The problem of gastric cancer (GC) prevention remains relevant for a long time. Various methods of population serological screening of atrophic gastritis and precancerous changes in the gastric mucosa have been created at present. Modern endoscopic and morphological methods of verification of the diagnosis of precancerous diseases and changes in the gastric mucosa have been introduced into the practice of gastroenterologists and oncologists. GC risk stratification systems allow the formation of risk groups that require population screening. Practical hints for population serological screening of atrophic gastritis, endoscopic and morphological verification of precancerous changes and diseases of the stomach recommend using it: When developing state programs for the prevention of stomach cancer; when implementing preventive measures for stomach cancer by doctors of all specialties; the authors also offer the possibility of use by anyone over the age of 40, provided that they seek methodological help from their doctor; in the work of health schools in any medical and preventive institutions. The use of an assessment system of certain risk factor signatures with prognostic value would add significant assistance to preventive measures against GC.

Gastric cancer represents a major public health burden globally, with a disproportionately high incidence and mortality observed in Asian countries. To analyze the epidemiology of gastric cancer across Asia using data from the GLOBOCAN 2020 database and explore the potential correlations with socioeconomic indicators. The study reported numbers of cases, 5-year prevalence, crude and age-standardized rates of incidence (ASIR) and mortality (ASMR), mortality-to-incidence ratio (MIR), and cumulative risk percentages. Asia had the highest ASIR and ASMR of gastric cancer in the world in 2020, with 14.30 and 10.00 per 100,000 population, respectively. The ASIRs were 20.40 and 8.70 in Asian males and females, respectively. The ASMRs were also 14.20 and 6.20 in males and females, respectively. The incidence and mortality rates increased with age and peaked in the > 70-year age group. There was a moderate inverse correlation between MIR and human development index (HDI). The incident cases of gastric cancer and its mortality numbers in Asia are estimated to increase by 72.20% and 75.90% by 2040, respectively. Gastric cancer burden varies across Asia, with high incidence and mortality rates in Eastern Asia. Lower MIRs in socioeconomically developed nations suggest the impact of early detection and treatment access to improve patients' outcomes.

Often referred to as 'the last unknown', Papua New Guinea's largely unexplored environments across its four distinct regions, the Highlands, New Guinea Islands, Momase, and Southern, exhibit remarkable diversity. Understanding this diversity is significant in contextualising the risk factors associated with developing non-communicable diseases. This review aims to map and summarise the literature to provide region-specific prevalence data for risk factors and non-communicable diseases. Four databases and grey literature were searched. Two reviewers completed the screening and data extraction. Twenty-one studies were included, with five reporting the data by region and the remaining reporting the data nationwide. Six studies reported on risk factors, thirteen reported on non-communicable diseases, and two reported on risk factors and non-communicable diseases. The Southern region, which includes the Capital, Port Moresby, reported the highest prevalence for most risk factors: anthropometric (overweight, obesity, and waist circumference), lifestyle (betel nut, alcohol, unhealthy diet, and stress), and biochemical (cholesterol, triglycerides, HbA1c, and metabolic syndrome). The findings of this review highlight the limited evidence base for region-specific risk factor data and the lack of objective diagnosis of non-communicable diseases. There were variations in the prevalence of specific risk factors by region; however, the Southern region stands out as requiring immediate attention for health promotion program interventions.

