This study aimed to evaluate the knowledge, attitudes, and practices (KAP) regarding nutritional management among patients with gastrointestinal cancer.

A descriptive cross-sectional study was conducted from December 2023 to May 2024 across hospitals in Jiangsu, Henan, Shanghai, and Tianjin, China. Participants completed questionnaires that collected demographic data and assessed their KAP toward nutritional management.

A total of 1239 valid questionnaires were analyzed. Among the participants, 769 (62.1%) were male, and 452 (36.5%) had been diagnosed with gastrointestinal cancer for less than six months. The proportion of participants demonstrating adequate knowledge, positive attitudes, and proactive practices were 1018 (82.1%), 328 (26.4%), and 403 (32.5%), respectively. Multivariate logistic regression identified several factors independently associated with proactive practices, including adequate knowledge, lack of insurance, a gastrointestinal tumor duration of 2-3 years or more, no doubts about nutritional management, absence of nutritional screening, and having others as primary caregivers. Structural equation modeling revealed direct effects of knowledge on both attitude (β ​= ​0.308, P ​< ​0.001) and practice (β ​= ​0.475, P ​< ​0.001), as well as of attitude on practice (β ​= ​0.286, P ​< ​0.001). Additionally, knowledge indirectly influenced practice through attitude (β ​= ​0.088, P ​< ​0.001).

While most gastrointestinal cancer patients demonstrated adequate knowledge regarding nutritional management, their attitudes were predominantly negative, and their practices were largely inactive. These findings highlight a critical need for targeted educational interventions to bridge knowledge gaps and encourage more active engagement with nutritional guidelines.

Gastric cancer (GC) is the fourth most common cause of cancer-related mortality and the fifth most common cancer worldwide. Despite efforts, the identification of biomarkers and new therapeutic approaches for GC remains elusive. Recent studies have begun to reveal the role of N6-adenosine methylation (m6A) in the regulation of gene expression.

The expression of the reader YT521-B homology domain-containing family 3 (YTHDF3) in GC was assessed in 331 patients using immunohistochemistry. GC cell lines depleted of YTHDF3 using CRISPR-Cas9 were evaluated for migration, metastasis, orientation of the mitotic spindle, and response to paclitaxel. The association between YTHDF3 and EZRIN (EZR) mRNA was shown using RNA sequencing, immunofluorescence, real-time PCR, and RNA immunoprecipitation. The single-base elongation- and ligation-based qPCR amplification (SELECT) method was used to map m6A in the EZR transcript.

YTHDF3 was significantly overexpressed in GC, and high levels of YTHDF3 were predictive of the response to chemotherapy. In GC cell lines, YTHDF3 was the most highly expressed reader protein. YTHDF3 depletion impaired cytoskeleton organization, cell migration and metastasis, and orientation of the mitotic spindle, leading to an increased response to paclitaxel. EZR was one of the downregulated targets in the YTHDF3 knockout cell models and was associated with the observed phenotype.

YTHDF3 contributes to cell motility and response to paclitaxel in GC cell lines, at least in part through EZR regulation. The YTHDF3-EZR regulatory axis is a novel molecular player in GC, with clinical relevance and potential therapeutic utility.

Gastric adenocarcinoma (GAC) ranks among the most common cancers worldwide. Hepatocyte growth factor receptor, also known as MET, plays crucial roles in GAC progression. Present study aimed to investigate whether urolithin A (UA), urolithin B (UB) and methyl UA (mUA) could induce anticancer effects on GAC cells via targeting MET. For computational analysis, potential molecular targets of urolithins and pathogenic targets of GAC were identified, PPI network was constructed, enrichment analyses were carried out and the expression of MET was assessed in MKN-45 cells. Additionally, pharmacokinetic and druglikeness of urolithins were evaluated, and molecular docking and dynamics simulations were performed. For in vitro analysis, urolithins were synthesized and viability of MKN-45, MG-63 and HFF-3 cells was investigated by alamarBlue assay, followed by apoptosis detection. MET was identified as one of the seven top hub genes for GAC and urolithins, and GO and KEGG enrichment analyses confirmed its involvement in several biological processes and pathways. Volcano plot revealed MET overexpression in MKN-45 cells. Web-based analyses revealed favorable lipophilicity, reasonable water solubility, intestinal absorption, moderate distribution and no significant toxicity concerns for urolithins. Viability assay indicated dose- and cell type-dependent cytotoxicity of urolithins, as the lowest IC50 values belonged to MKN-45 cells, which was confirmed by flow cytometry analysis. Molecular docking demonstrated favorable interactions between UA and UB within the active site of MET. Additionally, molecular dynamics simulations indicated both conformational flexibility and binding stability of UA-MET complex. Our comprehensive study suggests a potential mechanism for anticancer effects of urolithins through interaction with MET in GAC cells.

Gastric cancer (GC) is a leading cause of cancer-related death in Central America, with late-stage diagnosis common because of nonspecific early symptoms. Symptomatic screening guidelines validated in high-income settings have been used to identify patients requiring urgent referral for upper GI endoscopy.

This tool was piloted to assess feasibility for early detection of GC at a primary care clinic in Roatán, Honduras. If positive, a referral to endoscopy was placed, and patients contacted monthly for up to 4 months to collect information on demographics, GC risk factors, barriers to receiving endoscopy, and if they received an endoscopy. Provider questionnaires assessed endoscopy capacity and perceived patient barriers.

Five hundred patients were screened over 12 months. Nine screened positive, with seven clinically relevant to GC. Of these, four (57%) were female, average age was 49 years (IQR, 18), average number of years lived in Roatán was 29 (IQR, 34), and hypertension (57%) and hyperlipidemia (29%) were the most reported comorbidities. Two (29%) had a family history of cancer, four (57%) had a previous H. pylori infection, six (71%) took medication for acid reflux, and four (57%) had dietary risk factors for GC. All patients cited cost as a barrier to care, while two (29%) each reported difficulty traveling to a facility, lack of knowledge on which facilities did endoscopy, and uncertainty of whether they needed the procedure as other barriers.

Although symptomatic screening guidelines are feasible for screening GC in Honduras, limitations in endoscopy access and capacity pose barriers to early diagnosis. These findings highlight the need to increase diagnostic capacity and address financial barriers to endoscopy.

Gastric cancer (GC), one of the most prevalent malignancies worldwide, is distinguished by extensive genetic and phenotypic heterogeneity, posing persistent challenges to conventional diagnostic and therapeutic strategies. The significant global burden of GC highlights an urgent need to unravel its complex underlying mechanisms, discover novel diagnostic and prognostic biomarkers, and develop more effective therapeutic interventions. In this context, this review comprehensively examines the transformative roles of cutting-edge technologies, including radiomics, pathomics, genomics, transcriptomics, epigenomics, proteomics, and metabolomics, in advancing precision diagnosis and treatment for GC. Multiomics data analysis not only deepens our understanding of GC pathogenesis and molecular subtypes but also identifies promising biomarkers, facilitating the creation of tailored therapeutic approaches. Additionally, integrating multiomics approaches holds immense potential for elucidating drug resistance mechanisms, predicting patient outcomes, and uncovering novel therapeutic targets, thereby laying a robust foundation for precision medicine in the comprehensive management of GC.

