Development Of Stomach Cancer Research Articles

The effect of healthy eating on the development of stomach and colorectal cancer by the smoking and drinking status: Results from the Korean National Cancer Center (KNCC) community cohort study.

Determining the effect of dietary factors on cancer is a crucial issue when accounting for the effect of other major risks, such as smoking and drinking. A total of 15,563 adults from the Korean National Cancer Center Community Cohort were analyzed to determine and to compare the effect of dietary factors on stomach and colorectal cancer in overall and in the subgroup of non-smokers (or urinary cotinine concentrations <5 ng/mg) and non-drinkers with Cox proportional-hazard models. During the mean follow-up (13.7 years), 469 and 299 cases of stomach and colorectal cancer were identified, respectively. The preventive effect of vegetable, fish, and soybean/tofu intake on colorectal cancer was found in women after adjustment for smoking, drinking, BMI, and sociodemographic factors. In the subgroup analysis of non-smokers and non-drinkers, the effect on colorectal cancer was increased in women (≥1 time/week vs. almost never, vegetables: hazard ratio (HR) 0.30, 95% confidence interval (CI) 0.13-0.69; fish: HR 0.46, 95% CI 0.26-0.83), and the fresh fish intake effect on stomach cancer was newly identified in men (HR 0.36, 95% CI 0.15-0.86). These effects were more pronounced and additionally shown in other dietary factors such as soybean or tofu in women and vegetables and fish in men, when subjects with <5 ng/mg urinary cotinine concentrations applied. The protective effect of healthy eating on the risk of stomach and colorectal cancer were different by smoking and drinking status. Rigorous control of smoking and drinking effects is necessary when measuring the effect of dietary factors on cancer, properly.

The interactions between traditional Chinese medicine and gut microbiota in cancers: Current status and future perspectives

The gut microbiota, known as the “forgotten organ” and “human second genome,” comprises a complex microecosystem. It significantly influences the development of various tumors, including colorectal, liver, stomach, breast, and lung cancers, through both direct and indirect mechanisms. These mechanisms include the “gut-liver” axis, the “lung-intestine” axis, and interactions with the immune system. The intestinal flora exhibits dual roles in cancer, both promoting and suppressing its progression. Traditional Chinese medicine (TCM) can alter cancer progression by regulating the intestinal flora. It modifies the intestinal flora’s composition and structure, along with the levels of endogenous metabolites, thus affecting the intestinal barrier, immune system, and overall body metabolism. These actions contribute to TCM’s significant antitumor effects. Moreover, the gut microbiota metabolizes TCM components, enhancing their antitumor properties. Therefore, exploring the interaction between TCM and the intestinal flora offers a novel perspective in understanding TCM’s antitumor mechanisms. This paper succinctly reviews the association between gut flora and the development of tumors, including colorectal, liver, gastric, breast, and lung cancers. It further examines current research on the interaction between TCM and intestinal flora, with a focus on its antitumor efficacy. It identifies limitations in existing studies and suggests recommendations, providing insights into antitumor drug research and exploring TCM’s antitumor effectiveness. Additionally, this paper aims to guide future research on TCM and the gut microbiota in antitumor studies.

Immune evasion by proteolytic shedding of natural killer group 2, member D ligands in Helicobacter pylori infection.

Helicobacter pylori (H. pylori) uses various strategies that attenuate mucosal immunity to ensure its persistence in the stomach. We recently found evidence that H. pylori might modulate the natural killer group 2, member 2 (NKG2D) system. The NKG2D receptor and its ligands are a major activation system of natural killer and cytotoxic T cells, which are important for mucosal immunity and tumor immunosurveillance. The NKG2D system allows recognition and elimination of infected and transformed cells, however viruses and cancers often subvert its activation. Here we aimed to identify a potential evasion of the NKG2D system in H. pylori infection. We analyzed expression of NKG2D system genes in gastric tissues of H. pylori gastritis and gastric cancer patients, and performed cell-culture based infection experiments using H. pylori isogenic mutants and epithelial and NK cell lines. In biopsies of H. pylori gastritis patients, NKG2D receptor expression was reduced while NKG2D ligands accumulated in the lamina propria, suggesting NKG2D evasion. In vitro, H. pylori induced the transcription and proteolytic shedding of NKG2D ligands in stomach epithelial cells, and these effects were associated with specific H. pylori virulence factors. The H. pylori-driven release of soluble NKG2D ligands reduced the immunogenic visibility of infected cells and attenuated the cytotoxic activity of effector immune cells, specifically the anti-tumor activity of NK cells. H. pylori manipulates the NKG2D system. This so far unrecognized strategy of immune evasion by H. pylori could potentially facilitate chronic bacterial persistence and might also promote stomach cancer development by allowing transformed cells to escape immune recognition and grow unimpeded to overt malignancy.