Gastric cancer (GC) remains a significant health concern in Gansu province, China, with morbidity and mortality rates surpassing national averages. Despite the recognized health risks associated with ambient particulate matter with an aerodynamic diameter <1 μm (PM1), the relationship between PM1 exposure and GC incidence has not been extensively studied. Data on GC cases from 2013 to 2021 were gathered from 262 hospitals in Gansu, China. Concurrently, data on the normalized vegetation index (NDVI), gross domestic product (GDP), drinking and smoking behavioral index (DSBI), PM1, PM2.5, and PM2.5-1 were collected. Utilizing a Bayesian conditional autoregressive (CAR) combined generalized linear model (GLM) with quasi-Poisson regression, we evaluated the impact of PM1, PM2.5, PM2.5-1, NDVI, DSBI, and GDP on GC morbidity while adjusting for potential confounders. Our analysis indicated that exposure to PM1 (μg/m3) is significantly positively correlated with GC incidence in regions with an overall age-standardized incidence rate (ASIR) >40 (relative risks [RR]: 1.023, 95% confidence intervals [CI, 1.007, 1.039]), male ASIR >50 (RR: 1.014, 95% CI [1.009, 1.019]), and female ASIR >20 (RR: 1.010, 95% CI [1.002, 1.018]). PM2.5, PM2.5-1, DSBI, and GDP were positively correlated with GC incidence, while NDVI was negatively correlated in the study regions. Our findings provided evidence of a positive correlation between PM1 exposure and GC incidence in high-risk areas of GC within arid regions. Further research is warranted to elucidate the complex nonlinear relationships between environmental factors and GC. These insights could inform strategies for improving the control and prevention of GC in Gansu and similar regions.

BackgroundPancreatic cancer places a substantial global health and economic burden. However, the epidemiological characteristics and chronological trends of pancreatic cancer in high-income Asia-Pacific have not been systematically analyzed.MethodsData obtained from the GBD 2021 database were used for this cross-country secondary analysis. We used Joinpoint regression to analyze the temporal trends of pancreatic cancer disease burden in the high-income Asia-Pacific. Age-period-cohort model was used to estimate and describe the impact of age, period, and cohort effects on health outcomes. Bayesian age-period-cohort model was used for the projection of pancreatic cancer incidence from 2022 to 2036.ResultsIn high-income Asia-Pacific, the age-standardized prevalence rate (ASPR), mortality rate (ASMR), and disability-adjusted life-years (DALYs) rate (ASDR) were estimated to be 11.2 (95% UI, 9.69-12.17), 9.56 (95% UI, 8.34-10.34), and 197.6 (95% UI, 178.87-210.6) per 100 000 population, respectively, in 2021, which were all higher than those in across Asia. From 1990 to 2002, the age-standardized incidence rates (ASIRs) trend was rather stable. Instead, the ASIRs trend went up gradually from 2002 to 2011 in both males (APC = + 1.03, 95% CI: 0.85, 1.20) and females (APC = + 1.64, 95% CI: 1.40, 1.89). ASIRs and ASMRs went up considerably with increasing age, especially over 60. The ASIRs in the high-income Asia-Pacific region are predicted to go down in the years ahead, from approximately 12.81 in 2021 to approximately 11.11 in 2036 for males, and from approximately 8.97 in 2021 to approximately 8.42 in 2036 for females.ConclusionA comprehensive upward trend in ASIRs, ASPRs, ASMRs, and ASDRs of pancreatic cancer was observed in the high-income Asia-Pacific between 1990 and 2021. Given the poor prognosis of pancreatic cancer, prevention strategies are paramount, especially for modifiable factors like smoking, alcohol drinking, and obesity.

Gastric cancer represents a significant global health challenge due to its high mortality and incidence rates, particularly in Eastern Asia, Eastern Europe, and South America. This comprehensive review synthesizes the latest epidemiological data and explores both modifiable and non-modifiable risk factors associated with gastric cancer, aiming to delineate the multifactorial etiology of this disease. Modifiable risk factors include Helicobacter pylori infection, obesity, dietary habits, smoking and alcohol consumption, whereas nonmodifiable factors comprise genetic predispositions, age, family history and male gender. The interplay of these factors significantly impacts the risk and progression of gastric cancer, suggesting potential preventive strategies. The challenges in treating gastric cancer are considerable, largely because of the late-stage diagnosis and the heterogeneity of the disease, which complicate effective treatment regimens. Current treatment strategies involve a combination of surgery, chemotherapy, radiotherapy, and targeted therapies. The FLOT regimen (5-FU, Leucovorin, Oxaliplatin and Docetaxel) is now a standard for resectable cases in Europe and the US, showing superior survival and response rates over ECF and ECX regimens. For HER2-positive gastric cancer, trastuzumab combined with chemotherapy improves overall survival, as demonstrated by the ToGA trial. Additionally, immune checkpoint inhibitors like pembrolizumab and nivolumab offer promising results. However, the five-year survival rate remains low, underscoring the urgency for improved therapeutic approaches. Recent advancements in molecular biology and cancer genomics have begun to pave the way for personalized medicine in gastric cancer care, focusing on molecular targeted therapies and immunotherapy. This review also highlights the critical need for better screening methods that could facilitate early detection and treatment, potentially improving the prognosis. By integrating epidemiological insights with new therapeutic strategies, this article aims to thoroughly understand of gastric cancer's dynamics and outline a framework for future research and clinical management, advocating for a multidisciplinary approach to tackle this formidable disease.