Gastric cancer (GC) is the fourth most prevalent cancer and a leading cause of cancer-related fatalities in South Korea. Although periodic screening policies are in place, the early detection and prediction of GC remain challenging. This study evaluated the risk of GC incidence by utilizing longitudinal health check-up data from the National Health Insurance Service-Health Screening Cohort spanning from 2009 to 2019. The criteria selected for this study are general health examination candidates aged 40 or older who have been eligible for health insurance since 2009. The exclusion criteria included individuals diagnosed with cancer prior to 2009 or before their examination date, as well as those who did not complete the examination questionnaire. A time-dependent Cox proportional hazards model was employed to analyze the time from health examination to the first GC diagnosis, comparing our results with previous cohort studies that evaluated the GC risk through general check-up parameters. Significant risk factors for GC incidence in both genders were age, high levels of AST and γ-GTP, low levels of ALT and hemoglobin. Among males, dyslipidemia, smoking and physical activities were also significantly associated with GC risk. Although further evidence is needed, low hemoglobin levels emerged as a promising potential risk factor for GC, ascertainable through routine general health check-ups.

Gastric cancer (GC) prognosis is significantly influenced by intratumoral microbiomes, which modulate host-immune interactions. This study analyzed data from the The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to identify immune genes associated with GC prognosis and conducted prognostic immune subtypes. GC patients were classified into two distinct prognostic immune phenotypes C1 and C2 based on the non-negative matrix factorization consensus clusters. Phenotype C2 exhibited a better prognosis and distinct immune characteristics, including enhanced presence of Th2 and Th17 cells and improved response to chemotherapy. In contrast, phenotype C1 showed higher expression levels of PDCD1LG2 and TLR9, which were critical immune factors involved in immune regulation. Both phenotypes were linked to immune genes influencing intratumoral microbiomes and GC immunotherapy responses. A prediction risk model was constructed using the LASSO regression analysis and showed great prognostic value for GC patients. The key genes were correlated with immune cells and suppressed the function of the host immune system. The intratumoral microbiomes were strongly associated with the hosts' immune infiltration and significantly interacted with host immune genes to influence GC outcomes. Candidatus Nitrosotenuis plays a significant role in predicting the prognosis of GC patients. This research underscores the pivotal role of intratumoral microbiomes in GC prognosis and supports the development of future personalized therapeutic approaches.IMPORTANCEIncreasing evidence confirms the presence of intratumoral microbiomes. However, the role of the intratumoral microbiomes in the progression of gastric cancer and their relationship with the immune microenvironment remain unclear. Our study classified gastric cancer patients into two immune prognostic subtypes, C1 and C2, using non-negative matrix factorization consensus clusters. The C2 subtype exhibited a better prognosis and more pronounced immune characteristics. Microbiome analyses revealed associations between both subtypes and immune genes that affect intratumoral microbiomes and their responses to immunotherapy. The intratumoral microbiomes were closely linked with host immune infiltration and significantly interacted with immune genes, which influence the prognosis of gastric cancer. Notably, Candidatus Nitrosotenuis showed a significant prognostic value in gastric cancer patients. Our findings highlight the critical role of the intratumoral microbiomes in affecting gastric cancer prognosis and its interaction with the immune microenvironment, supporting future personalized therapeutic approaches.

Despite advancements in early detection and treatment, the prognosis and histological types for residual gastric cancer (GC) remains poor.

This case report presents a rare occurrence of residual GC featuring a combination of small cell neuroendocrine carcinoma (SCNEC) and squamous cell carcinoma (SCC) in a 60-year-old male patient. The patient, with a history of Billroth II gastrectomy for duodenal ulcer bleeding, presented with gastrointestinal bleeding. Preoperative computed tomography and positron emission tomography-computed tomography indicated adenocarcinoma with tumor and abdominal lymph node metastasis. The patient underwent laparoscopic total gastrectomy and lymph node dissection for residual GC. Histological examination of the resected tumor confirmed the presence of both SCNEC and SCC. Postoperatively, the patient underwent adjuvant chemotherapy four times. Two years later, the patient was found to occur esophageal cancer and was performed a small bowel stoma and radical esophagectomy.

In this case report, we detail a rare instance of residual GC with mixed SCNEC and SCC, emphasizing the complexity of diagnosis and treatment, and the need for ongoing research.

Gastric cancer is among the top five most important malignancies in the world due to the high burden of the disease and its lethality. Indeed, it is the fourth most common cause of death worldwide, characterized by a poor prognosis and low responsiveness to chemotherapy. Multidrug resistance limits the clinical management of the patient. Among these, the role of chronic activation of inflammatory pathways underlying gastric tumorigenesis should be highlighted. Furthermore, the gastric immunosuppressive TME influences the response to therapy. This review discusses the role of soluble cytokine receptors in the development and chemoresistance of gastric cancer, considered as a molecular marker and target of strategies to overcome resistance.

Background: Gastric cancer remains a leading global health challenge, despite advances in surgical techniques and perioperative care. Patients with gastric cancer present with a degree of postoperative complications, most notably anastomotic fistulas, which can lead to a high level of morbidity and mortality. Although significant advances have been made in their management by implementing less invasive methods, issues and debate remain regarding their early detection and treatment decisions. The purpose of this study was to emphasize the particularities of the treatment of postoperative fistulas in gastric cancer surgery, focusing on risk factors as well as management strategies. Methods: This retrospective study analyzed risk factors, diagnostic methods, and treatment strategies for anastomotic fistulas in 527 patients undergoing curative gastric cancer surgery over the span of five years, highlighting postoperative complication rates, the management of postoperative complications, and the primary risk factors for developing fistulas. Results: Conservative treatment combined with minimally invasive interventions achieved a primary success rate of over 65%, with surgical intervention being reserved for severe cases. The primary risk factors identified were an advanced tumor stage, total gastrectomy, type II diabetes mellitus, and a high number of transfusions required, as well as hypoalbuminemia. Conclusions: Although further research is required to standardize treatment protocols and reduce the morbidity and mortality associated with postoperative fistulas, understanding the primary elements of its causation can prove helpful in choosing the correct treatment.

Gastric cancer represents an aggressive malignancy and a leading contributor to cancer death. Ephrin-A4 (EFNA4) has been proposed to be related to the immune microenvironment and prognosis of gastric cancer. This study was undertaken to discuss the participation and mechanism of EFNA4 in the development of gastric cancer. RT-qPCR and western blot examined EFNA4 and Pygopus2 (Pygo2) expression in gastric cancer cells. After transfection of EFNA4 interference plasmids or co-transfection of EFNA4 interference plasmids and Pygo2 overexpression plasmids, cell proliferation was detected by the CCK-8 method and EDU staining. Wound healing, Transwell, TUNEL, and endothelial cell tube formation assays detected cell migration, invasion, apoptosis, and angiogenesis, respectively. Western blot examined the expression of metastasis-, apoptosis-, angiogenesis-, and Wnt signaling-associated proteins. Cell stemness was estimated by the sphere formation assay, RT-qPCR, and western blot. Through the experimental data, it was noticed that EFNA4 expression was increased in gastric cancer cells. Knockdown of EFNA4 suppressed the proliferation, migration, invasion, angiogenesis as well as stemness while aggravating the apoptosis of gastric cancer cells. Also, EFNA4 depletion reduced Pygo2 protein expression and then inactivated Wnt/β-catenin signaling. Further elevation of Pygo2 reversed the impacts of EFNA4 silencing on Wnt/β-catenin signaling, cell proliferation, apoptosis, migration, invasion, angiogenesis as well as stemness in gastric cancer. Accordingly, the knockdown of EFNA4 might downregulate Pygo2 and inactivate Wnt/β-catenin signaling to exert protective effects against gastric cancer.

