scholarly journals The Rationale and Efficacy of Primary and Secondary Prevention in Adenocarcinomas of the Upper Gastrointestinal Tract

2019 ◽  
Vol 37 (5) ◽  
pp. 381-393 ◽  
Author(s):  
Jan Bornschein ◽  
Elizabeth L. Bird-Lieberman ◽  
Peter Malfertheiner
Keyword(s):  
Gastric Cancer ◽  
Risk Factor ◽  
Secondary Prevention ◽  
Dietary Factors ◽  
Oesophageal Adenocarcinoma ◽  
Neoplastic Progression ◽  
Treatment Techniques ◽  
Risk Of Progression ◽  
H Pylori ◽  
Definition Of

While the primary risk factor for oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett’s oesophagus (BO) is gastro-oesophageal reflux, the infection with Helicobacter pylori (H. pylori) is the dominant risk factor for gastric cancer. Reduction of reflux by dietary measures and proton pump inhibitors has some merits in OAC prevention, and the chemopreventive effect of Aspirin and statins is being widely investigated; however, improved outcome in OAC occurs primarily as the result of secondary prevention. Early detection of neoplastic lesions in Barrett’s metaplasia can be achieved by surveillance endoscopies. Novel endoscopic imaging modalities carry similar importance as the endoscopic treatment techniques as without detection of early lesions, therapy cannot be applied. Minimally invasive approaches are currently being investigated to identify patients with BO who are at particular risk of neoplastic progression. While dietary factors also play an important role in the prevention of gastric cancer and chemoprevention seems to be promising, the most beneficial effect has been shown for the eradication of H. pylori infection, which results in at least a one third reduction of gastric cancer risk. This effect can be further improved if the eradication takes place prior to the development of pre-neoplastic gastric conditions such as mucosal atrophy or intestinal metaplasia (IM). The definition of the “point of no return”, after which eradication is less effective, is of high importance, although H. pylori eradication can still be beneficial even at more advance stages of mucosal changes. For this reason, patients with advanced atrophy and IM should undergo endoscopic surveillance in the same way as patients with BO. There is also need for development of non-invasive tests to identify patients at high risk of progression to gastric cancer to improve outcome of these surveillance approaches.

Role of vitamin C in gastric cancer

2018 ◽  
Vol 01 (1) ◽  
Author(s):  
Takalkar U Vidyadhar
Keyword(s):  
Gastric Cancer ◽  
Vitamin C ◽  
Gastric Juice ◽  
Oxidative Dna Damage ◽  
Preventive Measure ◽  
Dietary Factors ◽  
Preventive Strategy ◽  
H Pylori

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.

scholarly journals Long-term use of proton-pump inhibitors and risk of gastric cancer: a review of the current evidence

2019 ◽  
Vol 12 ◽  
pp. 175628481983451 ◽  
Author(s):  
Ka Shing Cheung ◽  
Wai K. Leung
Keyword(s):  
Gastric Cancer ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Randomized Clinical Trials ◽  
Bacterial Overgrowth ◽  
Current Evidence ◽  
Neoplastic Progression ◽  
Increased Risk ◽  
H Pylori

Gastric cancer remains one of the leading cancers in the world with a high mortality, particularly in East Asia. Helicobacter pylori infection accounts for the majority of the noncardia gastric cancers by triggering gastric inflammation and subsequent neoplastic progression. Eradication of H. pylori can reduce, but not totally eliminate, subsequent risk of developing gastric cancer. Proton-pump inhibitors (PPIs) are one of the most widely prescribed medications worldwide. With their profound gastric-acid suppression, there are concerns about a possible carcinogenic role in gastric cancer, due to induced hypergastrinemia, gastric atrophy and bacterial overgrowth in the stomach. While randomized clinical trials to establish causality between long-term PPI use and gastric cancer are lacking, current evidence based on observational studies suggests PPIs are associated with an increased gastric cancer risk. However, opinions on causality remain divergent due to unmeasured and possible residual confounding in various studies. Our recent study has showed that even after H. pylori eradication, long-term PPI use is still associated with an increased risk of gastric cancer by more than twofold. Hence, long-term PPIs should be used judiciously after considering individual’s risk–benefit profile, particularly among those with history of H. pylori infection. Further well-designed prospective studies are warranted to confirm the potential role of PPIs in gastric cancer according to baseline gastric histology and its interaction with other chemopreventive agents like aspirin, statins and metformin.