Although endoscopy is commonly used for gastric cancer screening in South Korea, predictive models that integrate endoscopy results are scarce. We aimed to develop a 5-year gastric cancer risk prediction model using endoscopy results as a predictor.

We developed a predictive model using the cohort data of the Kangbuk Samsung Health Study from 2011 to 2019. Among the 260,407 participants aged ≥20 years who did not have any previous history of cancer, 435 cases of gastric cancer were observed. A Cox proportional hazard regression model was used to evaluate the predictors and calculate the 5-year risk of gastric cancer. Harrell's C-statistics and Nam-D'Agostino χ2 test were used to measure the quality of discrimination and calibration ability, respectively.

We included age, sex, smoking status, alcohol consumption, family history of cancer, and previous results for endoscopy in the risk prediction model. This model showed sufficient discrimination ability [development cohort: C-Statistics: 0.800, 95% confidence interval (CI) 0.770-0.829; validation cohort: C-Statistics: 0.799, 95% CI 0.743-0.856]. It also performed well with effective calibration (development cohort: χ2 = 13.65, P = 0.135; validation cohort: χ2 = 15.57, P = 0.056).

Our prediction model, including young adults, showed good discrimination and calibration. Furthermore, this model considered a fixed time interval of 5 years to predict the risk of developing gastric cancer, considering endoscopic results. Thus, it could be clinically useful, especially for adults with endoscopic results.

Patients with gastric cancer experience different degrees of fear of cancer recurrence. The fear of cancer recurrence can cause and worsen many physical and psychological problems. We considered the "intimacy and relationship processes in couples' psychosocial adaptation" model.

The study aims to examine the effectiveness of a marital self-disclosure intervention for improving the level of fear of cancer recurrence and the dyadic coping ability among gastric cancer survivors and their spouses.

This is a quasiexperimental study with a nonequivalent (pretest-posttest) control group design. The study will be conducted at 2 tertiary hospitals in Taizhou City, Jiangsu Province, China. A total of 42 patients with gastric cancer undergoing chemotherapy and their spouses will be recruited from each hospital. Participants from Jingjiang People's Hospital will be assigned to an experimental group, while participants from Taizhou People's Hospital will be assigned to a control group. The participants in the experimental group will be involved in 4 phases of the marital self-disclosure (different topics, face-to-face) intervention. Patients will be evaluated at baseline after a diagnosis of gastric cancer and reassessed 2 to 4 months after baseline. The primary outcome is the score of the Fear of Progression Questionnaire-Short Form (FoP-Q-SF) for patients. The secondary outcomes are the scores of the FoP-Q-SF for partners and the Dyadic Coping Inventory.

Research activities began in October 2022. Participant enrollment and data collection began in February 2023 and are expected to be completed in 12 months. The primary results of this study are anticipated to be announced in June 2024.

This study aims to assess a marital self-disclosure intervention for improving the fear of cancer recurrence in Chinese patients with gastric cancer and their spouses. The study is likely to yield desirable positive outcomes as marital self-disclosure is formulated based on evidence and inputs obtained through stakeholder interviews and expert consultation. The study process will be carried out by nurses who have received psychological training, and the quality of the intervention will be strictly controlled.

ClinicalTrials.gov NCT05606549; https://clinicaltrials.gov/study/NCT05606549.

DERR1-10.2196/55102.

