• Journal of Gastric Cancer
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• v.1 no.2
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• pp.83-91
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• 2001

Purpose: This study was to observe whether the apoptotic function of tumor-infiltrating lymphocytes (TIL) is induced in human gastric epithelial dysplasia and gastric adenocarcinoma according to the role of FasL expression. Materials and Methods: A total of 56 gastric epithelial dysplasia and gastric adenocarcinoma patients were enrolled in this study: 9 cases of gastric epithelial dysplasia, 18 cases of early gastric carcinomas (EGC) and 29 cases of advanced gastric carcinomas (AGC). Immunohistochemical staining was performed for FasL and CD45, and the terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) method was used to detect cell death in tumor-infiltrating lymphocytes. Results: 1) Positive reactions of FasL to neoplastic cells were $88.9\%$ (8/9) in gastric epithelial dysplasia, $83.3\%$ (15/18) in EGC, and $75.9\%$ (22/29) in AGC. 2) Expression of TIL was decreased in the FasL positive region and was increased in the FasL negative region, and significant expression of TIL was observed in the AGC group (P=0.001). 3) Expression of apoptotic TIL was very similar to the FasL expression, and $100\%$ expression was observed in gastric epithelial dysplasia group. 4) Expression of apoptotic TIL was increased in the FasL positive region and decreased in the FasL negative region, and significant apoptotic expression was observed in the gastric epithelial dysplasia and EGC groups (P=0.0420, P=0.0263, respectively). Conclusion: These results suggest that FasL is a prevalent mediator of immune privilege in epithelial dysplasia and cancer of the stomach.

• Journal of Gastric Cancer
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• v.10 no.4
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• pp.175-181
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• 2010

Purpose: There is controversy over the treatment for low grade dysplasia, while resection is recommended for high grade dysplasia. But the concordance of the grade of dysplasia between pre- and post-resection is low because of sampling errors with endoscopic biopsy. We attempted to establish a clearer direction for the treatment of dysplasia by clarifying the discrepancy between the pre- and postresection diagnoses. Materials and Methods: We performed a retrospective review of 126 patients who had undergone resection with the diagnosis of dysplasia on biopsy at Bundang CHA Hospital from 1999 to 2009. Results: Seventy patients were diagnosed with low grade dysplasia and 56 patients were diagnosed with high grade dysplasia. Among the 33 patients who received gastrectomy with lymph node dissec-tion, 30 patients were revealed to have invasive cancers and 4 patients showed lymph node metastasis. Discordance between the diagnoses from biopsy and resection occurred in 55 patients (44%). There was no correlation on the comparative analysis between the size, location or gross type of lesion and the grade of dysplasia. Conclusions: The rate of discordance between the diagnoses of endoscopic biopsy and the post resection pathologic report was as high as 44%. Endoscopic mucosal resection was not sufficient for some patients who were diagnosed with dysplasia on biopsy due to the presence of lymph node metastasis. It is necessary to be prudent when determining the follow-up and treatment based solely on the result of the biopsy.

• Journal of Gastric Cancer
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• v.11 no.3
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• pp.141-145
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• 2011

Although the biological potential of gastric epithelial dysplasia (GED) as a precursor of gastric cancer has never been in doubt, the classification of these lesions has been controversial and fraught with marked variations in approach to diagnosis across the world. The complexity of cyto-architectural features has been considered to be of paramount importance for the diagnosis of carcinoma in Japan, while breach of the basement membrane and invasion into the lamina propria has been considered the sine qua non of malignancy and hence a pre-requisite for the diagnosis of cancer in the West. In Korea, although the incidence of gastric cancer is similar to Japan, the diagnostic approach to GED or cancer seems to lie midway between Western and Japanese criteria. In this review, we will discuss the difference in the diagnosis of GED and cancer between two pathologists working in the comprehensive cancer center located in Japan and Korea, one of the most prevalent areas in the world for gastric cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3549-3554
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• 2013

Background: It is generally accepted that gastric carcinomas are preceded by a sequential multistage process that includes chronic gastritis, gastric atrophy, usually with intestinal metaplasia (IM), and dysplasia. This series of changes in gastric carcinogenesis is often initiated by Helicobacter pylori (H pylori) infection. The aim of the present study was determination of gastric histopathologic changes in IM patients after at least one year in Guilan province, Iran. Materials and Methods: This case-series study was conducted in Guilan Gastrointestinal and Liver Disease Research Center (GLDRC) during 2010 to 2011. Gastric biopsy was performed for all 71 known cases of IM and precanceric lesions including gastric atrophy, IM, dysplasia and H pylori infection were determined after at least one year. Results: Of the total of 71 patients with established IM who were enrolled, 50 had complete-type IM and 21 had incomplete-type IM. Fifty two people had H pylori infection. H pylori eradication was achieved in 39 patients (75%). Secondary pathology findings of patients with IM were complete metaplasia (39.4%), incomplete metaplasia (32.4%), dysplasia (23.9%) and other precanceric lesions (4.2%). Dysplasia (20%vs 33%) occurred in patients who had complete and incomplete IM at baseline respectively (p>0.05). Age, gender, family history of gastric cancer(GC); smoking habits and NSAIDs use were not associated with gastric premalignant lesions in initial and secondary pathologies (p>0.05). The difference became statistically significant between H pylori infection in patients with more than 3 years diagnostic intervals (p<0.05). Statistical difference between eradicators and non-eradicators was not significant. Conclusions: We found that incomplete IM increased the risk of subsequent dysplasia in this study.