Immuno-histological Role of CD133 in Pathogenesis of Gastric Cancer

The spread of cancer is one of the biggest obstacles at the present time, which has caused panic to people on the health and psychological level, adding to the economic burdens and human losses at the level of most countries of the world. For this reason, most medical institutions and researchers have shown great interest in this field to find the appropriate way out by finding sincere treatments for this problem.The current study includes a review of the immuno-histological role of the CD133 indicator in the development and severity of stomach cancer in order to be a key for applied studies to employ this indicator in the diagnosis or treatment of gastric cancer.

Genetic susceptibility to Helicobacter pylori and the progression of gastrointestinal cancer

The Helicobacter pylori bacteria are spiral-shaped and grow in the stomach's mucus. During its life cycle, H. pylori produces an enzyme called urease that converts urea into ammonia. This enzyme allows the organism to survive a severe, acidic environment by converting urea into ammonia. Molecular genetic studies have identified polymorphisms functional as biomarkers of hereditary predisposition to stomach cancer. Several genes involved in inflammation have been linked to stomach cancer development. Recently, these genes' potential pathogenic and carcinogenic effects have been investigated (APC, CDH1, IL-1, BAX, NOS2, KRAS and MSH2). All these genes' processes have been researched to understand better their potential as biomarkers of gastric carcinogenesis. An in-depth analysis will be required to determine the genetic characteristics of stomach cancer related to H. pylori. It is imperative to research a variety of ethnicities to further use this influence as a critical and fundamental risk factor for stomach illness.

Remodeling of the gastric environment in Helicobacter pylori-induced atrophic gastritis.

Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry. We detected striking differences in the protein content of corpus and antrum tissues. Four hundred ninety-two proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared with infected corpus tissues exhibiting non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. The corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.IMPORTANCEA normal stomach is organized into distinct regions known as the corpus and antrum, which have different functions, cell types, and gland architectures. Previous studies have primarily used histologic methods to differentiate these regions and detect H. pylori-induced alterations leading to stomach cancer. In this study, we investigated H. pylori-induced gastric molecular alterations in a Mongolian gerbil model of carcinogenesis. We report the detection of numerous proteins that are preferentially localized to the gastric corpus but not the antrum in a normal stomach. We show that stomachs with H. pylori-induced atrophic gastritis (a precancerous condition characterized by the loss of specialized cell types) exhibit marked changes in the abundance and localization of proteins normally localized to the gastric corpus. These results provide new insights into H. pylori-induced gastric molecular alterations that are associated with the development of stomach cancer.

Goblet cells segmentation from confocal laser endomicroscopy with an improved U-Net

Gastric intestinal metaplasia (GIM) is regarded as a remarkable precursor for the development of intestinal-type stomach cancer. Goblet cell (GC) segmentation is the crucial step for assessing the degree of GIM by confocal laser endomicroscopy (CLE). However, GC segmentation by hand is difficult, unreliable, and time-consuming. Meanwhile, due to the high resolution and noise interference of CLE images, existing segmentation approaches perform poorly on this task. To tackle those issues, we collected 343 confocal laser endomicroscopy images of 62 patients from a Grade-A tertiary hospital. Each CLE image is manually annotated and then verified three times by skilled medical specialists. Then, U-Net is improved by incorporating the pixel gradient attention mechanism, which focuses on color gradient information around GC and captures color gradient features to direct feature maps in the skip connection layer. At last, the model output vector is used to calculate the possibility map and generate the final segmentation area. Compared with mainstream models, our proposed GC segmentation method from CLE with an improved U-Net (GCSCLE) performs the better segmentation result when tested on our CLE dataset and achieved an IOU of 87.95% and a DICE of 86.64%. Our result shows, the performance of the GCSCLE can be compared with the manual CLE image processing in clinical settings, and it can improve segmentation accuracy and save time and costs.

