 2019 based on GBD-reported population-based surveillance of gastric cancer in Asia. Obtained ASIR, ASMR, and mortality to incidence ratios (MIR) for gastric cancer in different countries in 2019, with association analysis by Kruskal-Wallis nonparametric test. ResultsThe annual percentage change in ASIR and ASMR in Asia from 1990 to 2019 was − 1.20% and − 1.91%. Male gastric cancer patients have higher ASIR and ASMR than female gastric cancer patients. Decreasing trends in ASIR and ASMR for the total population in five Asian regions. From 1990 to 2019, the average annual change in ASMR was − 2.45%, − 1.43%, − 0.53%, − 0.62%, and − 0.27% for Central Asia, East Asia, high-income Asia-Pacific, South Asia, and Southeast Asia, respectively (p < 0.05). Both incidence and mortality were concentrated in the age groups of 85–89 and 89–94 years. Classifying Asian countries into different levels of HDI, only MIR was associated with HDI levels. ConclusionASIR and ASMR of gastric cancer in the total population, different regions, and countries in Asia from 1990 to 2019 showed an overall decreasing trend. The MIR index is suggestive of survival rates and the role of cancer care in individual countries. Asian countries should develop different strategies for gastric cancer screening and prevention according to high-risk age, high-risk gender and HDI.

The Burden of Gastric Cancer Attributable to High Sodium Intake: A Longitudinal Study from 1990 to 2019 in China.

Excessive intake of sodium is a crucial risk factor of gastric cancer. However, it is still unclear whether the profile of gastric cancer burden is attributable to high sodium intake in China. This study aims to evaluate the levels and trends of gastric cancer burden attributable to high sodium intake across China from 1990 to 2019. We acquired data from the GBD (Global Burden of Disease Study) 2019 via the Global Health Data Exchange query tool. The details of regions from 1 January 1990 to 31 December 2019 from the China National Center for Food Safety Risk Assessment were also used. We conducted an integrated analysis on the gastric cancer burden attributable to high sodium intake among Chinese residents. The gastric cancer-related deaths, disability-adjusted life years (DALYs), age-standardized mortality rate (ASMR), and age-standardized DALYs rate (ASDR), all being calculated to be attributable to sodium intake, were reckoned as separated by age, sex, SDI, and regions. Then, the estimated annual percentage change (EAPC) was regarded as the secular trends of gastric cancer's ASMR and ASDR due to high sodium intake from 1990 to 2019. We further explored the associations between SDI (Socio-demographic index) and the ASMR and ASDR. The rates were calculated per 100,000 population as age-standardized rates. Briefly, the number of gastric cancer-related deaths and DALYs being attributed to high sodium intake were 37,131.48 (95% UI: 833.14 to 138,478.72) and 873,813.19 (95% UI: 19,283.13 to 3,220,231.82) in 2019; both have increased by a third since 1990. However, the ASMR decreased with an EAPC of -1.72% (95% CI: -2.11% to -1.33%), while ASDR increased with an EAPC of 0.36% (95% CI: 0.08% to 0.68%), respectively. The age-specific numbers and rates of deaths, as well as DALYs of gastric cancer being attributed to high sodium intake, elevated gradually with age. And, they were higher in males than in females. The gastric cancer burden being attributed to high sodium intake in 2019 and its temporal trends from 1990 to 2019 varied greatly by SDI quintile and geographic locations. There was a strong negative association between the EAPC in ASMR and SDI in 2019 (ρ = -0.642, p < 0.001). The EAPC in ASDR and SDI also exhibited a negative connection in 2019 (ρ = -0.538, p = 0.0012). Overall, using a longitudinal sample from different regions, the study presented that gastric cancer burden attributed to high sodium intake still exists seriously and varies remarkably by regions, sex, and age across China. The disparity of socioeconomic status on disease burden also exists. Integrated and precise approaches for gastric cancer prevention are anticipated in the future.