scholarly journals Role of vitamin C in gastric cancer

2018 ◽  
Author(s):  
Takalkar U Vidyadhar
Keyword(s):  
Gastric Cancer ◽  
Vitamin C ◽  
Gastric Juice ◽  
Oxidative Dna Damage ◽  
Preventive Measure ◽  
Dietary Factors ◽  
Preventive Strategy ◽  
H Pylori

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.

THE ASSOCIATION OF THE COMBINATION OF TP53 GENE CODON 72 POLYMORPHISM AND HELICOBACTER PYLORI INFECTION WITH GASTRIC CANCER

2017 ◽  
pp. 47-52
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Tp53 Gene ◽  
Codon 72 ◽  
Codon 72 Polymorphism ◽  
Pcr Rflp ◽  
Two Factors ◽  
Risk Patients ◽  
H Pylori

Background: The interaction of environment factor and host factor plays the important role in the pathogenesis of gastric cancer (GC). This study aimed to evaluate the association of the combination of TP53 gene codon 72 polymorphism and the H. pylori infection with GC risk. Patients and methods: 112 patients with GC and 136 patients without GC were extracted DNA from specimens of gastric mucosa, then were determined TP53 gene codon 72 polymorphism by PCR-RFLP and diagnosed H. pylori infection by PCR with ureC gene-specific primers. Results: There was no significant association between TP53 gene codon 72 polymorphism and GC risk, as well as between H. pylori infection and GC risk. The combination of two factors (TP53 gene codon 72 polymorphism and H. pylori infection) was found to be associated with GC risk: The combination of Pro/Pro genotype and H. pylori (+) was the GC risk factor, OR = 2.62 (95%CI: 1.20–5.71) as compared to other combinations. In the group of H. pylori-positive patients, Pro/Pro genotype was the GC risk factor, OR = 2.42 (95%CI: 1.05 – 5.59) as compared to (Arg/Arg + Arg/Pro) group, and OR = 3.48 (95%CI: 1.23 – 9.78) as compared to Arg/Arg genotype. Conclusion: The factors of TP53 gene codon 72 polymorphism and H. pylori infection were not associated with GC risk as assessed separately, but they had the interaction associated with GC risk. Key words: TP53 gene codon 72 polymorphism, Helicobacter pylori, gastric cancer

Su1214 - Emergence of Map-Like Redness is a Risk Factor for the Development of Gastric Cancer after H. Pylori Eradication

2018 ◽  
Vol 154 (6) ◽  
pp. S-504-S-505
Author(s):  
Tomoari Kamada ◽  
Ken Haruma ◽  
Noriaki Manabe ◽  
Jiro Hata ◽  
Akiko Shiotani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Risk Factor ◽  
H Pylori ◽  
Development Of Gastric Cancer

scholarly journals Pan-genomic analyses identify key Helicobacter pylori pathogenic loci modified by carcinogenic host microenvironments

Gut ◽  
2017 ◽  
Vol 67 (10) ◽  
pp. 1793-1804 ◽  
Author(s):  
Jennifer M Noto ◽  
Abha Chopra ◽  
John T Loh ◽  
Judith Romero-Gallo ◽  
M Blanca Piazuelo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Genetic Variation ◽  
Prolonged Exposure ◽  
Dietary Factors ◽  
High Salt ◽  
Premalignant Lesions ◽  
H Pylori

