Characteristics and predictors of gastric cancer after Helicobacter pylori eradication

Helicobacter pylori(H. pylori) eradication can reduce gastric cancer. However, gastric cancer still develops after eradication, and cases who received eradication therapy are increasing. In this study, we have reviewed the characteristics and predictors of primary gastric cancer developing after H. pylori eradication. In terms of the characteristics, endoscopic, histologic, and molecular characteristics are reported. Endoscopically, gastric cancer after eradication is often depressedtype and shows a gastritis-like appearance, which sometimes makes the diagnosis difficult. Histologically, most gastric cancer after eradication is intestinal type, and non-neoplastic epithelium, also called epithelium with low-grade atypia, is frequently seen over the tumor, which is presumably the cause of the endoscopic gastritis-like appearance. As for molecular characteristics, some markers, such as Ki67, MUC2, and Wnt5a expression, are lower in cancer from patients in whom H. pylori has been eradicated. In terms of predictors, several Japanese studies have reported that severe endoscopic atrophy at eradication is a risk factor for gastric cancer development. Histologic intestinal metaplasia, especially in the corpus, and long-term use of proton pump inhibitors, are also reported as risk factors for gastric cancer after H. pylori eradication. These studies on the characteristics and predictors of gastric cancer development will become the cornerstone for establishing a novel surveillance program based on the gastric cancer risk stratification specific to H. pylori-eradicated patients.     

Prevention of gastric cancer: a challenging but feasible task

Despite its declining incidence gastric cancer still ranks as the second most common malignancy of the digestive tract, accounting for 10% of cancer deaths worldwide. At the time of the diagnosis less than 15% of the patients are in the stage of early cancer, the only stage in which a definite cure of gastric cancer is possible. Therefore the challenges are either early detection or even better prevention of gastric cancer. H. pylori has become recognized as the major risk factor for gastric adenocarcinoma. Epidemiological, biological, histomorphologic, molecular-genetic, epidemiological evidence and more recently few clinical trails have shown that H. pylori eradication has the potential to prevent the development of gastric cancer. Currently H. pylori eradication is an indication for the prevention of gastric cancer in patients and groups of individuals with strongly increased risk, but further investigations are still required before an implementation of a general and global policy to eradicate H. pylori for the prevention of gastric cancer can be instituted. At present time, the main challenge remains to find out at what point mucosal abnormalities are no longer reversible and gastric cancer development cannot be prevented despite H. pylori eradication.     

Will treatment of Helicobacter pylori infection in childhood alter the risk of developing gastric cancer?

Helicobacter pylori has been classified as a group 1 carcinogen for gastric cancer. It is estimated that there is between a two- and sixfold increase in the risk of developing gastric cancer among infected patients. Among different populations, the risk of H. pylori-infected individuals developing gastric cancer varies greatly. However, on a worldwide scale, gastric cancer is the second most common cause of cancer-related death. Therefore, H. pylori eradication could help prevent up to three to four million gastric cancer deaths per year. H. pylori is usually acquired in childhood. Because infected children have not harboured the organism for long enough to have developed precancerous lesions, childhood is theoretically an attractive time for H. pylori eradication and, thus, could help prevent gastric cancer later in life. However, as H. pylori prevalence and the incidence of gastric cancer are falling rapidly in developed nations, widespread population screening programs aimed at the eradication of H. pylori in these countries would be enormously expensive. Therefore, except in groups with a high risk for development of gastric cancer (eg, Japanese or those with a strong positive family history of gastric cancer), a population-based test-and-treat policy is not justified.     

Helicobacter pylori infection and development of gastric cancer in Korea: long-term follow-up

BACKGROUND AND AIM: Infection of Helicobacter pylori is viewed as a major driver of progression to the precancerous state or to gastric cancer. This study was performed to investigate the effect of H. pylori infection on gastric cancer development and to determine to what extent H. pylori eradication is likely to reduce the prevalence of gastric cancer. METHODS: Gastric cancer development was investigated in 1790 Korean subjects who underwent gastroscopy and H. pylori testing between 1992 and 1998. The effects of H. pylori-positive and eradicated states on gastric cancer development were analyzed. RESULTS: Gastric cancer developed in 5 of the study cohort during a mean follow-up period of 9.4 years. All of these patients were positive for H. pylori infection, and 4 of the 5 had antral intestinal metaplasia (IM) at the time of study enrollment. One of these 5 patients was in an eradicated state when the gastric cancer was diagnosed, and had histologic IM before eradication therapy was performed. Gastric cancer was found to develop 10.9 times more frequently in the presence of IM than in its absence. CONCLUSIONS: The present study shows a close relationship between H. pylori infection and IM, and between IM and the development of gastric cancer. In addition, our finding suggests that chronic H. pylori infection looks like an important risk factor for the development of gastric cancer in Korea, where the prevalence of H. pylori remains high. This study indicates that to prevent gastric cancer H. pylori eradication is best performed before the development of IM.     