Currently, immune checkpoint inhibitors (ICIs) have excellent performance in the clinical treatment of advanced gastric cancer (AGC). However, precisely selecting AGC patients who can benefit from immunotherapy is an urgent difficulty. In this study, we investigated the immunoprognostic role of myeloid-to-lymphocyte ratio (M:L) in AGC patients.

We collected information on 268 AGC patients who were hospitalized in the Department of Medical Oncology of PLA General Hospital from December 2014 to May 2021. The patients were divided into low M: L group (< 3.76) and high M:L group (≥ 3.76). Survival differences between different M: L level groups at baseline and after treatment were analyzed by methods such as Kaplan-Meier, Cox or Logistic regression model.

Progression free survival (PFS) (5.8 months vs. 3.4 months, p = 0.001) and overall survival (OS) (14.1 months vs. 9.0 months, p = 0.001) were significantly longer in the low M:L group than in the high M:L group. After analyses of Cox regression modeling it was concluded that M:L was an independent prognostic factor for PFS (HR 1.371 95%CI 1.057-1.777 p = 0.017) and OS (HR 1.352 95%CI 1.003-1.824 p = 0.048), respectively. Subsequent subgroup analyses performed across immunotherapy lines, regimens, PD-1 inhibitor agents, and age groups revealed a poorer prognosis in the high M:L group. Notably, an increase in the value of M:L after treatment significantly increased the risk of poor prognosis.

M:L ≥ 3.76 is associated with poor prognostic outcomes in AGC patients receiving immunotherapy and may be a predictive biomarker of prognosis. This result needs to be confirmed by larger prospective studies.

Cancer remains a leading cause of mortality globally, necessitating ongoing research and development of innovative therapeutic strategies. Natural products from plants, herbs, and marine species have shown great promise as anti-cancer therapies due to their bioactive components that alter cellular pathways, particularly apoptosis. This review explores the mechanism by which natural chemicals trigger the apoptosis of cancerous cells, which is crucial for eliminating them and halting tumor growth. These can affect the mitochondrial process by controlling the Bcl-2 protein family, increasing cytochrome c release, and activating caspases. They also activate death receptors like Fas and TRAIL to enhance the extrinsic apoptotic pathway. We focus on the main signaling channels involved, such as the endoplasmic reticulum (ER) stress-mediated apoptosis, extrinsic death receptor, and intrinsic mitochondrial pathways. The review explores the role of natural substances such as polyphenols, terpenoids, alkaloids, and flavonoids in promoting apoptotic cell death and increasing cancer cell susceptibility, potentially aiding in cancer treatments and the potential of combining natural products with traditional chemotherapeutic medicines to combat medication resistance and enhance therapeutic efficacy. Understanding cancer development involves inhibiting cell proliferation, regulating it, targeting apoptosis pathways, and using plant and marine extracts as apoptotic inducers.

Early nutritional support holds paramount importance for postoperative gastric cancer (GC) patients. Peptidase M20 domain containing 1 (PM20D1) is a secretory enzyme associated with glucose and lipid metabolism. However, there is a dearth of clinical studies delving into the connection between PM20D1, lipid metabolism, and inflammatory factors in GC patients who have received enteral nutrition (EN). This research aimed to investigate the serum levels of PM20D1 in GC patients following early EN and their potential associations with lipid metabolism, nutritional markers, and inflammatory factors.

This prospective observational study enrolled 180 GC patients between May 2020 and July 2022. On the first postoperative day, all patients received EN support, which was maintained for a duration of 5 days. Serum levels of PM20D1, interleukin (IL)-6, IL-1β, and C-reactive protein were measured on the sixth day after surgery using an enzyme-linked immunosorbent assay. Data on demographics, clinical statistics, lipid metabolism, nutritional parameters, and the prognostic nutritional index (PNI) were collected. Patients were followed up for 12 months, and both overall survival and disease-free survival were recorded.

In the low PNI group, the serum levels of PM20D1, albumin (ALB), and blood lymphocytes (BL) showed significant reductions. Pearson analysis revealed a negative correlation between PM20D1 and IL-6 levels, whereas a positive correlation emerged between PM20D1 and ALB and BL levels. Furthermore, PM20D1 demonstrated potential as a biomarker for diagnosing poor nutritional status (PNI < 43) in GC patients and was a risk factor for poor nutritional status in GC patients.

Serum PM20D1 remarkably declined in GC patients after early EN and was associated with poor nutritional status.

Gastric cancer is a common malignancy disease with a poor prognosis. Deficient mismatch repair is a prognostic and predictive marker of response to systemic therapies. However, deficient mismatch repair frequency and the relationship between this status and microscopic characteristics are inconsistent across nations. We aimed to determine the rate of deficient mismatch repair and its association with histopathological features in gastric cancer patients. A cross-sectional study was conducted on 226 gastric cancer patients treated at Hue University of Medicine and Pharmacy Hospital and Hue Central Hospital from June 2020 to January 2024. Mismatch repair protein expression was evaluated using immunohistochemical staining, and any absence of mismatch repair proteins was regarded as deficient mismatch repair. The deficient mismatch repair rate was 12.8%. Deficient mismatch repair appeared to be more frequent in the intestinal subtype of Lauren classification odds ratio (OR) = 4.767 (95% confidence interval [CI], 1.086-20.921; p = 0.039), tubular/papillary adenocarcinoma (OR = 5.25; 95% CI, 1.185-23.251; p = 0.029), mucinous adenocarcinoma (OR = 6.19; 95% CI, 1.113-34.445; p = 0.037), and differentiated type (OR = 3.24; 95% CI, 1.324-7.931; p = 0.01). No statistically significant association was detected with histopathological features according to the Tumor Location-Modified Lauren classification and mucinous secreting morphology. Deficient mismatch repair status was unusual in gastric cancer. The degree of cell differentiation and microscopic characteristics based on the World Health Organization and Lauren classification could all impact the predictive power for microsatellite-instable status.

Gastric cancer is a highly prevalent malignancy in Asia; however, its incidence is rising in the United States. Traditionally, methods of treatment include surgery and chemotherapy. Endoscopy has become an alternative method with a low recurrence rate when used to treat early gastric cancers. Endoscopic mucosal resection and endoscopic submucosal dissection are the 2 mainstay methods of endoscopy treatment. They are advantageous compared to surgery as they are less invasive and maintain anatomic integrity for the patient. However, lesion selection is crucial for success. In this article, the authors describe the 2 methods in detail in the treatment of early gastric cancers.