ObjectiveHelicobacter pylori is the strongest risk factor for gastric cancer; however, the majority of infected individuals do not develop disease. Pathological outcomes are mediated by complex interactions among bacterial, host and environmental constituents, and two dietary factors linked with gastric cancer risk are iron deficiency and high salt. We hypothesised that prolonged adaptation of H. pylori to in vivo carcinogenic microenvironments results in genetic modification important for disease.DesignWhole genome sequencing of genetically related H. pylori strains that differ in virulence and targeted H. pylori sequencing following prolonged exposure of bacteria to in vitro carcinogenic conditions were performed.ResultsA total of 180 unique single nucleotide polymorphisms (SNPs) were identified among the collective genomes when compared with a reference H. pylori genome. Importantly, common SNPs were identified in isolates harvested from iron-depleted and high salt carcinogenic microenvironments, including an SNP within fur (FurR88H). To investigate the direct role of low iron and/or high salt, H. pylori was continuously cultured in vitro under low iron or high salt conditions to assess fur genetic variation. Exposure to low iron or high salt selected for the FurR88H variant after only 5 days. To extend these results, fur was sequenced in 339 clinical H. pylori strains. Among the isolates examined, 17% (40/232) of strains isolated from patients with premalignant lesions harboured the FurR88H variant, compared with only 6% (6/107) of strains from patients with non-atrophic gastritis alone (p=0.0034).ConclusionThese results indicate that specific genetic variation arises within H. pylori strains during in vivo adaptation to conditions conducive for gastric carcinogenesis.

scholarly journals Chronic gastritis and carcinogenesis issues

2019 ◽  
Vol 45 (4) ◽  
pp. 65-70
Author(s):  
M. M. Karimov ◽  
G. N. Sobirova ◽  
U. K. Abdullayeva
Keyword(s):  
Gastric Cancer ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Precancerous Conditions ◽  
Increased Risk ◽  
Operated Stomach ◽  
Increasing Risk ◽  
H Pylori ◽  
Definition Of

Risk factors contributing to the transformation of chronic atrophic gastritis into gastric cancer are analyzed. Detection and monitoring of patients with precancerous conditions/lesions (precancerous changes), proper screening of H. pylori make early diagnosis of gastric cancer real. Features of precancerous conditions are given in order of increasing risk of developing gastric cancer. Adenomatous polyps of the stomach take the first place. Subsequent precancerous conditions include: cancer of the operated stomach, Menetria disease (hypertrophic gastropathy), B12-deficient anemia, and gastric ulcer. A definition of intestinal metaplasia subtypes is proposed as a risk factor for gastric cancer, dividing into complete and incomplete one, taking into account reduction in the expression of gastric mucins MUC1, MUC5AC and MUC6. Currently, the development of gastric cancer (mainly of the “intestinal type”) is considered as a multistage process involving the sequence of mucosal change, such as chronic inflammation, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. Role of the organism’s genetic susceptibility to H. pylori infection, factors of pathogenicity contributing to epithelial metaplasia, are analyzed. Role of Toll-like type 4 receptors (TLR4) involved in the recognition of H. pylori is clarified. It is with this type of receptors that the development of an excessive immune response of the host is associated, resulting in damage to the mucous membrane in H. pylori-infected individuals. In particular, carriers of TLR4+896A> G polymorphism have a more severe atrophy of the stomach and degree of inflammation, as well as an increased risk of non-cardiac gastric cancer.