The effect of Helicobacter pylori eradication on reducing the incidence of gastric cancer

Epidemiologically, the association between chronic Helicobacter pylori infection and development of gastric cancer is well established. Although the possibility of preventing gastric cancer by eradicating H. pylori infection was recently investigated by several research groups, the results remain controversial. The aim of this study was to determine whether the eradication of H. pylori infection would reduce the incidence of gastric cancer. In total, 304 patients with persistent H. pylori infection and 404 patients with H. pylori infection eradicated were examined annually for gastric cancer by endoscopy. Over an average of 3.1 years for the first group and 3.2 years for the second group, 13 and 6 patients, respectively, were diagnosed as having new gastric cancer. The cumulative incidence of gastric cancer was statistically different between the groups (P=0.019; log-rank test). The hazard ratio of H. pylori eradication was 0.335 by Cox proportional hazards model (P=0.047). Differentiated gastric cancer was found in 11 patients in the persistent infection group and 3 patients in the eradicated group. The incidence of differentiated cancer was significantly different (P=0.017) between the groups, but not for undifferentiated cancer (P=0.847). The results of the current study suggest that the eradication of H. pylori infection reduces the incidence of gastric cancer.     

Can gastric cancer be prevented by Helicobacter pylori eradication?

Helicobacter pylori infection always causes chronic gastritis and triggers several gastroduodenal pathologies ranging from peptic ulcer disease to gastric cancer. It is well established that H. pylori eradication decreases the incidence of gastroduodenal ulcer and its recurrence. However, despite being accepted as the critical risk factor for gastric cancer, there is no conclusive evidence that H. pylori eradication decreases the incidence of gastric cancer. Bacterial virulence characteristics, as well as genetic predisposition of the host in conjunction with certain environmental conditions, are the major factors which influence the development of gastric cancer. Preclinical and clinical data suggest that reversibility of precancerous lesions (atrophic gastritis and intestinal metaplasia) is possible in some patients after H. pylori eradication. Since neoplastic lesions do not progress - or even regress in some cases - after H. pylori eradication, eradication therapy should be considered even in patients with precancerous lesions. Nonetheless, progression of atrophic gastritis and intestinal metaplasia into cancer has been also demonstrated in patients after H. pylori eradication, suggesting that there might be a point of no return where genetic changes have already happened and are irreversible despite elimination of the triggering carcinogen (H. pylori). At the present time the clinical decision to treat a patient is based on established risk profiles. A general screen-and-treat policy, although desirable, currently awaits a less complex treatment regimen.     

Kyoto classification in patients who developed multiple gastric carcinomas after Helicobacter pylori eradication

BACKGROUND Endoscopic Kyoto classification predicts gastric cancer risk; however, the score in the patients with primary gastric cancer after Helicobacter pylori(H. pylori) eradication therapy is unknown.AIM To elucidate the Kyoto classification score in patients with both single gastric cancer and multiple gastric cancers developed after H. pylori eradication.METHODS The endoscopist recorded the Kyoto classification at the endoscope and the Kyoto classification score at the time of the first diagnosis of gastric cancer after H. pylori eradication. The score was compared between single gastric cancer group and multiple gastric cancers group.RESULTS The Kyoto score at the time of diagnosis of 45 cases of gastric cancer after H. pylori eradication was 4.0 points in average. The score was 3.8 points in the single gastric cancer group, and 5.1 points in the multiple gastric cancers group. The multiple group had a significantly higher score than the single group(P = 0.016). In the multiple gastric cancers group, all the patients(7/7) had 5 or higher Kyoto score, while in single gastric cancer group, the proportion of patients with a score of 5 or higher was less than half, or 44.7%(17/38).CONCLUSION Patients diagnosed with gastric cancer after H. pylori eradication tended to have advanced gastritis. In particular, in cases of multiple gastric cancers developed after H. pylori eradication, the endoscopic Kyoto classification score tended to be 5 or higher in patients with an open type atrophic gastritis and the intestinal metaplasia extended to the corpus.     

