scholarly journals Intestinal metaplasia: A premalignant lesion involved in gastric carcinogenesis

2009 ◽  
Vol 24 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Rita A Busuttil ◽  
Alex Boussioutas
1998 ◽  
Vol 114 ◽  
pp. A676 ◽  
Author(s):  
IA Scotiniotis ◽  
T Rokkas ◽  
EE Furth ◽  
JW Plotkin ◽  
B Rigas ◽  
...  

2016 ◽  
Vol 16 (9) ◽  
pp. 1079-1084
Author(s):  
Ye Han ◽  
Qiaoming Zhi ◽  
Xiaofeng Xue ◽  
Bin Yuan ◽  
Hong Zhao ◽  
...  

2016 ◽  
Vol 51 (10) ◽  
pp. 949-960 ◽  
Author(s):  
Soichiro Sue ◽  
Wataru Shibata ◽  
Eri Kameta ◽  
Takeshi Sato ◽  
Yasuaki Ishii ◽  
...  

2016 ◽  
Vol 34 (4_suppl) ◽  
pp. 28-28
Author(s):  
Ji Hyun Song ◽  
Sang Gyun Kim ◽  
Eun Hyo Jin ◽  
Joo Hyun Lim ◽  
Sun Young Yang

28 Background: Atrophic gastritis and intestinal metaplasia were considered as premalignant lesions. The prevalence of chronic atrophic gastritis is very high in Korea. The aims of this study were to evaluate the risk factors of gastric carcinogenesis in underlying gastric mucosal atrophy. Methods: A total of 10187 subjects underwent upper gastrointestinal endoscopy for health checkup between 2003 and 2004 were enrolled in this retrospective cohort study. Follow-up endoscopy was performed between 2005 and 2014. Atrophic gastritis and intestinal metaplasia were assessed according to the Kimura-Takemoto classification by endoscopy. Helicobacter pylori (Hp) was evaluated by serum IgG antibody. Results: The number of atrophic gastritis was 3716 (36.5%) in baseline endoscopy, and 2146 were undergone follow-up endoscopy (82.8±38.3month); 1139 showed aggravation of atrophy and 1007 showed no change. A total of 71 subjects were diagnosed as gastric neoplasms (34 adenoma, 37 carcinoma). Age (HR = 1.019, 95%CI 1.010-1.028), alcohol intake (HR = 1.002, 95%CI 1.001-1.002), Salt intake (HR = 1.295, 95%CI 1.038-1.617) and Hp infection (HR = 1.584, 95%CI 1.220-2.057) were associated with aggravation of mucosal atrophy. The risk factors for gastric neoplasm in underlying mucosal atrophy were age (HR = 1.041, 95%CI 1.004-1.079), alcohol intake (HR = 1.003, 95% CI 1.001-1.005), Salt intake (HR = 2.553, 95% CI 1.141-5.712), Extent of mucosal atrophy (HR = 2.375, 95% CI 1.201-4.695 in C3-O1; HR = 4.255, 95% CI 1.612-11.229 in O2-O3), and intestinal metaplasia (HR = 2.599, 95% CI 1.286-5.251). Conclusions: Hp was a risk factor for aggravation of atrophy, but not for gastric neoplasm. Salt intake, extent of mucosal atrophy, and intestinal metaplasia were important risk factors for gastric neoplasm.


2011 ◽  
Vol 19 (19) ◽  
pp. 1981
Author(s):  
Ze-Li Gao ◽  
Cheng Zhang ◽  
Fei-Ying Sheng ◽  
Li-Wen Jin

Author(s):  
Beom Jin Kim

Atrophic gastritis (AG) and intestinal metaplasia (IM) are considered the main precursor lesions of gastric cancer, and the risk of gastric cancer in the gastric mucosa increases in the presence of AG and IM. The development of intestinal-type gastric adenocarcinoma represents the last step of an inflammation-metaplasia-dysplasia-carcinoma sequence, called the Correa cascade of multistep gastric carcinogenesis. The incidences of both AG and IM tend to increase with age. <i>Helicobacter pylori</i> is regarded the most important factor in the development of IM; the progression of AG to IM is also affected by numerous environmental factors and individual genetic factors. Therefore, understanding the natural course of AG and IM is very important, especially in areas with a high prevalence of gastric cancer such as Korea.


2000 ◽  
Vol 118 (4) ◽  
pp. A768
Author(s):  
Ivete B. Prado ◽  
Fabio P. Lopasso ◽  
Paulo Kassab ◽  
Kyoshi Iriya ◽  
Antonio A. Laudanna

2020 ◽  
Author(s):  
Heng Li ◽  
Xudong Dai ◽  
Jin Dou ◽  
Hualin Xu ◽  
Qi Min ◽  
...  

Abstract Background Aquaporin 3(AQP3) has been implicated in gastric intestinal metaplasia and gastric cancer, and considered as a biomarker to improve treatment strategy. Accumulating evidence suggests that AQP3 is involved in the gastric carcinogenesis and the disease progression. However, whether AQP3 is involved in the transformation from gastritis to gastric cancer remain elusive. In this study, we intended to realized the expression pattern and its significance of AQP3 in different gastric diseases. Methods A total of 101 patients diagnosed with gastric diseases were included in the study. A gastric tissue biopsy was taken from the gastric antrum during endoscopic examination. Expression of AQP3 protein is determined by immunohistochemistry using polyclonal rabbit anti-AQP3 antibody. Percentage of positive cells and staining intensity were counted and measured. Results The frequency of AQP3 positivity was similar between the disease types of chronic gastritis, gastric ulcer, gastric erosion, and atrophic gastritis, whereas the frequency of AQP3 positivity was significantly higher in patients with gastric intestinal metaplasia、gastric dysplasia 、gastric polyps and intestinal-type gastric adenocarcinoma than that in patients with gastritis, gastric ulcer, gastric erosion, or atrophic gastritis(p<0.0001, p=0.001, p=0.006, p=0.0009, respectively), especially in the patients with hyperplastic polyps (p<0.0001). Conclusion The frequency of AQP3 positivity was significantly higher in patients with gastric intestinal metaplasia, gastric dysplasia, and gastric adenocarcinoma, and the frequency between them was similar, suggesting that AQP3 expression is peaked at the stage of gastric intestinal metaplasia, which further confirmed that gastric intestinal metaplasia is a pivotal progression in gastric carcinogenesis pathologically. Interestingly, it is the first time to report AQP3 positive expression in patients with gastric polyps. In short, AQP3 is involved in the progression from gastritis to gastric adenocarcinoma, and might be a potential biomarker to improve the treatment strategy of gastric cancer.


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