The incorporation of plant-derived bioactive compounds into the food matrix is growing due to their benefits in improving human health. Agro-industrial avocado by-products are usually inexperienced waste and represent a 22-30% total fruit weight; however, they stand out for being high in bioactive and functional components such as lipid compounds, phenolic compounds, oxalates, and fiber, among others; Bioactive compound to be characteristic to preventive chronic disease proprieties. Besides, gastric cancer has anintermediate prevalence of 10-20 in 100,000 people, and isthe fifth most common cancer worldwide; health institutions recommend consuming fruits and vegetables as an effective strategy because their bioactive compounds exert chemopreventive activity. However, there is a knowledge gap regarding the bioaccessibility and chemical changes of phenolic compounds in ingredients and their implications in gastric cancer during the digestive process, mainly the gastric phase at different times. This study determined the bioaccessibility of phenolic compounds and evaluated the cytotoxicity in a transformed gastric cell line (CRL-1739) during oral-gastric digestion of ingredients from avocado seed. Principal phenolic compounds in the ingredient show high concentrations of catechin, rutin, ellagic, and chlorogenic acid; The phenolic compounds are more bioaccessible in gastric phases of 10 and 25 min, attributed to acid hydrolysis. The ingredient exhibited a maximum cytotoxicity potential in the gastric cancer cell line with the gastric phase at 10 min. Hence the ingredient from avocado seed has possible functional potential in gastric digestion.

This study is performed to research the biological role of KDM1A in the epithelial mesenchymal transition (EMT) of gastric cancer and investigate the mechanism involved.

The KDM1A, Vimentin and E-cadherin levels were studied, as well as the correlation among them in gastric cancer samples. Gastric cancer cells were transfected with KDM1A overexpression and knockdown, and the cellular infiltration, motility, morphology and F-actin expression were subsequently identified. For the protein level assessment of EMT, the western blot analysis combined with immunofluorescence was employed. The effect of KDM1A on TGF-β/Notch signaling was also detected.

KDM1A was overexpressed in gastric cancer tumor tissues. In the clinical gastric carcinoma samples, the level of KDM1A was linked negatively to the expression of E-cadherin, while positively to the expression of Vimentin. Among the gastric carcinoma population, the expression of KDM1A was linked to the lymph node metastasis, TNM stage and tumor differentiation. The KDM1A downregulation prohibited the cellular motility, infiltration and F-actin expression, and suppressed EMT process. KDM1A overexpression exhibited promoting effect on EMT in gastric cancer cells. KDM1A regulated TGF-β/Notch signaling to affect EMT in gastric cancer cells.

KDM1A acts as an oncogene and facilitates the epithelial mesenchymal transition process by regulating TGF-β/Notch signal pathway in gastric cancer cells.

Stomach cancer is the second most common cause of cancer-related death in Central Latin America and the fifth most common cancer by incident in the region. Understanding the epidemiology of stomach cancer is crucial to the appropriate planning, implementation and evaluation of comprehensive cancer control programs. The objective of this scoping review was to quantify the population-based incidence of stomach cancer in Central America from available data, identify reported risk factors, presentation and oncologic stage and explore the frequency of treatment used and survival outcomes for stomach cancer in Central America. Primary reports, cancer registries, hospital registries, endoscopy registries, case studies and case series focusing on the epidemiology of gastric cancer in Belize, Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua and Panama, along with its treatment modalities and mortality rates were included. After identifying 616 citations, 20 studies met the inclusion criteria and were selected for data extraction. 12 were from Costa Rica and 5 from Honduras, with few studies from other countries such as Belize, El Salvador and Panama. Crude rates of gastric adenocarcinoma varied widely across different studies, with rates ranging from 0.09/100,000 to 32.04/100,000 in Costa Rica between 1996 and 2015. Overall, there was a general decrease in crude rates over recent study periods. Studies in El Salvador and Panama reported lower crude rates compared to Costa Rica. Non-cardia cancers were more common than cardia cancers. Surgery was the main treatment discussed in the reviewed papers. Mortality data were limited. Our review highlights the need for reliable cancer registries in this region. Often, cancer registries provide the only opportunity for properly assessing the extent and nature of cancer burdens in developing countries. This information is crucial in creating priorities for cancer control public health programs.

Gastric cancer remains a significant global health challenge, with Helicobacter pylori (H. pylori) recognized as a major etiological agent, affecting an estimated 50% of the world's population. There has been a rapidly expanding knowledge of the molecular and pathogenetic mechanisms of H. pylori over the decades. This review summarizes the latest research advances to elucidate the molecular mechanisms underlying the H. pylori infection in gastric carcinogenesis. Our investigation of the molecular mechanisms reveals a complex network involving STAT3, NF-κB, Hippo, and Wnt/β-catenin pathways, which are dysregulated in gastric cancer caused by H. pylori. Furthermore, we highlight the role of H. pylori in inducing oxidative stress, DNA damage, chronic inflammation, and cell apoptosis-key cellular events that pave the way for carcinogenesis. Emerging evidence also suggests the effect of H. pylori on the tumor microenvironment and its possible implications for cancer immunotherapy. This review synthesizes the current knowledge and identifies gaps that warrant further investigation. Despite the progress in our previous knowledge of the development in H. pylori-induced gastric cancer, a comprehensive investigation of H. pylori's role in gastric cancer is crucial for the advancement of prevention and treatment strategies. By elucidating these mechanisms, we aim to provide a more in-depth insights for the study and prevention of H. pylori-related gastric cancer.

This study presents nanostructured lipid carrier (NLC) co-loaded with Docetaxel (DCT) and 5-Fluorouracil (5-FU) as a targeted therapeutic approach for gastric cancer (GC). Using nanoprecipitation, NLC-DCT/5-FU were synthesized and exhibited an average particle size of 215.3 ± 10.4 nm, a polydispersity index (PDI) of 0.29, and a zeta potential of - 17.1 mV. Encapsulation efficiency reached 95.9% for DCT and 5-FU, with a loading efficiency of 11.2%. In vitro release studies demonstrated a biphasic release profile, with an initial burst and sustained release, achieving 85.6% DCT and 75.8% 5-FU release over 72 h. Cytotoxicity assays in MKN45 cells showed a significantly lower half-maximal inhibitory concentration (IC50) for NLC-DCT/5-FU (0.3 µM) compared to free DCT (3.9 µM) and free 5-FU (19.5 µM), indicating enhanced efficacy. In vivo evaluation in a GC mouse model confirmed substantial tumor volume reduction to 213 mm3 with NLC-DCT/5-FU treatment, compared to 432 mm3 with the free-drug combination. Systemic safety assessment showed minimal adverse effects, suggesting the nanoparticles' enhanced therapeutic index. These results demonstrate that NLC-based co-delivery systems could substantially improve the clinical outcomes of GC therapy.

Gastric cancer (GC) remains a leading cause of morbidity and mortality worldwide. The current standard of care involves neoadjuvant chemotherapy (NACT) followed by radical gastrectomy. This study aims to evaluate the efficacy of neoadjuvant therapy with PD-1/PD-L1 inhibitors in comparison to chemotherapy alone for patients with locally advanced gastric cancer (LAGC).

We conducted a systematic search of PubMed, Web of Science, and Embase to identify studies examining the addition of PD-1/PD-L1 inhibitors to neoadjuvant therapy for LAGC. Odds ratios (OR) were calculated for binary outcomes, such as pathological complete response (pCR), with corresponding 95% confidence intervals (CI).