• Clinical Endoscopy
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• v.56 no.4
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• pp.470-478
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• 2023

Background/Aims: Metachronous recurrence incidences and risk factors following endoscopic submucosal dissection (ESD) for gastric adenocarcinoma and dysplasias were investigated. Methods: Retrospective review of electronic medical records of patients who underwent gastric ESD at The Catholic University of Korea, Yeouido St. Mary's Hospital. Results: A total of 190 subjects were enrolled for analysis during the study period. The mean age was 64.4 years and the male sex occupied 73.7%. The mean observation period following ESD was 3.45 years. The annual incidence rate of metachronous gastric neoplasms (MGN) was about 3.96%. The annual incidence rate was 5.36% for the low-grade dysplasia group, 6.47% for the high-grade dysplasia group, and 2.74% for the EGC group. MGN was more frequent in the dysplasia group than in the EGC group (p<0.05). For those with MGN development, the mean time interval from ESD to MGN was 4.1 (±1.8) years. By using the Kaplan-Meier model, the estimated mean MGN free survival time was 9.97 years (95% confidence interval, 8.53-11.40) The histological types of MGN were not related to the primary histology types. Conclusions: MGN following ESD developed in 3.96% annually and MGN was more frequent in the dysplasia group. The histological types of MGN did not correlate with those of primary neoplasm.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.19
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• pp.8027-8034
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• 2014

Genetic instability contributes to the development and progression of gastric cancer, one of the leading causes of cancer death worldwide. Microsatellite instability (MSI) has been hypothesized to be involved in carcinogenesis, althgough its mechanisms and exact roles in gastric cancer remain largely unknown. Our aim was to identify associated clinicopathological characteristics and prognostic value of MSI in gastric cancer and precancerous lesions including gastritis, metaplasia, dysplasia, and adenoma. Because mitochondrial DNA has a different genetic system from nuclear DNA, the results of both nuclear MSI and mitochondrial MSI in gastric cancer were reviewed. This review provides evidence that genetic instability of nuclear and mitochondrial DNAs contributes to early stages of gastric carcinogenesis and suggests possible roles in predicting prognosis.

• 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.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.13 no.10
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• pp.4897-4900
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• 2012

Objective: In this study, anticancer effects of mirtazapine on rats were investigated in an adenocarcinoma model induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and compared with those of cisplatin. Materials and Methods: For this purpose, 10 mg/kg doses of mirtazapine were administered orally to one group of rats, while 1 mg/kg doses of cisplatin were administered intraperitoneally to another group. At 1 hour after administration, 200 mg/kg doses of MNNG were given orally to both groups. MNNG administration was repeated once every 10 days through 3 months, after which period, gastric tissue was taken and pathologically evaluated. Results: Mirtazapine prevented adenocarcinoma induction by MNNG in rats to a greater extent than cisplatin. Some of the rats receiving cisplatin demonstrated severe dysplasia in gastric samples and others exhibited mild dysplasia. Rats given mirtazapine were not observed to suffer severe dysplasia, only mild dysplasia being observed. Conclusion: For adenocarcinoma induced by MNNG on rats, mirtazapine was determined more effective than cisplatin. In order to make statement about mechanism of anticancer activity of mirtazapine, wider studies are required.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.1
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• pp.247-250
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• 2012

Objective: To determine whether CDX2 and villin protein expression are associated with intestinal metaplasia (IM) in gastric cardiac mucosa and to explore the relationship with evolution of gastric cardiac adenocarcinoma (GCA). Methods: We studied 143 gastric cardiac biopsy or resection specimens from Henan province China, including 25 cardiac gastritis specimens with IM, 65 dysplasia specimens with IM and 35 gastric cardiac adenocarcinoma specimens and stained them for CDX2 and villin by the immunohistochemical SP method. 15 normal gastric cardiac biopsy specimens were also collected as control. Results: (1) Normal gastric mucosa presented no CDX2 and villin expression. The positive rates of CDX2 protein in cardiac gastritis with IM, dysplasia with IM, and carcinoma tissues were 84.0% (21/25), 66.7% (32/48) and 36.4% (20/55), respectively. While the positive rates of villin protein in cardiac gastritis with IM, dysplasia with IM, and carcinoma tissues were 76.0% (19/25), 70.8% (34/48) and 45.5% (25/55), respectively. There were significant differences among the three groups for both CDX2 and villin (P<0.01). Spearman's rank correlation coefficient(rho) showed a close correlation between the two proteins (r=0.843, P<0.01) and both were positively related with tumor differentiation (both P<0.05), but not associated with age, sex, invasion and metastasis of lymph node (P>0.05). Conclusion: Our results suggest that ectopic expression of CDX2 and villin may be involved in early-stage IM and tumorigenesis in gastric cardia and the expression of villin may be regulated by CDX2.