Systematic review: <i>Helicobacter pylori</i> eradication for the prevention of gastric cancer

Fuccio, Lorenzo; Zagari, Rocco Maurizio; Minardi, Me; Bazzoli, Franco

doi:10.1111/j.1365-2036.2006.03183.x

Cited by 109 publications

(89 citation statements)

References 62 publications

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“…Hwang et al [95] reported that peptic ulcer patients had lower atrophy scores than patients with simple gastritis, whereas Brooks [96] reported that patients with gastric ulcer generally have more severe atrophy than do duodenal ulcer patients, and furthermore, Fuccio et al [11] reported that many patients with gastric ulcer also have atrophic gastritis or intestinal metaplasia. Hussein [1] has shown that gastric ulcer is associated with a high risk, but duodenal ulcer with a low risk, of gastric cancer, and patients with gastric ulcers typically have atrophic gastritis and corpus-predominant gastritis, whereas patients with duodenal ulcers have antral-predominant gastritis, but few atrophic changes.…”

Section: Failure To Notice Lesionsmentioning

confidence: 99%

“…Uemura et al [6] conducted a 5-year follow-up of many Japanese subjects with H. pylori infections and found that all those with duodenal ulcers were also infected with H. pylori; however, none of the patients with duodenal ulcer developed gastric cancer, although 3.4% of the patients with gastric ulcer did, and gastric cancer subsequently appeared in 5% of the patients with H. pylori infections. Fuccio et al [11] indicated that the risk of gastric cancer was higher in patients with gastric ulcer than in those with duodenal ulcer. Therefore, gastric cancer concomitant with duodenal ulcer appears to be very rare.…”

Section: Frequencies Of Duodenal Ulcer and Gastric Cancermentioning

confidence: 99%

“…Fuccio et al [11] appropriately summarized the mechanisms of gastric cancer and duodenal ulcer after H. pylori infection as follows: H. pylori infection is usually established during childhood, so that antral gastritis and duodenal ulcers are common among young patients with a relatively short history of H. pylori infection; they speculated that continuous infection with H. pylori may result in the development of corpus gastritis in patients with antral gastritis associated with duodenal ulcer, so that middle-aged and elderly patients with duodenal ulcer often have gastritis in the corpus, and these conditions may place a patient at high risk of the development of gastric cancer. This explanation is considered to be widely accepted at the present time.…”

Section: Failure To Notice Lesionsmentioning

confidence: 99%

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Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

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Section: Failure To Notice Lesionsmentioning

confidence: 99%

Section: Frequencies Of Duodenal Ulcer and Gastric Cancermentioning

confidence: 99%

Section: Failure To Notice Lesionsmentioning

confidence: 99%

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Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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“…Fuccio, et al investigated this idea. 10 In previous work by them and others, it has been demonstrated that E-cadherin, a tumor suppressor gene, is aberrantly methylated in H. pylori infected gastric specimens as well as in gastric tumor specimens. A decrease in methylation of E-cadherin has been demonstrated after treatment of H. pylori infection, suggesting the possibility that methylation changes induced by infection can be mitigated by treatment directed against the bacteria.…”

Section: Inflammation and Methylation Changesmentioning

confidence: 97%

DNA Methylation: Its Role in Cancer Development and Therapy

Kurkjian¹,

Kummar²,

Murgo³

2008

Current Problems in Cancer

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Inflammation and Methylation ChangesChanges in the genome which result in cancer promotion remain a complex interplay of aberrant methylation in the setting of a multitude of epigenetic changes. The events leading to these disruptions in methylation have been postulated; though remain to be fully elucidated. A causal relationship between inflammation and cancer has long been accepted in multiple tumor types, most prominently colon cancer; an association supported by the evidence that non-steroidal anti-inflammatory medications can potentially stop the development of colon cancer. Investigations in patients with ulcerative colitis who have a predisposition to the development of colon cancer have established a potential link between inflammation and cancer by the demonstration of hypermethylated gene promoters in early dysplastic lesions. 1 The mechanisms responsible for the contribution of inflammation to cancer remain to be fully understood. Mutagenesis resulting from the production of halogenated nucleotide precursors in activated neutrophils and eosinophils with subsequent incorporation into DNA has been demonstrated in vitro. 2,3 The link between inflammation-induced halogenated nucleotides and aberrant methylation stems from the demonstration that methyl-binding proteins cannot distinguish between methylated cytosine residues and chlorinated or brominated cytosine nucleotides. Furthermore, DNMT1 also could not distinguish between 5-methylcytosine and some 5-halocytosine products which could potentially result in mistaken methylation at sites of inflammation. 4 These halogenated cytosine residues were not recognized by DNA repair enzymes suggesting the possibility of accumulation of heritable changes within the genome.Infection with Helicobacter pylori has been implicated in the development of gastric cancer with a relative risk increase of 2.2-to 6 fold when infection is detected. 5-8 The mechanism of cancer development in this setting has been attributed to inflammation leading to cell proliferation resulting in a propensity for gene mutation. Aberrant methylation due to H. pylori infection has been suggested as an additional mechanism bridging the gap between inflammation and cancer. In a series of 154 healthy volunteers and 72 patients with gastric cancer, methylation of 8 regions of 7 CpG islands was assessed. 14 Among the healthy volunteers, the extent of DNA methylation was 5.4-to 303-times higher in the H. pylori positive cases compared to the H. pylori negative cases (p<0.0001) suggesting an increase in methylation levels due to the presence of H. pylori. However, the comparison of methylation levels between healthy volunteers and patients with gastric cancer stratified by H. pylori status

