Helicobacter Pylori Infection and Gastric Cancer

Goldstone, Antony R; Quirke, Philip; Dixon, M. F.

doi:10.1002/(sici)1096-9896(199606)179:2<129::aid-path504>3.0.co;2-c

Cited by 59 publications

(21 citation statements)

References 85 publications

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“…1995). Chronic gastritis due to H. pylor also precedes IM and cancer (Sipponen et al 1992: Goldstone et al 1996. and accumulating evidence has shown that geographic variation in diet may influence the development of the intestinalized gastritis associated w%ith GC (Stemmermann et al 1990 (Antonioli.…”

Section: Materials and Methods Patients And Tissuesmentioning

confidence: 99%

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

Shun²,

Lee³

et al. 1998

Br J Cancer

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(Correa. 1992). In sequential changes from superficial gastritis to dysplasia and cancer. intestinal metaplasia (TM) plays a pivotal role. This is testified by a high frequency of IM in patients with GC and in their relatives. a similar topographic distribution of IM and GC. and a high IM occurrence in endemic areas with a high risk of GC (Dobrilla et al. 1994). Although most investigators agree with Stemmermann ( 1994) that the risk of GC is proportional to the extent of IM and although IM has been intensively explored as a possible premalignant lesion of GC. controversy exists because of many confounding factors in previous retrospective studies (Antonioli. 1994). Because of the heterogeneous nature of IM. a recent interest has been focused on the interrelationship between GC and different subtypes of IM (Jass et al. 1979: Turani et al. 1986: Filipe et al. 1994 patients were finally included in this study. Tumorous. adjacent and non-tumorous portions were resected from surgical specimens and stored for further examination. Controls matched one-to-one with cases on age (within 3 years). sex. ethnic group and residential area were also selected from subjects receiving endoscopic examinations that did not reveal any ulcer nor tumour in the stomach. During this procedure. five specimens were biopsied including two from the lesser curvature of the antrum. one from the incisura angularis and two from the lesser curvature of the corpus of the stomach. An aliquot of 5 ml of heparinized blood wvas collected from each study subject. and the serum was separated on the same day and stored at -70°C until further testing. The titre of serum IgG antibody against H. pylorn was determined using an enzyme-linked immunosorbent assay as previously described (Lin et al. 1993).Histopathological determination of intestinal metaplasia and its subtypes Specimens from patients and controls were fixed in 10% buffered formalin. embedded in paraffin. sectioned and stained with haematoxylin and eosin (H&E). If IM was present in H&E staining, a fther section was stained using the high iron diamine (HID)alcian Table 2. There were 57 patients with diffuse type GC and 78 with intestinal type GC. According to the depth of invasion. the frequency of early lesion in diffuse type GC (42 .1%) was higher than that of intestinal type GC (29.5%7. P = 0.18).Intestinal type GC had a significantly higher frequency of coexistent IM (91.0%) than diffuse type (33.3%. P = 0.0001).As shown in Table 3

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Section: Materials and Methods Patients And Tissuesmentioning

confidence: 99%

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

Shun²,

Lee³

et al. 1998

Br J Cancer

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“…H. pylori infection is related not only to gastric ulcers but also, probably, to gastric cancer (Goldstone et al 1996). There can be little doubt that, in the gastrointestinal tract, mucous secretions play an important role in restricting the movement of bacteria to the surface epithelium.…”

Section: Localization Of Fucosylated Oligosaccharidesmentioning

confidence: 99%

Lectin-Gold Localization of Fucose Residues in Human Gastric Mucosa

Madrid

Leis

Díaz‐Flores

et al. 1998

J Histochem Cytochem.

