scholarly journals Trefoil Factor Family in Pre-neoplastic Lesions and Gastric Cancer

2018 ◽  
Vol 4 ◽  
Author(s):  
Zahra Behrooznia ◽  
Pouya Ghaderi ◽  
Narges Jafarzadeh ◽  
Azra Izanloo ◽  
Sepideh Mansoori Majoofardi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastrointestinal Tract ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Suppressor Activity ◽  
Neoplastic Lesions ◽  
Tumor Suppressor Activity ◽  
Trefoil Factor Family

Gastric cancer is the fourth most common cancer and the second leading cause of cancer death worldwide. Although the global incidence of gastric cancer has been decreased dramatically in recent decades, north and northwest of Iran have the highest incidence rate of gastric cancer. Whilst the surgical procedures for gastric cancer have been improved, there is no cure for that. The intestinal type of GC results from pre-neoplastic conditions including atrophic gastritis, intestinal metaplasia and dysplasia. Trefoil Factors Family proteins (TFFs) are small and stable molecules secreted by the mammalian gastrointestinal tract. TFFs constitute a family of three peptides (TFF1, TFF2and TFF3) that are widely expressed in a tissue specific manner in the gastrointestinal tract. Variable TFFs expression in gastric cancer and pre-neoplastic lesions has been found. TFF1 has a tumor suppressor activity and inhibits tumorogenesis in gastric cancer. Its expression decreases in gastritis, gastric atrophy, dysplasia, intestinal metaplasia and gastric cancer.TFF2 has a protective effect on gastrointestinal epithelium. As a prognostic factor, TFF2 expression decreases in gastric ulcer, chronic atrophic gastritis and gastric cancer. TFF3 is considered as an oncogenic factor in gastric tissues. Whilst the normal gastric tissues don’t express TFF3, it increases in intestinal metaplasia. Therefore, more studies are necessary to clarify the role of TFFs in GC and pre-neoplastic conditions. This review has focused on elucidating the important role of TFFs in gastric cancer and pre-neoplastic lesions.

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.

NTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION IN PATIENTS WITH CHRONIC GASTRITIS.

2011 ◽  
pp. 63-71
Author(s):  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Significant Relationship ◽  
Precancerous Lesion ◽  
Chronic Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Antral Gastritis

Background: Intestinal metaplasia is a precancerous lesion. Helicobacter pylori is identified as an important cause of gastric cancer. This study is aimed at assessing the intestinal metaplasia and Helicobacter pylori infection and their relation in patients with chronic gastritis. Patients and methods: Study includes 75 patients with chronic gastritis diagnosed by clinical, endoscopic and histopathological criteria. Intestinal metaplasia is diagnosed by HE stain. Hp infection is tested by CLO-test from Viet A Ltd. Results: Hp infecton rate in this study is 66.67% and is highest in patients with antral gastritis. Intestinal metaplasia is found in 29.33% of patients with chronic gastritis with the predominance of complete intestinal metaplasia. The rate of intestinal metaplasia is the highest in the group with chronic atrophic gastritis. There is a significant relationship between intestinal metaplasia and Hp ìnfection. Conclusion: Hp and intestinal metaplasia are found at significant rates in chronic gastritis. The rate of intestinal metaplasia is clearly higher in the group with Hp-positive chronic gastritis.

scholarly journals Pathways of Gastric Carcinogenesis, Helicobacter pylori Virulence and Interactions with Antioxidant Systems, Vitamin C and Phytochemicals

2020 ◽  
Vol 21 (17) ◽  
pp. 6451 ◽  
Author(s):  
James W. T. Toh ◽  
Robert B. Wilson
Keyword(s):  
Gastric Cancer ◽  
Ascorbic Acid ◽  
Helicobacter Pylori ◽  
Vitamin C ◽  
Atrophic Gastritis ◽  
Chronic Atrophic Gastritis ◽  
Gastric Carcinogenesis ◽  
Antioxidant Systems ◽  
H Pylori

Helicobacter pylori is a class one carcinogen which causes chronic atrophic gastritis, gastric intestinal metaplasia, dysplasia and adenocarcinoma. The mechanisms by which H. pylori interacts with other risk and protective factors, particularly vitamin C in gastric carcinogenesis are complex. Gastric carcinogenesis includes metabolic, environmental, epigenetic, genomic, infective, inflammatory and oncogenic pathways. The molecular classification of gastric cancer subtypes has revolutionized the understanding of gastric carcinogenesis. This includes the tumour microenvironment, germline mutations, and the role of Helicobacter pylori bacteria, Epstein Barr virus and epigenetics in somatic mutations. There is evidence that ascorbic acid, phytochemicals and endogenous antioxidant systems can modify the risk of gastric cancer. Gastric juice ascorbate levels depend on dietary intake of ascorbic acid but can also be decreased by H. pylori infection, H. pylori CagA secretion, tobacco smoking, achlorhydria and chronic atrophic gastritis. Ascorbic acid may be protective against gastric cancer by its antioxidant effect in gastric cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosation, reducing toxic effects of ingested nitrosodimethylamines and heterocyclic amines, and preventing H. pylori infection. The effectiveness of such cytoprotection is related to H. pylori strain virulence, particularly CagA expression. The role of vitamin C in epigenetic reprogramming in gastric cancer is still evolving. Other factors in conjunction with vitamin C also play a role in gastric carcinogenesis. Eradication of H. pylori may lead to recovery of vitamin C secretion by gastric epithelium and enable regression of premalignant gastric lesions, thereby interrupting the Correa cascade of gastric carcinogenesis.

scholarly journals Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Anna Alakoski ◽  
Teea T. Salmi ◽  
Kaisa Hervonen ◽  
Hannu Kautiainen ◽  
Maarit Salo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Dermatitis Herpetiformis ◽  
Villous Atrophy ◽  
Chronic Atrophic Gastritis ◽  
Controlled Study ◽  
Gastric Corpus ◽  
H Pylori

Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia.Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, andHelicobacter pylori. Duodenal biopsies were taken.Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp.,P<0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%,P=0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P=0.038) andH. pyloriin 17 (18.3%) and 17 (9.3%) (P=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer.Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum.H. pyloriwill partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.

scholarly journals Dominant Role of Oncogene Dosage and Absence of Tumor Suppressor Activity in Nras-Driven Hematopoietic Transformation

2013 ◽  
Vol 3 (9) ◽  
pp. 993-1001 ◽  
Author(s):  
Jin Xu ◽  
Kevin M. Haigis ◽  
Ari J. Firestone ◽  
Megan E. McNerney ◽  
Qing Li ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Dominant Role ◽  
Suppressor Activity ◽  
Tumor Suppressor Activity
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