Seven studies were included, encompassing a total of 1772 patients. Baseline median age ranged from 31 to 75 years. Most patients had an ECOG performance status score of 0 (942 patients), while 294 had an ECOG score of 1. The estimated pCR (OR 5.94, 95% CI 3.98-8.87; p < 0.000001) significantly favored the PD-1/PD-L1 inhibitors combined with chemotherapy over chemotherapy alone. Additionally, the incidence of certain adverse events increased significantly in the intervention group, including any-grade hypothyroidism (OR 4.55, 95% CI 2.27-9.10; p = 0.000019) and rash (OR 1.74, 95% CI 1.10-2.76; p = 0.017). Conversely, the control group showed a statistically significant lower incidence of grade ≥ 3 fatigue (OR 2.80, 95% CI 1.15-6.85; p = 0.024) compared to the intervention group.

This systematic review and meta-analysis indicate that the addition of PD-1/PD-L1 inhibitors to neoadjuvant chemotherapy is associated with a higher pathological complete response rate compared to chemotherapy alone in patients with locally advanced gastric cancer.

Gastric cancer (GC) is one of the most common cancers in the world. It is a multi-factorial disease influenced by both genetic and environmental factors such as diet, obesity, radiation exposure, and infectious agents. Viral infections usually lead to chronic inflammation, which can initiate the development of cancers. To date, only a few studies have been published about Epstein-Barr virus (EBV) and human papillomavirus (HPV) infections in the context of the development of GC. In particular, research on the development of cancer among people under 45 years of age, including the impacts of EBV and HPV, is rare, and clear results have not been obtained. The aim of this study was to analyze the frequency of occurrence of EBV and HPV in GC, particularly in early-onset gastric cancer (EOGC). Tissue material from 135 patients with GC, including 84 men and 51 women, was examined. RT-PCR was performed to detect EBV, and PCR was performed to detect HPV. There were no significant impacts of EBV and HPV infections on any subtype of GC. There was also no statistically significant dependence of gender and location of the tumor on any subtype of GC. Further research on the impacts of infectious agents such as EBV and HPV on GC should be conducted using larger populations.

Helicobacter pylori (H. pylori) infection is a well-established risk factor for gastric cancer, primarily due to its virulence factor, cytotoxin-associated gene A (CagA). Although PD-L1/PD-1-mediated immune evasion is critical in cancer development, the impact of CagA on PD-L1 regulation remains unclear. This study revealed that H. pylori CagA upregulated squalene epoxidase (SQLE) expression, a key enzyme in the cholesterol biosynthesis pathway. Elevated SQLE activity increased cellular palmitoyl-CoA levels, enhancing PD-L1 palmitoylation while decreasing its ubiquitination. This ultimately increases PD-L1 stability, suppressing T cell activity and facilitating immune evasion in gastric cancer. In summary, our findings highlight the crucial role of the CagA-SQLE-PD-L1 axis in gastric cancer progression, suggesting potential therapeutic strategies for targeting CagA-positive gastric cancer.

The aim of this study was to establish a primary mouse gastric carcinoma cell line.

Gastric adenocarcinoma in the body region was induced in immunocompetent BALB/c mice using N-Methyl-N-nitrosourea and a 2% NaCl solution. Fresh gastric cancer tissue samples were cultured in 1640 medium supplemented with 10% fetal bovine serum for primary culture and subculture. Cellular morphology was assessed via light microscopy, and a cell growth curve was established. Genomic and proteomic analyses were conducted to characterize the molecular features of the cell lines. This cell line demonstrated a 100% success rate in forming subcutaneous tumors in BALB/c mice. By integrating proteomic profiles from clinical gastric cancer patients and the murine subcutaneous tumor model, several molecular targets suitable for preclinical investigation were identified. Trametinib, a MEK inhibitor, was employed as a model compound in our preclinical study.

A novel gastric carcinoma cell line, designated MCC, was established from BALB/c mice. This cell line exhibited a doubling time of approximately 33 h. Genomic and proteomic analyses identified mutations frequently observed in clinical gastric cancer patients, such as Kras, Egfr, and Ccnd3. Additionally, MCC overexpresses proteins, including SLC1A5, MCM6, and ITGA2, which are significantly upregulated in gastric cancer tissues compared to adjacent non-cancerous tissues. The MCC cell line demonstrated stable tumorigenicity in immunocompetent BALB/c mice, forming subcutaneous tumors that closely resemble the proteomic profile of clinical gastric cancer samples. This high concordance facilitated the identification of several potential therapeutic targets for gastric cancer. Preclinical studies with trametinib revealed that treatment effectively inhibited gastric cancer growth, likely mediated through the activation of immune cells, particularly neutrophils and T cells.

The MCC cell line serves as an indispensable model for gastric cancer research, offering a robust platform for investigating tumor development and progression. Its exceptional tumorigenic capacity and strong concordance with clinical proteomic profiles underscore its significance in translational research, facilitating the discovery of novel therapeutic targets and elucidation of molecular pathways critical for developing effective treatment strategies.

Gastric cancer (GC) is one of the leading causes of cancer-related deaths worldwide because of its high morbidity and the absence of effective therapies. Even though paclitaxel is a powerful anticancer chemotherapy drug, recent studies have indicated its ineffectiveness against GC cells. Long non-coding RNA (lncRNA) PVT1 has a high expression in GC cells and increases the progression of tumors via inducing drug resistance. In the present study, the effects of the siRNA-mediated lncRNA PVT1 gene silencing along with paclitaxel treatment on the rate of apoptosis, growth, and migration of AGS GC cells were investigated. AGS cells were cultured and then transfected with siRNA PVT1 using electroporation. The MTT test was used to examine the effect of treatments on the viability of cultured cells. Furthermore, the flow cytometry method was used to evaluate the impact of treatments on the cell cycle process and apoptosis induction in GC cells. Finally, the mRNA expression of target genes was assessed using the qRT-PCR method. The results showed that lncRNA PVT1 gene suppression, along with paclitaxel treatment, reduces the viability of cancer cells and significantly increases the apoptosis rate of cancer cells and the number of cells arrested in the G2/M phase compared to the control group. Based on the results of qRT-PCR, combined treatment significantly decreased the expression of MMP3, MMP9, MDR1, MRP1, Bcl-2, k-Ras, and c-Myc genes and increased the expression of the Bax gene compared to the control group. The results of our study showed that lncRNA PVT1 gene targeting, together with paclitaxel treatment, induces apoptosis, inhibits growth, alleviates drug resistance, and reduces the migratory capability of GC cells. Therefore, there is a need for further investigations to evaluate the feasibility and effectiveness of this approach in vivo in animal models.

Gastric cancer (GC) is a significant global health issue with high incidence rates and poor prognoses, ranking among the top prevalent cancers worldwide. Due to undesirable side effects and drug resistance, there is a pressing need for the development of novel therapeutic strategies. Understanding the interconnectedness of the JAK2/STAT3/mTOR/PI3K pathway in tumorigenesis and the role of Astaxanthin (ASX), a red ketocarotenoid member of xanthophylls and potent antioxidant and anti-tumor activity, can be effective for cancer treatments. This study aimed to investigate the effect of ASX-loaded nanoparticles on the survival of MKN-45 GC cells and the expression of JAK2/STAT3/mTOR/PI3K, offering insights into potential targeted therapies for GC.