Nutrition and Helicobacter pylori infection in gastric disease

H. pylori is a highly prevalent bacterial infection among humans. It is considered the major etiological factor in the development of chronic gastritis, peptic ulcers, and stomach cancer. Nutritional therapy is important for the prevention of gastritis, as well as for reducing stomach irritation (irritation) in the treatment of gastritis, and it plays an important role by helping to eradicate or strengthen the stomach wall. Chronic gastritis should be diagnosed before it progresses and causes fatal diseases such as peptic ulcer or cancer, and it should be treated with both a healthy diet and appropriate medications.

Evolution of precancerous changes in the gastric mucosa. A case report

To present the experience of long-term observation of a patient with atrophic and dysplastic measurements of the gastric mucosa, to try to analyze the correctness of treatment, dynamic observation.&#x0D; The analysis included the period from 2008 to 2022. 19 esophagogastroduodenoscopies were performed. A histological study was conducted according to the Operative Link for Gastritis Assessment. Neoplastic changes were evaluated according to the World Health Organization classification of gastrointestinal tumors of 2019. The evolution of changes was observed under conditions of limited possibility of eradication of Helicobacter pylori due to intolerance to antibacterial drugs.&#x0D; During 14 years of follow-up, the endoscopic picture did not demonstrate significant changes. In each study, atrophy of the gastric mucosa was noted; in most cases no intestinal metaplasia and hyperplasia, erosion, ulcers, and neoplasms of the examined segments were detected. According to the histology, atrophy, intestinal metaplasia and hyperplastic changes in the gastric mucosa, Helicobacter pylori were constantly present from 2008 to 2013. Unsuccessful attempts of eradication were made. In 2013 low-grade intraepithelial neoplasia was detected, and in 2014 local high-grade intraepithelial neoplasia. Due to the small-scale nature of the changes, the observation tactics were continued. In 2015, against the background of persistent intraepithelial neoplasia of an indeterminate nature, an attempt was made to eradicate Helicobacter pylori. In 2016, a regression of neoplastic changes to low-grade intraepithelial neoplasia was recorded. From 2016 to 2022, there was a stabilization of inflammatory and atrophic changes. Intraepiteal neoplasia of the gastric mucosa and Helicobacter pylori did not recur.&#x0D; The observation is notable for the fact that for 7 years it was impossible to carry out Helicobacter pylori eradication therapy. There was no negative dynamics for 5 years. In the period from 2013 to 2015, high-grade intraepithelial neoplasia of gastric mucosa was formed. The situation changed with the introduction of antibacterial therapy, after which neoplastic changes regressed and a stable picture was observed over the next 6 years. Despite the observations of various specialists, the availability of objective and reliable information, and the decisions made on its basis allowed to prevent the development of stomach cancer.

HELICOBACTER PYLORI PREVALENCE IN GASTRODUODENAL PERFORATIONS

In India, gastro-duodenal ulcers are among the most prevalent diseases affecting people. Although much research has been done on the etiology of this disorder, especially in our region of the country, no single etiological agent can be blamed for the development of this particular sickness. Because stress is the single most signicant factor in producing peptic ulcers and because modern life is so stressful and demanding, this condition is becoming more common. One of the devastating events that can happen to a person with gastroduodenal ulcers is perforation. The infection with H. pylori has a signicant role in the development of stomach cancer and peptic ulcer disease. Even while the virus may be found in more than 50% of the world's population, only a small percentage of those people would experience ulcer disease or stomach cancer. This investigation aims to determine H. Pylori's contribution to the development of gastroduodenal perforation(1,2).