Gastric cancer (GC), ranking as the third deadliest cancer globally, faces challenges of late diagnosis and limited treatment efficacy. Long non-coding RNAs (lncRNAs) emerge as valuable treasured targets for cancer prognosis, diagnosis, and therapy, given their high specificity, convenient non-invasive detection in body fluids, and crucial roles in diverse physiological and pathological processes. Research indicates the significant involvement of lncRNAs in various aspects of GC pathogenesis, including initiation, metastasis, and recurrence, underscoring their potential as novel diagnostic and prognostic biomarkers, as well as therapeutic targets for GC. Despite existing challenges in the clinical application of lncRNAs in GC, the evolving landscape of lncRNA molecular biology holds promise for advancing the survival and treatment outcomes of gastric cancer patients. This review provides insights into recent studies on lncRNAs in gastric cancer, elucidating their molecular mechanisms and exploring the potential clinical applications in GC.

More than half of the world's population is infected with Helicobacter pylori (H. pylori), which may lead to chronic gastritis, peptic ulcers, and stomach cancer. LeoA, a conserved antigen of H. pylori, aids in preventing this infection by triggering specific CD3+ T-cell responses. In this study, recombinant plasmids containing the LeoA gene of H. pylori are created and conjugated with chitosan nanoparticle (CSNP) to immunize BALB/c mice against the H. pylori infection. We used the online Vaxign tool to analyze the genomes of five distinct strains of H. pylori, and we chose the outer membrane as a prospective vaccine candidate. Afterward, the proteins' immunogenicity was evaluated. The DNA vaccine was constructed and then encapsulated in CSNPs. The effectiveness of the vaccine's immunoprotective effects was evaluated in BALB/c mice. Purified activated splenic CD3+ T cells are used to test the anticancer effects in vitro. Nanovaccines had apparent spherical forms, were small (mean size, 150-250 nm), and positively charged (41.3 ± 3.11 mV). A consistently delayed release pattern and an entrapment efficiency (73.35 ± 3.48%) could be established. Compared to the non-encapsulated DNA vaccine, vaccinated BALB/c mice produced higher amounts of LeoA-specific IgG in plasma and TNF-α in splenocyte lysate. Moreover, BALB/c mice inoculated with nanovaccine demonstrated considerable immunity (87.5%) against the H. pylori challenge and reduced stomach injury and bacterial burdens in the stomach. The immunological state in individuals with GC with chronic infection with H. pylori is mimicked by the H. pylori DNA nanovaccines by inducing a shift from Th1 to Th2 in the response. In vitro human GC cell development is inhibited by activated CD3+ T lymphocytes. According to our findings, the H. pylori vaccine-activated CD3+ has potential immunotherapeutic benefits.

Gastric cancer (GC) is the fourth leading cause of death worldwide, with more than 1 million cases diagnosed every year. Helicobacter pylori represents the main risk factor, being responsible for 78% of the cases. Increased amounts of salt, pickled food, red meat, alcohol, smoked food, and refined sugars negatively affect the stomach wall, contributing to GC development. Several gene mutations, including PIK3CA, TP53, ARID1A, CDH1, Ras, Raf, and ERBB3 are encountered in GC pathogenesis, leading to phosphatidylinositol 3-kinase (PI3K) protein kinase B (AKT)/mammalian target of rapamycin (mTOR)-PI3K/AKT/mTOR-and mitogen-activated protein kinase (MAPK) signaling pathway activation and promoting tumoral activity. Helicobacter pylori, growth factors, cytokines, hormones, and oxidative stress also activate both pathways, enhancing GC development. In clinical trials, promising results have come from monoclonal antibodies such as trastuzumab and ramucirumab. Dual inhibitors targeting the PI3K/AKT/mTOR and MAPK signaling pathways were used in vitro studies, also with promising results. The main aim of this review is to present GC incidence and risk factors and the dysregulations of the two protein kinase complexes together with their specific inhibitors.

We aimed to identify the associated single nucleotide polymorphisms (SNPs) with gastric cancer (GC) risk by genome-wide association study (GWAS) and to explore the pathway enrichment of implicated genes and gene-sets with expression patterns.

The study population was comprised of 1,253 GC cases and 4,827 controls from National Cancer Center and an urban community of the Korean Genome Epidemiology Study and their genotyping was performed. SNPs were annotated, and mapped to genes to prioritize by three mapping approaches by functional mapping and annotation (FUMA). The gene-based analysis and gene-set analysis were conducted with full GWAS summary data using MAGMA. Gene-set pathway enrichment test with those prioritized genes were performed.