The growth status and survival rate of MKN-45 GC cell lines were determined using the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide(MTT) assay, and the optimal IC50 concentration of ASX, PLGA, and ASX + PLGA was estimated. Also, the clonogenic assay was performed to determine the reproductive power and colony formation of under-treatment cells. Apoptosis and necroptosis of cells were evaluated using acridine orange (AO) staining. The western blot assessed the protein's level of expression and intensity (JAK2/STAT3/mTOR/PI3K). SPSS version 16 software was used for statistical analysis, P-value was considered lower than 0.05.

Based on the results, increasing concentrations of ASX and ASX + PLGA led to a decrease in the viability of MKN-45 cells compared to the control group (P < 0.001). This value was lower for cells treated with ASX + PLGA (P = 0.003). The IC50 values for each of the studied groups (ASX, ASX + PLGA, and PLGA) were 81.45 µg/ml, 51.45 µg/ml, and 3.383 mg/ml, respectively. The levels of expression and intensity of JAK2, STAT3, and mTOR proteins in the Western blotting analysis under ASX + PLGA treatment increased compared to the control group. Conversely, the levels of expression and intensity of P-JAK2, P-STAT3, and P-mTOR proteins in the ASX + PLGA treatment group decreased by 41%, 34%, 37%, and 43%, respectively, compared to the control group. Protein expression levels and intensities of JAK2, STAT3, and mTOR significantly increased when treated with PLGA, ASX, and ASX + PLGA compared to the control group (P < 0.001).

The encapsulation of ASX in PLGA nanoparticles enhances drug stability, enables targeted delivery, and allows for sustained release. This study highlights the therapeutic potential of ASX-loaded nanoparticles in targeting JAK2/STAT3/mTOR/PI3K pathways in GC treatment. Further research is needed to understand the mechanisms and clinical applications of this novel immunotherapy strategy.

Few studies have been designed to predict the survival of Chinese patients initially diagnosed with metastatic gastric cancer (mGC). Therefore, the objective of this study was to construct and validate a new nomogram model to predict cancer-specific survival (CSS) in Chinese patients.

We collected 328 patients with mGC from Northern Jiangsu People's Hospital as the training cohort and 60 patients from Xinyuan County People's Hospital as the external validation cohort. Multivariate Cox regression was used to identify risk factors, and a nomogram was created to predict CSS. The predictive performance of the nomogram was evaluated using the consistency index (C-index), the calibration curve, and the decision curve analysis (DCA) in the training cohort and the validation cohort.

Multivariate Cox regression identified differentiation grade (P < 0.001), T-stage (P < 0.05), N-stage (P < 0.001), surgery (P < 0.05), and chemotherapy (P < 0.001) as independent predictors of CSS. Nomogram of chemotherapy regimens and cycles was also designed by us for the prediction of mGC. Thus, these factors are integrated into the nomogram model: the C-index value was 0.72 (95% CI 0.70-0.85) for the nomogram model and 0.82 (95% CI 0.79-0.89) and 0.73 (95% CI 0.70-0.86) for the internal and external validation cohorts, respectively. Calibration curves and DCA also demonstrated adequate fit and ideal net benefit in prediction and clinical applications.

We established a practical nomogram to predict CSS in Chinese patients initially diagnosed with mGC. Nomograms can be used to individualize survival predictions and guide clinicians in making therapeutic decisions.

The development of cancer has been a multistep process involving mutation, proliferation, survival, invasion, and metastasis. Of all the characteristics of cancer, metastasis is believed to be the hallmark as it is responsible for the highest number of cancer-related deaths. In connection with this, Matrix metalloproteinases (MMPs), that has a role in metastasis, are one of the novel therapeutic targets. MMPs belong to the family of zinc-dependent endopeptidases and are capable of degrading the components of the extracellular matrix (ECM). The role of MMPs in ECM remodeling includes tissue morphogenesis, uterine cycling, growth, tissue repair, and angiogenesis. During pathological conditions, MMPs play a critical role in the excessive degradation of ECM which includes arthritis, tumour invasion, tumour metastasis, and several other autoimmune disorders. Moreover, they are believed to be involved in many physiological aspects of the cell, such as proliferation, migration, differentiation, angiogenesis, and apoptosis. It is reported that dysregulation of MMP in a variety of cancer subtypes have a dual role in tumour growth and metastasis processes. Further, multiple studies suggest the therapeutic potential of targeting MMP in invading cancer. The expression of MMP-2 correlates with the clinical characteristics of cancer patients, and its expression profile is a new diagnostic and prognostic biomarker for a variety of human diseases. Hence, manipulating the expression or function of MMP-2 may be a potential treatment strategy for different diseases, including cancers. Hence, the present review discusses the therapeutic potential of targeting MMP in various types of cancers and their recent patents.

RNA methylation is a dynamic and ubiquitous post-transcriptional modification that plays a pivotal role in regulating gene expression in various conditions like cancer, neurological disorders, cardiovascular diseases, viral infections, metabolic disorders, and autoimmune diseases. RNA methylation manifests across diverse RNA species including messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA), exerting pivotal roles in gene expression regulation and various biological phenomena. Aberrant activity of writer, eraser, and reader proteins enables dysregulated methylation landscape across diverse malignancy transcriptomes, frequently promoting cancer pathogenesis. Numerous oncogenic drivers, tumour suppressors, invasion/metastasis factors, and signalling cascade components undergo methylation changes that modulate respective mRNA stability, translation, splicing, transport, and protein-RNA interactions accordingly. Functional studies confirm methylation-dependent alterations drive proliferation, survival, motility, angiogenesis, stemness, metabolism, and therapeutic evasion programs systemically. Methyltransferase overexpression typifies certain breast, liver, gastric, and other carcinomas correlating with adverse clinical outcomes like diminished overall survival. Mapping efforts uncover nodal transcripts for targeted drug development against hyperactivated regulators including METTL3. Some erasers and readers also suitable lead candidates based on apparent synthetic lethality. Proteomic screens additionally highlight relevant methylation-sensitive effector pathways amenable to combinatorial blockade, reversing compensatory signalling mechanisms that facilitate solid tumour progression. Quantifying global methylation burdens and responsible enzymes clinically predicts patient prognosis, risk stratification for adjuvant therapy, and overall therapeutic responsiveness.