Helicobacter pylori Infection: Current Status and Future Prospects on Diagnostic, Therapeutic and Control Challenges.

Helicobacter pylori (H. pylori) infection, which affects approximately half of the world's population, remains a serious public health problem. As H. pylori infection leads to a number of gastric pathologies, including inflammation, gastroduodenal ulcers, and malignancies, early detection and treatment are crucial to preventing the spread of the infection. Multiple extragastric complications, such as iron deficiency anaemia, immune thrombocytopenic purpura, vitamin B12 deficiency, diabetes mellitus, cardiovascular diseases, and certain neurological disorders, have also been linked to H. pylori infection. An awareness of H. pylori and associated health hazards is necessary to minimize or even eradicate the infection. Therefore, there is an urgent need to raise the standards for the currently employed diagnostic, eradication, alternative treatment strategies. In addition, a brief overview of traditional and cutting-edge approaches that have proven effective in identifying and managing H. pylori is needed. Based on the test and laboratory equipment available and patient clinical characteristics, the optimal diagnostic approach requires weighing several factors. The pathophysiology and pathogenic mechanisms of H. pylori should also be studied, focusing more on the infection-causing virulence factors of this bacterium. Accordingly, this review aims to demonstrate the various diagnostic, pathophysiological, therapeutic, and eradication tactics available for H. pylori, emphasizing both their advantages and disadvantages. Invasive methods (such as quick urease testing, biopsy, or culture) or noninvasive methods (such as breath tests, stool investigations, or serological tests) can be used. We also present the most recent worldwide recommendations along with scientific evidence for treating H. pylori. In addition to the current antibiotic regimens, alternative therapies may also be considered. It is imperative to eradicate the infections caused by H. pylori as soon as possible to prevent problems and the development of stomach cancer. In conclusion, significant advances have been made in identifying and treating H. pylori. To improve eradication rates, peptide mass fingerprinting can be used as a diagnostic tool, and vaccines can also eliminate the infection.

Mechanisms of microbial interactions between probiotic microorganisms and Helicobacter pylori

Infection caused by Helicobacter pylori is currently one of the most common infection in the world, but the clinical picture can vary from asymptomatic manifestations to the development of stomach cancer. In order to eradicate the pathogen various regimens of antibacterial therapy have been proposed, but recent studies indicate a decrease in efficiency of this therapy due to the increasing rate of H. pylori resistance to antibiotics, the appearance of side effects, including the development of dysbiosis. One of the perspective directions of an alternative approach to the treatment of helicobacteriosis is probiotic therapy. The usage of probiotic therapy of H. pylori infection has two main directions. The first one is associated with the usage of probiotics to reduce the frequency of undesirable effects from the gastrointestinal tract during H. pylori antimicrobial therapy and the second one is the potentiation of the eradication effect due to the antagonistic effect on H. pylori. The purpose of this review was to summarize the latest data about the mechanisms of microbial interactions between probiotic microorganisms and H. pylori. The review examines the influence of H. pylori on the gastrointestinal microbiota, interspecific interactions of microorganisms in microbial consortia, mechanisms of antagonistic action of probiotic cultures on H. pylori, as well as the analysis of experience of using probiotics in the treatment of helicobacteriosis. At the same time, there will be many unresolved questions about the choice of the specific composition of the probiotic cocktail, dosage, duration of therapy, mechanisms of antimicrobial action of probiotics, as well as possible negative sides of this therapy, which requires further research.

Genetically predicted testosterone and cancers risk in men: a two-sample Mendelian randomization study.