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“…About 50% of the world population is affected with this bacterium. Although eradication of H. pylori has shown a benefi cial effect in experimental studies, metaanalyses have not found a signifi cant benefi t for human beings [4]. Only after endoscopic mucosal resection for early gastric cancer, eradication of H. pylori proved benefi cial to prevent metachronic gastric cancer [5].…”

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confidence: 99%

Improving outcome for scirrhous gastric cancer

Hartgrink

2009

Gastric Cancer

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The curative treatment of gastric cancer has been basically only surgical. Many trials and comparative studies have tried to fi nd out to what extent surgery should be performed. There is a great difference between results from the East and the West. Comparative studies from Japan in the early 1990s showed an improved survival for D2 lymph node dissections over D1 and D0 dissections. In the Dutch gastric cancer and the British MRC gastric cancer randomized trials no signifi cant difference was found between D1 and D2 lymph node dissections [7,8]. It was suggested that the higher morbidity and mortality for D2 dissections probably had offset the possible benefi t in survival. Indeed, a subgroup analysis of patients who did not have a pancreatico-splenectomy showed a signifi cant survival benefi t after a D2 lymph node dissection over a D1.A more recent randomized trial from Taiwan by Wu et al. did show a signifi cant survival benefi t after a D3 lymph node dissection [9]. This result could probably be reached because there was no mortality in either arm; therefore, the theoretical benefi t of an extended lymph node dissection does become evident if mortality can be avoided. However, Sasako et al. found no difference in survival for a D2 dissection and a D2 dissection with para-aortal lymph node dissection in a large randomized trial in Japan [10]. The extent of surgery therefore seems to have reached its limits. The results for gastric cancer surgery remain poor especially for the more advanced stages.To further improve outcome, (neo-)adjuvant treatment with radiotherapy and/or chemotherapy has been tested in many regimens. Radiotherapy alone in an adjuvant setting has a modest favorable impact on locoregional control, but survival benefi t has not been proven. Radiotherapy preceding surgery, however, did show a signifi cant improvement in 3-and 5-year survival in a meta-analysis by Fiorica et al. [11]. Compliance of radiotherapy was 100% and there was no increase in anastomotic leakage or mortality. Despite these results Gastric cancer is still the second most common cause of cancer death in the world. Survival is related to the stage of the disease at diagnosis and to the histological profi le. From Japanese registry data it was shown that about 11% of all gastric cancers are scirrhous [1]. Together with lymphatic invasive forms of gastric cancer, they lead to metastasis even in earlier stages and therefore have poor prognosis. Improvement of survival could be achieved through prevention, early detection, and optimization of treatment.Prevention of gastric cancer seems to be the most logical approach to decrease cancer-related death. The exact cause of gastric cancer, however, is not always known. Epidemiologic studies show that smoking, food preservation, and low consumption of fresh fruit and vegetables are associated with an increased gastric cancer risk [2]. In addition, Helicobacter pylori is a major risk factor for the development of gastric cancer [3]. About 50% of the world population is affected with t...

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Systematic review: Helicobacter pylori eradication for the prevention of gastric cancer

Abstract: SUMMARY BackgroundHelicobacter pylori is recognized as one of the most significant risk factors for gastric cancer, and H. pylori eradication has been proposed as a possible primary chemo-preventive strategy to reduce gastric cancer incidence.

Cited by 109 publications

References 62 publications

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

DNA Methylation: Its Role in Cancer Development and Therapy

Improving outcome for scirrhous gastric cancer

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