NEK2 is a serine/threonine protein kinase that is involved in regulating the progression of various tumors. Our previous studies have found that NEK2 is highly expressed in gastric cancer and suggests that patients have a worse prognosis. However, its role and mechanism in gastric cancer are only poorly studied. In this study, we established a model of ferroptosis induced by RSL3 or Erastin in AGS cells in vitro, and konckdown NEK2, HOMX1, Nrf2 by siRNA. The assay kit was used to analyzed cell viability, MDA levels, GSH and GSSG content, and FeRhoNox™-1 fluorescent probe, BODIPY™ 581/591 C11 lipid oxidation probe, CM-H2DCFDA fluorescent probe were used to detected intracellular Fe2+, lipid peroxidation, and ROS levels, respectively. Calcein-AM/PI staining was used to detect the ratio of live and dead cells, qRT-PCR and Western blot were used to identify the mRNA and protein levels of genes in cells, immunofluorescence staining was used to analyze the localization of Nrf2 in cells, RNA-seq was used to analyze changes in mRNA expression profile, and combined with the FerrDb database, ferroptosis-related molecules were screened to elucidate the impact of NEK2 on the sensitivity of gastric cancer cells to ferroptosis. We found that inhibition of NEK2 could enhance the sensitivity of gastric cancer cells to RSL3 and Erastin-induced ferroptosis, which was reflected in the combination of inhibition of NEK2 and ferroptosis induction compared with ferroptosis induction alone: cell viability and GSH level were further decreased, while the proportion of dead cells, Fe2+ level, ROS level, lipid oxidation level, MDA level, GSSG level and GSSG/GSH ratio were further increased. Mechanism studies have found that inhibiting NEK2 could promote the expression of HMOX1, a gene related to ferroptosis, and enhance the sensitivity of gastric cancer cells to ferroptosis by increasing HMOX1. Further mechanism studies have found that inhibiting NEK2 could promote the ubiquitination and proteasome degradation of Keap1, increase the level of Nrf2 in the nucleus, and thus promote the expression of HMOX1. This study confirmed that NEK2 can regulate HMOX1 expression through Keap1/Nrf2 signal, and then affect the sensitivity of gastric cancer cells to ferroptosis, enriching the role and mechanism of NEK2 in gastric cancer.

Gastric cancer (GC) has been a major health burden all over the world but there are fewer promising chemotherapeutic drugs due to its multidrug resistance. It has been reported that WYC-209 suppresses the growth and metastasis of tumor-repopulating cells but the effect on GC was not explored. MTT, colony formation, and transwell assays were performed to examine the effects of WYC-209 on the proliferation, colony growth, and mobility of GC cells. Western blotting and qRT-PCR were used to detect the expression of proteins and mRNA. RNA-seq and enrichment analyses were conducted for the differentially expressed genes and enriched biological processes and pathways. The rescue experiments were carried out for further validation. Besides, we constructed xenograft model to confirm the effect of WYC-209 in vivo. The dual-luciferase reporter and Chromatin immunoprecipitation were implemented to confirm the underlying mechanism. WYC-209 exerted excellent anti-cancer effects both in vitro and in vivo. Based on RNA-seq and enrichment analyses, we found that Wnt family member 4 (WNT4) was significantly down-regulated. More importantly, WNT4 overexpression breached the inhibitory effect of WYC-209 on GC progression. Mechanically, WYC-209 significantly promoted the binding between retinoic acid receptor α (RARα) and WNT4 promoter. WYC-209 exerts anti-tumor effects in GC by down-regulating the expression of WNT4 via RARα.

Gastric adenocarcinoma is the fourth leading cause of global cancer mortality and leading infection-associated cancer. Gastric cancer has significant geographic variability, with a high incidence in East Asia and mountainous regions of Latin America. In the United States, gastric cancer represents a marked disparity with incidence rates that are two to three times higher in Hispanics compared to non-Hispanic Whites.

We conducted a national retrospective study of incident gastric cancer in El Salvador from to 2000 to 2014 to estimate the age-standardized incidence rate (ASIR) by using a combination of pathology and endoscopy databases. A unique multisectorial coalition was formed between the Ministry of Health (MINSAL) and ES Gastroenterology Society (AGEDES), representing public hospitals (n = 5), governmental employee hospitals (ISSS, n = 5), and private facilities (n = 6), accounting for >95% of national endoscopy capacity. HER2 and EBV tumor status was ascertained in a representative sample during 2014 to 2016.

A total of 10,039 unique cases of gastric cancer were identified, 45.5% female, and mean age of 65. 21% and 9.4% were <55 and <45 years old, respectively. ASIRs (M, F) were 18.9 (95% CI, 14.4-20.7) and 12.2 per 100,000 persons (95% CI, 10.9-13.5), respectively, in the period 2010 to 2014 with all centers operational. Intestinal gastric cancer was 2.8 times more common than diffuse gastric cancer; 23.2% had partial or complete pyloric obstruction. The HER2 2+/3+ status was 16.7% and EBV-encoded RNA positivity was 10.2%.

A high incidence of gastric cancer was confirmed in El Salvador and nearly half of the patients were female.

The findings have implications for cancer control in the Central America LMICs and for US Latino populations. See related commentary by Riquelme and Abnet, p. 1550.

To evaluate the image quality of ultra-high-resolution CT (U-HRCT) images reconstructed using an improved deep-learning-reconstruction (DLR) method. Additionally, we assessed the utility of U-HRCT in visualizing gastric wall structure, detecting gastric cancer, and determining the depth of invasion.

Forty-six patients with resected gastric cancer who underwent preoperative contrast-enhanced U-HRCT were included. The image quality of U-HRCT reconstructed using three different methods (standard DLR [AiCE], improved DLR-AiCE-Body Sharp [improved AiCE-BS], and hybrid-IR [AIDR3D]) was compared. Visualization of the gastric wall's three-layered structure in four regions and the visibility of gastric cancers were compared between U-HRCT and conventional HRCT (C-HRCT). The diagnostic ability of U-HRCT with the improved AiCE-BS for determining the depth of invasion of gastric cancers was assessed using postoperative pathology specimens.

The mean noise level of U-HRCT with the improved AiCE-BS was significantly lower than that of the other two methods (p < 0.001). The overall image quality scores of the improved AiCE-BS images were significantly higher (p < 0.001). U-HRCT demonstrated significantly better conspicuity scores for the three-layered structure of the gastric wall than C-HRCT in all regions (p < 0.001). In addition, U-HRCT was found to have superior visibility of gastric cancer in comparison to C-HRCT (p < 0.001). The correct diagnostic rates for determining the depth of invasion of gastric cancer using C-HRCT and U-HRCT were 80%.

U-HRCT reconstructed with the improved AiCE-BS provides clearer visualization of the three-layered gastric wall structure than other reconstruction methods. It is also valuable for detecting gastric cancer and assessing the depth of invasion.

Few studies have been conducted on the prevention of bile reflux in gastric cancer patients who have undergone gastrectomy. The aim of this study was to evaluate the efficacy and safety of ursodeoxycholic acid (UDCA) in preventing bile reflux after gastrectomy in patients with gastric cancer.

This study was a secondary analysis of the PEGASUS-D trial, a randomized, double-blind, placebo-controlled clinical trial. Adults with a diagnosis of gastric cancer who underwent gastrectomy were enrolled. Eligible participants were randomly assigned to receive 300 mg of UDCA, 600 mg of UDCA, or placebo at a ratio of 1:1:1. UDCA and placebo were administered daily for 52 weeks. The primary outcomes included bile reflux symptoms at each time point, the percentage of participants with bile reflux, and the grade of gastritis.

Among 521 participants who underwent randomization, 151, 164, and 150 participants were analyzed from the 300 mg UDCA, 600 mg UDCA, and placebo groups, respectively. The difference in symptoms between the three groups was not significant. Bile reflux was less evident in the UDCA group than in the placebo group; however, this difference was significant only in the 300 mg group at 12 months postoperation (odds ratio, 0.44; P =0.0076). A significant reduction in gastritis was also observed in the 300 mg group at 12 months postoperation (odds ratio, 0.50; P =0.0368) compared to the placebo group.