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SUMMARYThe oligosaccharides of the mucous gastric glycoproteins are involved in the protection of the gastric mucosa and are altered in different diseases. Therefore, it is important to know their composition in health, to better determine the alterations induced by the disease. Moreover, analysis of the molecular composition of the fundic gland cells has been previously used to obtain new insights into the origin of the different cell types. The aim of the present study was the localization in the subcellular structures of the fucose residues of the oligosaccharides in human fundic glands. For this, lectin cytochemical methods were used at the light and electron microscopic levels. They were combined with enzymatic and chemical treatments to characterize the nature of the oligosaccharide chains containing the fucose residues. The presence of this carbohydrate belonging to N-or O-linked oligosaccharides has been demonstrated in the secretory granules of the surface, gastric pit, mucous neck, and transitional cells of the fundic mucosa, and in the intracellular canaliculi and tubulovesicular system of the parietal cells. These fucose residues were added in the trans-Golgi regions to the elongating chains. The term "mucosal defense" refers to the factors that permit the gastric mucosa to withstand frequent exposure to substances with a wide range of properties including, e.g., pH, osmolarity, and detergent properties. The first level of defense consists of the factors secreted into the lumen, including acid, bicarbonate, mucus, immunoglobulins, and other antibacterial substances (Wallace and Granger 1996). Mucous secretions form a barrier that traps bicarbonate secreted by the epithelium and stops acid retrodiffusion from the gastric lumen. Moreover, bacteria become trapped in the mucus and are eventually excreted in the feces (Wallace and Granger 1996).

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“…The human gastric pathogen Helicobacter pylori causes type B chronic gastritis and is associated with peptic ulcer disease as well as gastric cancer (7,9,38). Some epidemiological studies have shown the difference between the prevalence of H. pyloriassociated diseases and intake of certain vitamins and antioxidants in various populations (10,28,33) and that a high intake of vitamin C, ␣-tocopherol, or ␤-carotene in food reduces the risk of gastric carcinoma (2,30).…”

mentioning

confidence: 99%

Astaxanthin-Rich Algal Meal and Vitamin C Inhibit Helicobacter pylori Infection in BALB/cA Mice

Wang

Wïllén

Wadström

2000

Antimicrob Agents Chemother

138

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Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma. A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies. The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model. Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95. At 2 weeks postinoculation mice were treated orally once daily for 10 days (i) with different doses of algal meal rich in astaxanthin (0.4, 2, and 4 g/kg of body weight, with the astaxanthin content at 10, 50, and 100 mg/kg, respectively), (ii) with a control meal (algal meal without astaxanthin, 4 g/kg), or (iii) with vitamin C (400 mg/kg). Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment. Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment. Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.The human gastric pathogen Helicobacter pylori causes type B chronic gastritis and is associated with peptic ulcer disease as well as gastric cancer (7,9,38). Some epidemiological studies have shown the difference between the prevalence of H. pyloriassociated diseases and intake of certain vitamins and antioxidants in various populations (10,28,33) and that a high intake of vitamin C, ␣-tocopherol, or ␤-carotene in food reduces the risk of gastric carcinoma (2, 30). H. pylori infection in humans is characterized by a marked infiltration of neutrophilic leukocytes of the gastric mucosa, and the generation of reactive oxygen metabolites (ROMs) may play a part in the development of severe chronic type B gastritis (15,26).Astaxanthin is a carotenoid found in many different organisms in nature, but the main dietary sources for humans are found in crustaceans and other seafood, especially salmon. Astaxanthin is a powerful lipid-soluble antioxidant in vitro (8,16,19) and was shown to be most effective in stimulating immune defenses when different carotenoids were compared (12,13,23). Vitamin C is a water-soluble antioxidant required for many biological functions such as the normal synthesis of hormones, neurotransmitters, collagen, and carni...

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Helicobacter Pylori Infection and Gastric Cancer

Cited by 59 publications

References 85 publications

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

Lectin-Gold Localization of Fucose Residues in Human Gastric Mucosa

Astaxanthin-Rich Algal Meal and Vitamin C Inhibit Helicobacter pylori Infection in BALB/cA Mice

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