S1643 The Higher Number of EPIYA-C Segments of the H. pylori cagA Protein is a Risk Factor for Gastric Cancer and the Eastern cagA-Multimerization (CM) Sequence is Associated With Tumor Diffuse Type

2010 ◽  
Vol 138 (5) ◽  
pp. S-245
Author(s):  
Dulciene M. Queiroz ◽  
Gifone A. Rocha ◽  
Andreia Maria C. Rocha ◽  
Sérgio A. Batista ◽  
Fabricio F. Melo
Keyword(s):  
Gastric Cancer ◽  
Risk Factor ◽  
Diffuse Type ◽  
Caga Protein ◽  
C Segments ◽  
H Pylori

Stomach Cancer

2018 ◽  
Author(s):  
Weimin Ye ◽  
Olof Nyrén ◽  
Hans-Olov Adami
Keyword(s):  
Risk Factor ◽  
Stomach Cancer ◽  
Fruits And Vegetables ◽  
Human Genetics ◽  
Risk Groups ◽  
Dietary Factors ◽  
Bacterial Genetics ◽  
Modifying Factors ◽  
Primary Prevention Strategy ◽  
H Pylori

The epidemiology of stomach cancer is characterized by its wide variation of incidence by geography and population. Despite a declining secular trend of incidence in most Western populations, it is still one of the most common cancers worldwide. Helicobacter pylori infection is the strongest and most important risk factor known today. Although eradication of H. pylori might be an efficient primary prevention strategy, a deeper understanding of effect-modifying factors, including bacterial genetics, human genetics, and environmental risk factors, may enable us to focus even more precisely on the relevant high-risk groups. Dietary factors, particularly the low intake of antioxidant-rich fruits and vegetables and high intake of salt, are likely to be important. The roles of microbes other than H. pylori in the oral cavity and stomach have recently gained increasing attention. A subtype of stomach cancer, cardia cancer, appears to have a different epidemiology and risk factor profile.

Gastritis staging in the endoscopic follow-up for the secondary prevention of gastric cancer: a 5-year prospective study of 1755 patients

Gut ◽  
2018 ◽  
Vol 68 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Massimo Rugge ◽  
Alberto Meggio ◽  
Cecilia Pravadelli ◽  
Mattia Barbareschi ◽  
Matteo Fassan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Prospective Study ◽  
Stage Iv ◽  
Intraepithelial Neoplasia ◽  
Stage Iii ◽  
Low Grade ◽  
Neoplastic Progression ◽  
Gastric Epithelial Neoplasia ◽  
Neoplastic Lesions ◽  
H Pylori

ObjectiveOperative link on gastritis assessment (OLGA) staging for gastritis ranks the risk for gastric cancer (GC) in progressive stages (0–IV). This prospective study aimed at quantifying the cancer risk associated with each gastritis stage.DesignA cohort of 1755 consecutive patients with dyspepsia underwent initial (T-0) oesophagogastroduodenoscopy with mapped gastric biopsies, OLGA staging and assessment of Helicobacter pylori infection. Patients were followed for 55 months (median); patients with stages II III and IV underwent a second endoscopy/restaging (T-1), and those with stages 0 and I were followed clinically and through in-depth clinical and record checking. Endpoints were OLGA stage at T-1 and development of gastric epithelial neoplasia.ResultsAt T-0, 77.6% of patients had stage 0, 14.4% stage I, 5.1% stage II, 2.1% stage III and 0.85% stage IV. H. pylori infection was detected in 603 patients at T-0 and successfully eradicated in 602 of them; 220 had a documented history of H. pylori eradication; and 932 were H. pylori naïve-negative. Incident neoplastic lesions (prevalence=0.4%; low-grade intraepithelial neoplasia (IEN)=4; high-grade IEN=1; GC=2) developed exclusively in patients with stages III–IV. The risk for epithelial neoplasia was null in patients at stages 0, I and II (95% CI 0 to 0.4), 36.5 per 1000 person-years in patients at stage III (95% CI 13.7 to 97.4) and 63.1 per 1000 person-years in patients at stage IV (95% CI 20.3 to 195.6).ConclusionsThis prospective study confirms that OLGA staging reliably predicts the risk for development of gastric epithelial neoplasia. Although no neoplastic lesions arose in H. pylori-naïve patients, the H. pylori eradication in subjects with advanced stages (III–IV) did not abolish the risk for neoplastic progression.

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