In observational studies, testosterone has been reported to be associated with some types of cancers. However, the direction and magnitude of the causal association between testosterone and different types of cancer remain unclear. This Mendelian randomization study assessed the causal associations of total testosterone (TT) and bioavailable testosterone (BT) with cancer risk in men. We performed two-sample Mendelian randomization using publicly available GWAS summary statistics to investigate the genetically causal association between testosterone and the risk of 22 kinds of cancers in men. Causal estimates were calculated by the inverse variance weighted method. We also performed additional sensitivity tests to evaluate the validity of the casualty. Genetically predicted BT level were significantly associated with an increased risk of prostate cancer [odds ratio (OR) = 1.17 95% confidence interval (CI): 1.09-1.26, P = 2.51E-05] in the MR analysis with the IVW method. TT was found to be the suggestive protective factor against stomach cancer (OR = 0.66, 95% CI: 0.48-0.93, P = 0.0116) as well as pancreatic cancer (OR = 0.59, 95% CI: 0.36-0.96, P = 0.0346). A suggestive association was found between TT and the occurrence of small intestine cancer (OR = 1.0004, 95% CI: 1.0001-1.0007, P = 0.0116). However, testosterone had no significant association with other cancers. This study investigated the role of testosterone in the development of prostate cancer, stomach cancer, pancreatic cancer, and small intestine cancer but found no strong association with the other cancers in men.

Trace element levels in serum and gastric mucosa in patients with Helicobacter pylori positive and negative gastritis

BackgroundMost trace elements are inhibited by Helicobacter pylori-infection, and variations in specific element levels are linked to the development of stomach cancer. This is the first study to show the relationship between serum and tissue concentrations of twenty-five trace elements and H. pylori infection status. This study purposed to define serum and tissue trace element levels of 25 healthy individuals with Helicobacter pylori-positive gastritis and Helicobacter pylori-negative gastritis and to reveal their relationship with the disease. MethodsStudy groups consisted of sixty-two patients with Helicobacter pylori-positive, thirty-seven patients with Helicobacter pylori-negative, and thirty healthy individuals. Serum and tissue concentrations of twenty-five elements (aluminum, boron, arsenic, barium, calcium, beryllium, copper, cadmium, iron, chromium, mercury, lithium, potassium, magnesium, sodium, manganese, nickel, phosphorus, lead, scandium, strontium, selenium, tellurium, titanium, zinc) were defined by inductively coupled plasma optical emission spectrometry. ResultsExcept for copper, lithium, and strontium elements in serum samples, other trace elements differed significantly between the groups (p < 0.05). The serum chromium (p = 0.002), mercury (p = 0.001), boron (p < 0.001), and cadmium (p < 0.001) levels of H. pylori-negative gastritis and H. pylori-positive gastritis participants were significantly different, and their serum concentrations were less than 0.5 µ/l. Boron, barium, beryllium, chromium, lithium, phosphorus and strontium elements in tissue samples did not differ significantly between the groups (p > 0.05). Manganese, nickel, tellurium and titanium elements were not detected in tissue and serum samples. The mean concentrations of calcium, beryllium, chromium, iron, potassium, lithium, magnesium, scandium, and selenium were higher in the tissues of patients with H. pylori gastritis compared to healthy control tissues. Also, cadmium could not be detected in tissue samples. There was a significant difference between H. pylori-infected tissue and serum chromium levels (p = 0.001), with lower levels detected in tissue samples. ConclusionThis is the first study that we are knowledgeable of that reports the concentrations of twenty five elements in both serum and tissue samples, as well as the relationship between trace elements and Helicobacter pylori-infection status. Dietary adjustment is indicated as an adjunct to medical therapy to stabilize trace elements because Helicobacter pylori bacteria cause inflammation and impair element absorption in gastritis patients. We also think that this study will shed light on studies on the relationship between Helicobacter pylori-trace elements and serum-tissue/healthy serum-tissue trace element levels of patients with Helicobacter pylori gastritis.

Risk factors modification as a preventive strategy in mortality reduction caused by digestive organs malignant neoplasms