Treatment of Helicobacter pylori and prevention of gastric cancer

Gastric cancer is the second commonest fatal malignancy in the world with a high incidence in China. Helicobacter pylori infection is an important factor in the pathogenesis of gastric cancer. Epidemiological studies have shown a strong causal relationship between H. pylori infection and gastric cancer. Animal studies also show that eradication of H. pylori infection, especially at the early stage, is effective in preventing H. pylori-related gastric carcinogenesis. H. pylori eradication leads to regression and prevents the progression of gastric precancerous lesions, but only in a minority of cases. H. pylori eradication appears to be the most promising approach in gastric cancer prevention. The current available data in human studies showed that H. pylori eradication can reduce the risk of developing gastric cancer and this strategy is more useful in patients without atrophic gastritis or intestinal metaplasia. A longer follow-up and additional studies are needed for better understanding this issue.     

根除幽门螺杆菌在预防胃癌中的作用

胃癌在全球恶性肿瘤致死亡的原因中位居第二位,幽门螺杆菌（H．pylori）感染是胃癌发生的重要病因。动物研究显示根除H.pylori,特别是在早期阶段,能有效预防胃癌的发生。部分病例通过根除npylori可阻止胃癌前病变的发展并可能使其逆转。最新研究表明根除H．pylori可降低胃癌发生的风险,对无萎缩或肠化生者可能尤其有效。本文就根除H．p）tori在预防胃癌中作用的研究进展作一综述。     

The effect of eradicating helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease

OBJECTIVES: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. METHODS: Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women; mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. RESULTS: A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p= 0.04; log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p= 0.005; Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35; 95% confidence interval: 1.00-11.22; p= 0.04; Cox's proportional-hazards model). CONCLUSION: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted.     

Prevention of gastric cancer by Helicobacter pylori eradication

The evidence supporting the important role of Helicobacter pylori causing gastric cancer is getting stronger. The mechanisms by which H. pylori can influence the progression to severe changes in the gastric mucosa are under investigation. An increased gastric epithelial cell proliferation has been observed in individuals infected with H. pylori. This lifelong increased cell turnover is deemed to be a major risk factor for increased mutational changes and may lead to the development of gastric cancer. Successful eradication of H. pylori infection induces the healing of the gastritis and a significant decrease in gastric epithelial cell proliferation. Nevertheless, it is right now unknown at which time the point of no return, meaning at which time an eradication therapy leads to a benefit for the individual to prevent gastric cancer, has been reached. Therefore the major question that arises is to whom an eradication therapy should be offered to prevent gastric cancer. A general elimination of the infection might be worthwhile, but seems to be unrealistic now because of the high prevalence of the infection and the missing of a vaccine. This review reflects possible mechanisms of gastric cancer development induced by chronic H. pylori infection and recent investigational trials for prevention of gastric cancer by H. pylori eradication therapy will be discussed.     

Does Helicobacterpylori eradication therapy for peptic ulcer prevent gastric cancer？

AIM： TO investigate the effects of Helicobacter pylori （H pylori） eradication therapy for treatment of peptic ulcer on the incidence of gastric cancer. METHODS： A multicenter prospective cohort study was conducted between November 2000 and December 2007 in Yamagata Prefecture, Japan. The study included patients with H pylori-positive peptic ulcer who decided themselves whether to receive Hpylori eradication （eradication group） or conventional antacid therapy （non-eradication group）. Incidence of gastric cancer in the two groups was determined based on the results of annual endoscopy and questionnaire surveys, as well as Yamagata Prefectural Cancer Registry data, and was compared between the two groups and by results of Hpylori therapy.RESULTS： A total of 4133 patients aged between 13 and 91 years （mean 52.9 years） were registered, and 56 cases of gastric cancer were identified over a mean follow-up of 5.6 years. The sex- and age-adjusted incidence ratio of gastric cancer in the eradication group, as compared with the non-eradication group, was 0.58 （95% CI： 0.28-1.19） and ratios by follow-up period （〈 1 year, 1-3 years, 〉 3 years） were 1.16 （0.27-5.00）, 0.50 （0.17-1.49）, and 0.34 （0.09-1.28）, respectively. Longer follow-up tended to be associated with better prevention of gastric cancer, although not to a significant extent. No significant difference in incidence of gastric cancer was observed between patients with successful eradication therapy （32/2451 patients, 1.31%） and those with treatment failure （11/639 patients, 1.72%）. Among patients with duodenal ulcer, which is known to be more prevalent in younger individuals, the incidence of gastric cancer was significantly less in those with successful eradication therapy （2/845 patients, 0.24%） than in those with treatment failure （3/216 patients, 1.39%）. CONCLUSION： H pylori eradication therapy for peptic ulcer patients with a mean age of 52.9 years at registration did not significantly decrease the incidence of gastric cancer.     

