• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7635-7638
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• 2014

Background: The aim of this study was to investigate the value of serum gastric markers to differentiate between patients with precancerous lesions and nonatrophic chronic gastritis. Materials and Methods: Serum samples of 128 patients with dyspepsia who were candidates for endoscopic examination were tested for pepsinogen (PG I and PG II), PG I/II ratio, gastrin 17(G-17), anti-Helicobacter pylori (anti-H pylori ) and anti-CagA antibodies. Two sample t-tests, chi-square tests and Pearson's correlation analyses were used for analysis using SPSS (version 20). Results: PGI, PG I/II ratio values were decreased significantly in the precancerous lesion group (0.05, 0.001 respectively). The frequency of H pylori infection was significantly (p=0.03) different between the two groups ofthe study. Conclusions: We suggest PGI and the PG I/II ratio as valuable markers for screening of premalignant gastric lesions.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.4
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• pp.1571-1574
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• 2015

Background: Treatment of Helicobacter pylori (H. pylori) decreases the prevalence of gastric cancer, and may inhibit gastric precancerous lesions progression into gastric cancer. The aim of this study was to determine the effect of treatment on subsequent gastric precancerous lesion development. Materials and Methods: We prospectively studied 27 patients who had low grade dysplasia at the time of enrollment, in addition to dysplasia atrophic gastritis and intestinal metaplasia observed in all patients. All were prescribed quadruple therapy to treat H. Pylori infection for 10 days. Patients underwent endoscopy with biopsy at enrollment and then at follow up two years later. Biopsy samples included five biopsies from the antrum of lesser curvature, antrum of greater curvature, angularis, body of stomach and fundus. Results of these biopsies were compared before and after treatment. Results: Overall, the successful eradication rate after two years was 15/27 (55.6%). After antibiotic therapy, the number of patients with low grade dysplasia decreased significantly (p=0.03), also with reduction of the atrophic lesions (p=0.01), but not metaplasia. Conclusions: Treatment of H. pylori likely is an effective therapy in preventing the development of subsequent gastric premalignant lesions.

• Journal of Gastric Cancer
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• v.9 no.2
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• pp.46-50
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• 2009

During carcinogenesis, precancers (premalignant lesions) are the morphologically identifiable lesions that precede invasive cancers. In theory, the successful treatment of precancers would result in the eradication of most human cancers. Despite the importance of these lesions, there has been no effort to list and classify all of the precancers. In 2001, the NCI sponsored a workshop on the classification of precancers. When considering all the possible classes of precancers, it is worth noting that not all precancers are neoplastic. In fact, precancers need not progress to cancer, and precancerous lesions often have a high rate of regression. Thus, the following five classes were adopted: 1) acquired microscopic precancers; 2) acquired large lesions with microscopic atypia; 3) Precursor lesions occurring with inherited hyperplastic syndromes that progress to cancer; 4) acquired diffuse hyperplasias and diffuse metaplasias; and 5) currently unclassified entities. In this review paper, precancerous lesions of the stomach are classified and their clinical significance is described.

• Journal of Gastric Cancer
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• v.1 no.3
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• pp.129-135
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• 2001

Purpose: Dysplasia or flat adenoma of the stomach is regarded as a precancerous lesion. However, the frequency and the evolutionary process of malignant transformation of gastric dysplasia are still debated. In order to see whether the lesion was a monoclonal or a polyclonal proliferation, clonality was assayed by X-linked HUMARA polymorphism. Materials and Methods: DNA was extracted from the paraffin-embedded tissue of 16 consecutive cases of endoscopic biopsy, eight of which supplied both dysplastic and nondysplastic tissue for comparison. HUMARA was amplified by PCR with or without pretreatment with methylationsensitive restriction enzyme, HpaII. The amplification products were electrophoresed on polyacrylamide gel and silver-stained. Results: Among the 16 cases, 13 cases were informative and 3 cases noninformative. Of the 13 cases, one case showed skewed lyonization, rendering 12 cases to be analyzed further. A monoclonal band pattern was noted in 2 cases, and a polyclonal band pattern in 10 cases. A review of the histopathologies of the monoclonal and the polyclonal cases did not reveal features discriminating the two groups. Conclusion: These results suggest that gastric dysplasia is a disease entity heterogeneous in the genetic level, and many cases may be non-neoplastic.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6983-6987
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• 2014

Background: Modified toluidine blue staining (MTBs) is a simple, inexpensive and time saving method to detect H. pylori in gastric biopsy specimens. As a metachromatic stain, it simultaneously highlights intestinal metaplasia, a gastric cancer precancerous lesion. The aim of this study was to assess the reliability of MTBs compared with hematoxylin-eosin (H&E) for H. pylori detection using immunoperoxidase staining as the gold standard. This technique would be beneficial for a routine diagnosis and confirmation of H. pylori eradication in developing countries where endoscopic-based approaches are dominant. Materials and Methods: Esophagogastroduodenoscopy with triple site gastric biopsies was undertaken in 207 dyspeptic patients at Thammasat University Hospital, Thailand between 1997 and 1999. H&E, MTBs and immunoperoxidase staining were applied to each specimen. The presence or absence of H. pylori with each stain was interpreted separately and the sensitivity, specificity, positive and negative predictive values of H&E and MTBs were calculated. Results: A total of 282 specimens from 207 patients were evaluated. Using immunoperoxidase staining, organisms were positive in 117 specimens (41%). MTBs proved almost equally sensitive as immunoperoxidase (99%) and significantly more sensitive than H&E (85%). It has comparable specificity (96% vs 96%), PPV (95% vs 94%), and NPV (99% vs 90%) to H&E, using immunoperoxidase staining as gold standard. MTBs compared with immunoperoxidase staining, is cheaper (2 USD vs 12 USD) and faster (20 min vs 16 hrs) compared to immunoperoxidase staining. Conclusions: MTBs is effective, economical and easy to use in daily practice for the detection of H. pylori in gastric biopsy specimens. In addition to saving time in evaluating H. pylori associated gastritis, with a high sensitivity and ability to demonstrate intestinal metaplasia, the technique may have a role in confirmation of H. pylori eradication for gastric cancer prevention in a developing country setting.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3931-3936
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• 2013

Background: Iran is a country with very high incidences of stomach cancer, especially in Northern parts. Here we assessed prognostic value of serum screening biomarkers among people >50 years old for early detection of precancerous lesions in a hot spot for gastric carcinoma in Guilan Province, North Iran. Methods: A cross-sectional population-based survey was conducted on 1,390 residents of Lashtenasha city with the mean age (SD) of 61.8 (9.02) years old (50.8% females) to assess the association of gastrin and the pepsinogen (PG) I/II ratio with premalignant gastric lesions. Blood samples were taken for CBC, blood group, and serologic exams (PGI, PGII, and gastrin 17) from each subject. Expert gastroenterologists performed upper GI endoscopy and ROC curves were generated to determine appropriate cutoff points. Results: Mean values of PGI, PGII, PGI/PGII and gastrin were significantly different between patients with and without atrophy or metaplasia (P<0.05). To diagnose atrophy and intestinal metaplasia, a significantly higher AUC was observed for the PGI/PGII ratio (70 and 72%, respectively) compared to the PGI (56, 55%), PGII (63, 64%) and gastrin (59, 61%) (all p<0.001). Conclusions: Biomarker tests such as the PGI/II ratio can be used in the screening and diagnosis of subjects at high gastric cancer risk in our region.

• Journal of Gastric Cancer
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• v.2 no.2
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.