Purpose of this study is to research contribution of chronic non-communicable diseases (CNCDs) risk factors (RF) to the prevalence rate of digestive organs diseases and risks of digestive system malignant neoplasms development in the context of Omsk region municipal districts. Material and methods: the analysis includes following risk factors (RF): unhealthy diets, overweight, harmful use of alcohol, physical inactivity with proved causal relationship with of digestive organs diseases such as stomach and duodenal ulcer, gastritis and duodenitis, liver fibrosis and liver cirrhosis, and with digestive organs malignant neoplasms (MNP): esophageal cancer, stomach cancer, colon cancer, rectal cancer, liver cancer and intrahepatic bile ducts cancer. This research used Russian Federation Federal State Statistics Service statistic material. Statistic material processing was conducted using traditional correlation analysis and the estimation of reliability of data differences method. Correlation analysis was carried out using online-calculator of statistics on the www.medstatistic.ru website. Results: the group of region municipal districts with the most unfavorable population mortality rates for malignant neoplasms has “unhealthy diets” RF associated with high risk of stomach cancer development, “overweight” RF associated with high risk of colorectal cancer and liver cancer development, “harmful use of alcohol” RF associated with high risk of stomach cancer and pancreatic cancer development, “physical inactivity” RF associated with high risk of stomach cancer development. Conclusion: the analysis made it possible to determine priorities in primary prevention of oncological diseases strategy in Omsk region municipal districts and to form key MNP development risk groups among region population to be targeted by preventive measures.

Epidemiological review on Gastric cancer

The mortality rate of the patients with gastric cancer is reduced dramatically from past few years. Still the gastric cancer the major concern that is in front of health care professionals and is the second leading cause of cancer death across the world. But the trend of infection and the severity of infection differ as per location and histology. While there has been a marked decline in distal, intestinal type gastric cancers, the incidence of proximal, diffuse gastric carcinoma has been increasing, particularly in the Western countries. The severities of gastric cancer infection also differ by change in geographical location, social and economic status of the respective race as well. The main risk factors for distal gastric cancer include Helicobacter pylori infection and dietary factors; whereas gastro esophageal reflux disease and obesity play important roles in the development of proximal stomach cancer. The main aim of this review is to determine the epidemiology of gastric cancer and to discuss about available strategies for its prevention.

Risk factors for early gastric cancer: focus on Helicobacter pylori gastritis

Background: Gastric cancer is a global health problem, and the incidence and geographical distribution of different types of gastric cancer varies. Particularly, noncardiac gastric cancer is more prevalent in East Asia, Central and Eastern Europe, Latin America, and Africa. Infection with Helicobacter pylori, which was discovered in 1982, is a common cause of chronic gastritis, and the association between H. pylori infection and gastric adenocarcinoma is well established.Current Concepts: Gastric cancer is histologically divided into 2 types: intestinal and diffuse. H. pylori infection is considered as the main risk factor for the development of both types of gastric tumors. The most documented course of development of stomach cancer is following cellular metaplasia due to chronic inflammation, damage, and repair. Various molecular alterations caused by H. pylori are identified not only in gastric cancer but also in precancerous lesions. Recently, many studies have attempted to diagnose H. pylori gastritis and precancerous lesions using endoscopy.Discussion and Conclusion: Recent studies have shown that eradication therapy stabilizes or reduces the risk of developing gastric cancer. Therefore, the diagnosis and understanding of gastritis and precancerous lesions caused by H. pylori are the first step in the prevention of gastric cancer.

Probiotics mitigate Helicobacter pylori-induced gastric inflammation and premalignant lesions in INS-GAS mice with the modulation of gastrointestinal microbiota.

Dysbiosis of gastric microbiota including Helicobacter pylori (H. pylori) infection is associated with the development of stomach cancer. Probiotics have been shown to attenuate H. pylori-induced gastritis, although their role in cancer prevention remains unclear. Thus, we aimed to explore the effects of probiotics on H. pylori-induced carcinogenesis and the alterations of gastrointestinal microbiota. Male INS-GAS mice were randomly allocated to H. pylori-infected and non-infected groups. After 4 weeks, probiotic combination (containing Lactobacillus salivarius and Lactobacillus rhamnosus) was administered in drinking water for 12 weeks. Stomachs were collected for RNA-Sequencing and the differentially expressed genes were validated using RT profiler PCR array. 16S rRNA gene sequencing was performed to assess the alterations of gastrointestinal microbiota. Probiotics significantly alleviate H. pylori-induced gastric pathology, including reduced infiltration of inflammation and lower incidence of precancerous lesions. RNA-Sequencing results showed that probiotics treatment decreased expressions of genes involved in pro-inflammatory pathways, such as NF-κB, IL-17, and TNF signaling pathway. Of note, probiotics did not suppress the growth of H. pylori, but dramatically reshaped the structure of both gastric and gut microbiota. The microbial diversity was increased in H. pylori-infected group after probiotics treatment. While gastric cancer-associated genera Lactobacillus and Staphylococcus were enriched in the stomach of H. pylori-infected group, the beneficial short-chain fatty acids-producing bacteria, including Bacteroides, Alloprevotella, and Oscellibacter, were more abundant in mice treated with probiotics. Additionally, probiotics restored the H. pylori-induced reduction of anti-inflammatory bacterium Faecalibaculum in the gut. Probiotics therapy can protect against H. pylori-associated carcinogenesis probably through remodeling gastrointestinal microbiota, which in turn prevent host cells from malignant transformation.