Faecal calprotectin: factors affecting levels and its potential role as a surrogate marker for risk of development of Crohn’s Disease

Infection with Helicobacter pylori is associated with severe digestive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer. Successful eradication of this common gastric pathogen in individual patients is known to prevent the occurrence of peptic ulcer disease and gastric cancer. With half of the world’s population being infected with H, pylori and only few antibiotics result in an effective eradication, a successful antibiotic driven worldwide eradication program seems unlikely. In addition, H. pylori eradication is not always beneficial as it has been described that eradication can be associated with an increased frequency of other disorders such as pediatric asthma, inflammatory bowel diseases and Barrett’s Esophagus. We have to accept that eradication of this infection is a two-edged sword that is both useful and harmful and we should therefore focus our H. pylori eradication policy toward selectively identify and destroy only the virulent strains. In order to still be able to effectively treat H. pylori infections in the future we need an alternative diagnostic/treatment algorithm. This would involve a shift towards more precise and enhanced disease predicting diagnosis that tries to identify patients with chance of developing severe diseases such as gastric cancer, rather than the current regime that is geared towards find and destroy all H. pylori.     

Causal role of Helicobacter pylori infection in gastric cancer

Gastric cancer is the second most frequent cancer in the world, accounting for a large proportion of all cancer cases in Asia, Latin America, and some countries in Europe. Helicobacter pylori(H pylori) is regarded as playing a specific role in the development of atrophic gastritis, which represents the most recognized pathway in multistep intestinal-type gastric carcinogenesis. Recent studies suggest that a combination of host genetic factors, bacterial virulence factors, and environmental and lifestyle factors determine the severity of gastric damage and the eventual clinical outcome of H pylori infection. The seminal discovery of H pylori as the leading cause of gastric cancer should lead to effective eradication strategies. Prevention of gastric cancer requires better screening strategies to identify candidates for eradication.     

Helicobacter pylori-related diseases: dyspepsia, ulcers and gastric cancer

This article summarizes the main conclusions drawn from the presentations on Helicobacter pylori infection at Digestive Disease Week 2011. In developed countries, the prevalence of H. pylori infection has decreased, but seems to have reached a plateau at a fairly high level. Antibiotic resistance is increasing in several countries. H. pylori eradication does not contribute to the development of gastroesophageal reflux disease or worsen its course. The frequency of idiopathic peptic ulcers seems to be increasing. H. pylori eradication eliminates almost all episodes of peptic ulcer rebleeding; nevertheless, the use of non-steroidal anti-inflammatory drugs or H. pylori reinfection can lead to bleeding recurrence. H. pylori-negative patients with peptic ulcer bleeding more frequently have bleeding recurrences and higher mortality. In each particular population, there is a close correlation between the prevalence of H. pylori infection and the incidence of gastric cancer. H. pylori eradication is associated with a higher and faster healing rate of ulcerous lesions caused by endoscopic submucosal dissection. In patients undergoing endoscopic submucosal dissection for early gastric cancer, H. pylori eradication decreases the incidence of metachronous tumors. In a high proportion of cases, H. pylori eradication induces MALT lymphoma regression, and long-term tumoral recurrences are exceptional. Narrow-band imaging allows visualization of the mucous and vascular pattern in H. pylori-infected patients during the endoscopic examination. The electrochemical properties of H. pylori allow these lesions to be rapidly and accurately detected in gastric biopsies. The efficacy of "traditional" triple therapies currently leaves much to be desired. The superiority of "sequential" therapy over the standard triple therapy should be confirmed in distinct environments. The "concomitant" quadruple therapy seems to be as effective as "sequential" therapy, but with the advantage of being simpler. Both the "sequential" and the "concomitant" regimens are relatively effective even when clarithromycin resistance is present. Second-line rescue therapy with levofloxacin for 10 days is effective and is simpler and better tolerated than quadruple therapy. In patients allergic to penicillin, a combination with levofloxacin and clarithromycin is a promising rescue alternative. The new-generation quinolones, such as moxifloxacin and sitafloxacin, could be useful as eradication treatment. After two eradication treatment failures, an empirical third-line rescue therapy may be a valid option in clinical practice. Even after three previous H. pylori eradication failures, an empirical fourth-line rescue treatment with rifabutin may be effective.     

Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis

OBJECTIVE: Helicobacter pylori and duodenogastric reflux (DGR) are both associated with chronic gastritis, peptic ulcer and gastric cancer. The nature of their interrelationship remains unclear. H. pylori eradication has also been reported to result in new or worsening acid gastro-oesophageal reflux (GOR). The aim of this study was to investigate the relationship between GOR, DGR and H. pylori infection. METHOD: 25 patients with H. pylori gastritis underwent ambulatory 24-hour oesophageal and gastric pHmetry and gastric bilirubin monitoring before and 12 weeks after H. pylori eradication, confirmed by 14C urea breath testing (UBT). Ten healthy subjects served as a control group. RESULTS: There were no differences between patient and control groups for gastric alkaline exposure or gastric bilirubin exposure (P> 0.25 in all categories). Oesophageal acid reflux was higher in the study group (P< 0.02). No differences were detected in oesophageal acid reflux, gastric alkaline exposure, or gastric bilirubin exposure (P = 0.35, 0.18 and 0.11, respectively) before and after eradication. CONCLUSIONS: Acid GOR is not increased by H. pylori eradication. DGR in patients with H. pylori gastritis is similar to that in healthy, non-infected subjects. H. pylori eradication produces no change in GOR or DGR. In patients with chronic gastritis, H. pylori infection and DGR appear to be independent of each other.     

Association of Helicobacter pylori with gastroduodenal diseases

Helicobacter pylori was first cultured in vitro in 1982. This bacterium is a spiral gram-negative rod which grows under microaerophilic conditions. The ecological niche is the mucosa of the human stomach which had been thought to be aseptic before the discovery of this bacterium. This organism causes a long-lasting infection throughout a person's life if there is no medical intervention. Numerous persons are infected with the organism around the world, and the rate of infection in Japan is nearly 50% of the population. However, the route of infection remains unclear because the organism has not been isolated from any environment other than several animals. H. pylori is now recognized as a causative agent of gastritis and peptic ulcers. Though gastritis, and especially chronic active gastritis, is observed at least histologically in all persons with H. pylori, peptic ulcers develop in only some infected persons. Specific factors in the host and/or the bacteria are needed for the development of peptic ulcer disease. Furthermore, H. pylori is considered to be related to the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, especially those of low grade. Also, H. pylori infection is a major determinant for initiating the sequence of events leading to gastric cancer. In some patients with low-grade gastric MALT lymphoma, the eradication of H. pylori led to a regression of lesion. Gastric cancer has been induced in Mongolian gerbils with long-term H. pylori infection. The combinations of drugs, which consist of an antisecretory agent (acid-suppressing agent) and antimicrobial agents, are used for the eradication of the organism. Eradication therapy is recommended at least for patients with peptic ulcers.     

Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer in Japan

This article describes the characteristics of H. pylori infection dynamics in early gastric cancer cases in Japan and the reduced likelihood of metachronous cancer development and growth inhibition by H. pylori eradication based on healing of background gastric mucosa. In the future, these clinical studies and experimental studies in Mongolian gerbils and mice should elucidate the role of H. pylori infection in the development of gastric carcinogenesis to clinical cancer on the genetic level so that gastric cancer prevention by H. pylori eradication is established.     

What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers?

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.     

Endoscopic surveillance of gastric cancers after Helicobacter pylori eradication

The incidence and mortality of gastric cancer remains high in East Asian countries. Current data suggest that Helicobacter pylori(H. pylori) eradication might be more effective for preventing gastric cancer in young people before they develop atrophic gastritis and intestinal metaplasia. However, the long-term effect of H. pylori eradication on metachronous cancer prevention after endoscopic resection(ER) of early gastric cancer remains controversial, with some discordance between results published for Japanese and Korean studies.The detection ability of synchronous lesions before ER and eradication of H. pylori directly influences these results. After eradication, some gastric cancers are more difficult to diagnose by endoscopy because of morphologic changes that lead to a flat or depressed appearance. Narrow-band imaging with magnifying endoscopy(NBI-ME) is expected to be useful for identifying metachronous cancers. However, some gastric cancers after eradication show a "gastritislike"appearance under NBI-ME. The gastritis-like appearance correlates with the histological surface differentiation of the cancer tubules and superficial non-neoplastic epithelium atop or interspersed with the cancer. Till date, it remains unclear whether H.pylori eradication could prevent progression of gastric cancer. Until we can establish more useful endoscopic examination methodologies, regular endoscopic surveillance of high-risk groups is expected to be the most beneficial approach for detection.