In GWAS, rs2303771, a nonsynonymous variant of KLHDC4 gene was top SNP associated significantly with GC (odds ratio, 2.59; p=1.32×10-83). In post-GWAS, 71 genes were prioritized. In gene-based GWAS, seven genes were under significant p < 3.80×10-6 (0.05/13,114); DEFB108B had the lowest p=5.94×10-15, followed by FAM86C1 (p=1.74×10-14), PSCA (p=1.81×10-14), and KLHDC4 (p=5.00×10-10). In gene prioritizing, KLDHC4 was the only gene mapped with all three gene-mapping approaches. In pathway enrichment test with prioritized genes, FOLR2, PSCA, LY6K, LYPD2, and LY6E showed strong enrichment related to cellular component of membrane; a post-translation modification by synthesis of glycosylphosphatidylinositol (GPI)-anchored proteins pathway.

While 37 SNPs were significantly associated with the risk of GC, genes involved in signaling pathways related to purine metabolism and GPI-anchored protein in cell membrane are pinpointed to be playing important role in GC.

Metastasis of gastric cancer (GC) is one of the major causes of death among GC patients. GC metastasis involves numerous biological processes, yet the specific molecular biological mechanisms have not been elucidated. Here, we report a novel tumor suppressor, retinoic acid-induced 2 (RAI2), which is located in the Xp22 region of the chromosome and plays a role in inhibiting GC growth and invasion. In this study, integrated analysis of The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) datasets and immunohistochemistry staining data suggested that RAI2 expression in GC samples was low. Moreover, the immune infiltration analysis indicated that low expression of RAI2 in GC was associated with a higher intensity of tumor-infiltrating lymphocytes (TILs) and an abundance of Programmed death ligand 1 (PD-L1) expression. Gene set enrichment analysis (GSEA) analysis further revealed that RAI2 regulated some pathways including the GAP junction, focal adhesion and ECM receptor interaction pathway, immune regulation, PI3K-Akt signaling, MAPK signaling, cell cycle, and DNA replication. Furthermore, the knockdown of RAI2 promoted GC cell proliferation, migration, and invasion in vitro. Taken together, these results suggest that the tumor suppressor RAI2 could be a potential target for the development of anti-cancer strategies in GC.

The prevalence of gastric cancer has markedly declined, but due to the high mortality rates associated with gastric cancer, it is still a serious disease. The preferred classification of gastric cancer is according to Lauren into either the intestinal type, which has a glandular growth pattern, or the diffuse type, which does not have glandular structures. Both types have been classified as adenocarcinomas, with the latter type based on periodic acid-Schiff (PAS) positivity presumed to reflect mucin. However, the presence of mucin in the diffuse type, in contrast to neuroendocrine/enterochromaffin-like (ECL) cell markers, has not been confirmed by immunohistochemistry and in situ hybridization. The ECL cells are probably prone to becoming cancerous because they do not express E-cadherin. Gastric cancer is unique in that a bacterium, Helicobacter pylori, is thought to be its main cause. H. pylori predisposes infected individuals to cancer only after having caused oxyntic atrophy leading to gastric hypoacidity and hypergastrinemia. No single H. pylori factor has been convincingly proved to be carcinogenic. It is probable that gastrin is the pathogenetic factor for gastric cancer due to H. pylori, autoimmune gastritis, and long-term prolonged inhibition of gastric acid secretion. Hypergastrinemia induces ECL cell hyperplasia, which develops into neuroendocrine tumors (NETs) and then into neuroendocrine carcinomas in rodents, a sequence that has also been described in humans. During carcinogenesis, the tumor cells lose specific traits, requiring that sensitive methods be used to recognize their origin. Gastric cancer occurrence may hopefully be prevented by H. pylori eradication at a young age, and by the reduced use of inhibitors of acid secretion and use of a gastrin antagonist in those with previous long-term H. pylori infection and those with autoimmune gastritis.