Waterpipe Tobacco Smoking and Risk of Stomach Cancer: A Case-Control Study in Vietnamese Men

Objective:This study investigated the impacts of waterpipe tobacco (WTP) and cigarette smoking on stomach cancer development in Vietnamese men. Methods: A total of 80 stomach cancer cases and 146 controls were recruited in a hospital-based case-control study. Data on sociodemographic, anthropometric characteristics, tobacco smoking, and the dietary pattern was obtained based on a semi-quantitative food frequency and demographic lifestyle questionnaire; and venous anti-Helicobacter pylori IgG antibodies were tested by ELISA. Unconditional logistic regression analysis with adjustments for potential confounding was performed to estimate the association between target exposures and stomach cancer. Results:Compared to the never tobacco smokers, the risk of stomach cancer significantly increased among tobacco smokers (OR 2.95, 95%CI 1.26-6.90, p=0.013). Those who early started tobacco smoking before 26 years old had a high risk of SC (OR 3.04, 95%CI 1.29-7.20, p for trend=0.011). For types of tobacco, It was increased risk in exclusively cigarette smokers (OR 2.85, 95%CI 1.19-6.85, p=0.019) and in WPT smokers (OR 3.09, 95%CI 1.24-7.68, p=0.015). The daily frequency and longer duration of exclusively WPT or cigarette smoking tended to be significantly higher SC risk. Conclusions:The findings suggest that tobacco smoking, particularly water pipe tobacco smoking, dramatically and independently increased the risk of stomach cancer.

Interaction of Helicobacter pylori Infection with Waterpipe Tobacco Smoking in the Development of Stomach Cancer in Vietnamese Men.

This study aims to examine the joint effect of H. pylori infection and tobacco smoking on the development of stomach cancer among Vietnamese men. A total of 80 stomach cancer cases and 146 controls were recruited in a case-control study conducted in a general hospital. Information on sociodemographic, anthropometric characteristics, tobacco smoking, and the dietary pattern was obtained based on a semi-quantitative food frequency and demographic lifestyle questionnaire; and venous anti-H. pylori IgG antibodies were tested by ELISA. Unconditional logistic regression analysis with adjustment for potential confounding was performed to estimate the association between target exposures and stomach cancer. An increase in antibody level was related to an elevated odds of stomach cancer (Fifth versus bottom quintile, OR=3.07; 95%CI: 1.16, 8.12; p for trend = 0.032). Compared to participants who were negative with both H. pylori infection and tobacco smoking (either cigarette or waterpipe tobacco), individuals exposed to both these factors showed significantly greater odds of stomach cancer (OR=3.58. (95%CI: 1.32, 9.76, p=0.013). A similar combined impact of H. pylori infection and tobacco smoking was found in individuals who smoked a cigarette (excluded exclusive waterpipe tobacco smokers, ORs = 3.17; 95%CI: 1.13, 8.94, p=0.029) or waterpipe tobacco (excluded exclusive cigarette smokers; OR= 3.96, 95%CI: 1.28, 12.26, p=0.017). The present study suggests an interaction between H. pylori infection and tobacco smoking, even waterpipe tobacco, to induce stomach cancer.