This study showed that UDCA administration significantly reduced bile reflux and gastritis by ~50% at the 12 months-postoperative follow-up in patients who underwent gastrectomy for gastric cancer.

Gastrointestinal cancers are one of the most frequent cancer types and seriously threaten human life and health. Recent studies attribute the occurrence of gastrointestinal cancers to both genetic and environmental factors, yet the intrinsic etiology remains unclear. Mendelian randomization is a powerful well-established statistical method that is based on genome-wide association study (GWAS) to evaluate the causal relationship between exposures and outcomes. In the present study, we aimed to conduct a systematic review of Mendelian randomization studies investigating any causal risk factors for gastrointestinal cancers.

We systematically searched Mendelian randomization studies that addressed the associations of genetically predicted exposures with five main gastrointestinal cancers from September 2014 to March 2024, as well as testing the research quality and validity.

Our findings suggested robust and consistent causal effects of body mass index (BMI), basal metabolic rate, fatty acids, total cholesterol, total bilirubin, insulin like growth factor-1, eosinophil counts, interleukin 2, alcohol consumption, coffee consumption, apolipoprotein B on colorectal cancer risks, BMI, waist circumference, low-density lipoprotein (LDL), total testosterone, smoking on gastric cancer risks, BMI, fasting insulin, LDL, waist circumference, visceral adipose tissue (VAT), immune cells, type 2 diabetes mellitus (T2DM) on pancreatic cancer risks, waist circumference, smoking, T2DM on esophageal adenocarcinoma risks, and VAT, ferritin, transferrin, alcohol consumption, hepatitis B virus infection, rheumatoid arthritis on liver cancer risks, respectively.

Larger, well-designed Mendelian randomization studies are practical in determining the causal status of risk factors for diseases.

Talin-1 (TLN1) is crucial in cell migration, metastasis, and cancer development. This study evaluated Talin-1 expression and its clinical significance in gastric cancer (GC), along with human epidermal growth factor receptor-2 (HER-2) expression and its correlation with Talin-1.

Bioinformatics analysis assessed the potential prognostic value of Talin-1 and HER-2 in GC patients. The study included 223 GC patients (Signet Ring Cells and Intestinal subtypes) and 29 non-malignant tissue samples. Immunohistochemistry (IHC) on tissue microarray slides evaluated Talin-1 and HER-2 expression and clinical significance. Receiver operating characteristic (ROC) curves assessed their diagnostic value.

Bioinformatics identified Talin-1 as a potential prognostic factor and HER-2 as an oncogene in GC. Talin-1 and HER-2 expression increased in SRC-type GC samples compared to non-malignant tissues. High cytoplasmic Talin-1 expression inversely correlated with tumor expansion and invasion in SRC-type GC. Increased HER-2 expression positively correlated with metastasis. ROC curves showed significant diagnostic values for both proteins.

Higher cytoplasmic Talin-1 expression is associated with less invasive tumor behavior, while increased membranous HER-2 expression is associated with metastasis in SRC-type GC. These findings suggest potential use in assessing diagnosis and screening high-risk cancer patients, particularly those with SRC-type GC.

This study aims to create and assess machine learning models for predicting lymph node metastases following neoadjuvant treatment in advanced gastric cancer (AGC) using baseline and restaging computed tomography (CT). We evaluated CT images and pathological data from 158 patients with resected stomach cancer from two institutions in this retrospective analysis. Patients were eligible for inclusion if they had histologically proven gastric cancer. They had received neoadjuvant chemotherapy, with at least 15 lymph nodes removed. All patients received baseline and preoperative abdominal CT and had complete clinicopathological reports. They were divided into two cohorts: (a) the primary cohort (n = 125) for model creation and (b) the testing cohort (n = 33) for evaluating models' capacity to predict the existence of lymph node metastases. The diagnostic ability of the radiomics-model for lymph node metastasis was compared to traditional CT morphological diagnosis by radiologist. The radiomics model based on the baseline and preoperative CT images produced encouraging results in the training group (AUC 0.846) and testing cohort (AUC 0.843). In the training cohort, the sensitivity and specificity were 81.3% and 77.8%, respectively, whereas in the testing cohort, they were 84% and 75%. The diagnostic sensitivity and specificity of the radiologist were 70% and 42.2% (using baseline CT) and 46.3% and 62.2% (using preoperative CT). In particular, the specificity of radiomics model was higher than that of conventional CT in diagnosing N0 cases (no lymph node metastasis). The CT-based radiomics model could assess lymph node metastasis more accurately than traditional CT imaging in AGC patients following neoadjuvant chemotherapy.

Most gastric cancers (95%) are related to an initial Helicobacter pylori infection worldwide. Treatments against this pathogen include a mix of antibiotics, antimicrobials, and proton-pump inhibitors. Over time, H. pylori mutated, generating resistance to treatments and making it hard to combat its infection. The purpose of this review is Hibiscus sabdariffa, commonly known as hibiscus, as a potential agent for anti-H. pylori activity. Scientific interest has increased toward plant-derived bioactive compounds, which have the ability to enhance the antibiotic effect and can lead to the development of new drugs, such is the case for H. sabdariffa. In general, studies show that natural products, such as plant-derived bioactive compounds, can be used as alternative treatments from natural origin against the pathogen. The specific action mechanism of these bioactive compounds is still controversial, but it is suggested that they have an anti-inflammatory effect, and they also act as antibiotic coadjutants. Research has been conducted regarding different bioactive compounds such as polyphenols, epicatechins, alkaloids, and caryophyllenes. H. sabdariffa contains several of these compounds; therefore, more studies are needed to establish its effect against H. pylori.

Despite the remarkable improvement in gastric adenocarcinoma treatment modalities, the prognosis of gastric adenocarcinoma remains poor. The purpose of this study was to determine the prevalence of HER2 immunohistochemical expression and its association with clinicopathological features of patients with gastric adenocarcinoma.

This was a cross-sectional study which was conducted at the department of pathology. A total of 86 formalin fixed paraffin embedded tissue blocks of the patients who were confirmed histologically with gastric adenocarcinoma from January 2009 to December 2019 were included in the analysis. Laboratory requisition form and patients' files were used to extract the clinical and pathological data of the cases. Immunohistochemistry to assess HER2 overexpression was done using monoclonal (SP3 clone) rabbit anti-HER2/neu (Thermo Fisher Scientific-USA). Chi-square statistical test was used to determine the association of the clinicopathological characteristics with HER2 expression. P <0.05 was considered statistically significant.

Mean age of the patients included in the study was 58.5 ± 14.3 years, and over half 54.7% (n= 47) of the patients were males. Poorly cohesive non-signet ring types contributed most (47.7%) (n= 41) of the cases, and diffuse/mixed histological subtypes were more prevalent (57%) (n= 49) subtypes. Poorly differentiated cases accounted for the majority (66.3%) (n= 57) of the cases. The prevalence of HER2 immunohistochemical expression was 8.1% (n= 7). None of the clinicopathological characteristics were associated with HER2 expression.

This study has shown almost every one in 10 patients with gastric adenocarcinoma may express HER2 when using immunohistochemistry test. However, the HER2 in this study was not associated with age, sex, tumor location, the nature of biopsy, histological subtypes, and tumor grade.