Background: Gastric cancer stands as a primary cause of cancer-related deaths worldwide, making the discovery of new therapeutic agents essential for enhancing treatment outcomes. Curcumin, a polyphenolic compound found in turmeric (Curcuma longa), has demonstrated potential in multiple cancer types due to its anti-cancer characteristics. This research aimed to examine the impact of curcumin on gastric cancer cell growth, migration, and invasion, as well as its influence on the phosphoinositide 3-kinase (PI3K) signaling cascade. Methods: Gastric cancer cell lines were exposed to varying curcumin concentrations, followed by assessments of cell viability, migration, and invasion. Furthermore, gene and protein expression levels associated with the PI3K signaling cascade were evaluated using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. Results: The findings revealed a dose-dependent decrease in cell viability, migration, and invasion in gastric cancer cells treated with curcumin. Additionally, curcumin administration led to the downregulation of key genes and proteins within the PI3K signaling process, such as PI3K, Akt, and mTOR. Conclusion: These findings propose that curcumin may exercise its anti-cancer effects on gastric cancer cells, partly by suppressing the PI3K signaling pathway. This study's outcomes support curcumin's potential as a therapeutic agent for gastric cancer and encourage further exploration of its underlying molecular mechanisms and in vivo effectiveness.

Hp0521 is the number of cag pathogenicity island (cagPAI) family in Helicobacter pylori (H. pylori, Hp), which encoded Cag2 protein. The aim of this study was to investigate the role of hp0521 on the H. pylori 26,695 strain. We constructed the recombinant prokaryotic expression plasmid pET-32a-hp0521 and pET-32a-hpc0521. Then, we co-cultured the H. pylori wild strain 26,695 and Δhp0521 strain with GES-1 cells to detect CagA protein transport and IL-8 secretion. We found that Δhp0521 mutation increased the expression of cagA, rpoB and promoted the transportation of CagA protein in GES-1 cells. In addition, we also observed that Δhp0521 mutation had no effect on other cagPAI protein stability and the expression of IL-8. Our findings suggested that hp0521 may down-regulated the expression of cagA, rpoB and inhibited the transportation of CagA protein in GES-1 cells and had no effect on growth.

Microelectrode-based cell chip studies for cellular responses often require improved adhesion and growth conditions for efficient cellular diagnosis and high throughput screening in drug discovery. Cell-chip studies are often performed on gold electrodes due to their biocompatibility, and stability, but the electrode-electrolyte interfacial capacitance is the main drawback to the overall sensitivity of the detection system. Thus, here, we developed reduced graphene oxide-polyaniline-modified gold microelectrodes for real-time impedance-based monitoring of human gastric adenocarcinoma cancer (MKN-1) cells. The impedance characterization on modified electrodes showed 28-fold enhanced conductivity than the bare electrodes, and the spectra were modeled with proper equivalent circuits to extrapolate the values of circuit elements. The impedance of both time-and frequency-dependent measurements of cell-covered modified electrodes with equivalent model circuits was analyzed to achieve cellular behavior, such as adhesion, spreading, proliferation, and influence of anti-cancer agents. The normalized impedance at 41.5 kHz (|Z|_{norm 41 kHz}) was selected to monitor the cell growth analysis, which was found linear with the proliferation of adherent cells along with the influence of the anticancer drug agent on the MKN-1 cells. The synergistic effects and biocompatible nature of PANI-RGO modifications improved the overall sensitivity for the cell-growth studies of MKN-1 cells.

Previous research has revealed the role of statins in cancer prevention and treatment. This study aimed to determine the relationship between statins exposure and the incidence and prognosis of gastric cancer (GC).

Relevant articles until January 2022 were systematically searched in PubMed, EBSCO, Web of Science, and Cochrane Library databases for comparison in GC with or without statins exposure. The primary referred outcomes were the occurrence of GC and the survival rate. A total of 19 articles were included in this meta-analysis.

The analysis showed that statins were associated with reduced GC incidence and increased GC survival rate. Subgroup analysis suggested a decreased incidence of GC in both Eastern and Western countries exposed to statins. Furthermore, the risk of GC was reduced in those exposed to lipophilic statins, yet not in those exposed to hydrophilic statins.

Statins were found to help lower the incidence and improve the survival rate of GC. Furthermore, the incidence of GC was influenced by the population's origin region and the type of statins used.