scholarly journals Microsatellite Instability in Gastric Intestinal Metaplasia in Patients with and without Gastric Cancer

2000 ◽  
Vol 156 (2) ◽  
pp. 537-543 ◽  
Author(s):  
Wai K. Leung ◽  
Jae J. Kim ◽  
Jong G. Kim ◽  
David Y. Graham ◽  
Antonia R. Sepulveda
Gut ◽  
2021 ◽  
pp. gutjnl-2021-324057
Author(s):  
Jonathan W J Lee ◽  
Feng Zhu ◽  
Supriya Srivastava ◽  
Stephen KK Tsao ◽  
Christopher Khor ◽  
...  

ObjectiveTo investigate the incidence of gastric cancer (GC) attributed to gastric intestinal metaplasia (IM), and validate the Operative Link on Gastric Intestinal Metaplasia (OLGIM) for targeted endoscopic surveillance in regions with low-intermediate incidence of GC.MethodsA prospective, longitudinal and multicentre study was carried out in Singapore. The study participants comprised 2980 patients undergoing screening gastroscopy with standardised gastric mucosal sampling, from January 2004 and December 2010, with scheduled surveillance endoscopies at year 3 and 5. Participants were also matched against the National Registry of Diseases Office for missed diagnoses of early gastric neoplasia (EGN).ResultsThere were 21 participants diagnosed with EGN. IM was a significant risk factor for EGN (adjusted-HR 5.36; 95% CI 1.51 to 19.0; p<0.01). The age-adjusted EGN incidence rates for patients with and without IM were 133.9 and 12.5 per 100 000 person-years. Participants with OLGIM stages III–IV were at greatest risk (adjusted-HR 20.7; 95% CI 5.04 to 85.6; p<0.01). More than half of the EGNs (n=4/7) attributed to baseline OLGIM III–IV developed within 2 years (range: 12.7–44.8 months). Serum trefoil factor 3 distinguishes (Area Under the Receiver Operating Characteristics 0.749) patients with OLGIM III–IV if they are negative for H. pylori. Participants with OLGIM II were also at significant risk of EGN (adjusted-HR 7.34; 95% CI 1.60 to 33.7; p=0.02). A significant smoking history further increases the risk of EGN among patients with OLGIM stages II–IV.ConclusionsWe suggest a risk-stratified approach and recommend that high-risk patients (OLGIM III–IV) have endoscopic surveillance in 2 years, intermediate-risk patients (OLGIM II) in 5 years.


2012 ◽  
Vol 75 (4) ◽  
pp. AB240
Author(s):  
Justin M. Gomez ◽  
James T. Patrie ◽  
Jeanetta Frye ◽  
Bryan G. Sauer ◽  
Vanessa M. Shami ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Tarek Almouradi ◽  
Tadd Hiatt ◽  
Bashar Attar

Gastric intestinal metaplasia is an important stage in the development of gastric cancer. Limited data is available regarding the prevalence of gastric intestinal metaplasia in the United States. We conducted a retrospective review of esophagogastroduodenoscopies performed in our endoscopy unit between the months of April and October 2010 to evaluate the prevalence and the epidemiologic and endoscopic features of gastric intestinal metaplasia in an underserved population in the United States.


2016 ◽  
Vol 62 (1) ◽  
pp. 56-59
Author(s):  
Silvia Cosmina Drasovean ◽  
Diana Elena Morărașu ◽  
Ofelia Daniela Pascarenco ◽  
Olga Brsunic ◽  
Danusia Maria Onișor ◽  
...  

AbstractBackground and Aim: Gastric intestinal metaplasia represents a risk factor for intestinal type of gastric cancer. Gastric intestinal metaplasia seems to be associated with Helicobacter pilory infection in relatives of patients with gastric cancer. The aim of this study was to determine the prevalence, clinical, endoscopic and histological features of gastric intestinal metaplasia. Material and Methods: We retrospectively analyzed the esophagogastroduodenoscopies with biopsies performed between January 1, 2014 and October 31, 2014. Collected and analyzed data included age, gender, symptoms, endoscopic and histological findings. Results: Four hundred eighty-two patients were included in the study. One hundred thirty-seven patients had gastric intestinal metaplasia, which presented a prevalence was 28,4%. A similar distribution between gender was observed with a significant increase of gastric intestinal metaplasia with age (p=0,0001). Regarding the indication for endoscopy, the prevalence of gastric intestinal metaplasia was: 17 % among patients with dyspeptic syndrome, 2 % in patients with anemia and 5 % in patients examined for other symptoms. Endoscopic findings showed gastric intestinal metaplasia was significantly associated with atrophic gastritis (p=0.0001), erythematous gastritis (p=0.0079), while there was no association with erosive gastritis (p=0.24) and peptic ulcer (p=0.19). Conclusions: Gastric intestinal metaplasia is frequently recorded in patients undergoing in esophagogastroduodenoscopies with associated biopsies. Endoscopic findings like erythema and atrophy is strongly associated with gastric intestinal metaplasia emphasizing the importance of sampling biopsies.


Gut ◽  
2020 ◽  
Vol 69 (10) ◽  
pp. 1738-1749
Author(s):  
Vaidehi Krishnan ◽  
Debbie Xiu En Lim ◽  
Phuong Mai Hoang ◽  
Supriya Srivastava ◽  
Junichi Matsuo ◽  
...  

Objective Intestinal metaplasia (IM) is a premalignant stage that poses a greater risk for subsequent gastric cancer (GC). However, factors regulating IM to GC progression remain unclear. Previously, activated DNA damage response (DDR) signalling factors were shown to engage tumour-suppressive networks in premalignant lesions. Here, we interrogate the relationship of DDR signalling to mutational accumulation in IM lesions. Design IM biopsies were procured from the gastric cancer epidemiology programme, an endoscopic surveillance programme where biopsies have been subjected to (epi)genomic characterisation. IM samples were classified as genome-stable or genome-unstable based on their mutational burden/somatic copy-number alteration (CNA) profiles. Samples were probed for DDR signalling and cell proliferation, using the markers γH2AX and MCM2, respectively. The expression of the gastric stem cell marker, CD44v9, was also assessed. Tissue microarrays representing the GC progression spectrum were included. Results MCM2-positivity increased during GC progression, while γH2AX-positivity showed modest increase from normal to gastritis and IM stages, with further increase in GC. γH2AX levels correlated with the extent of chronic inflammation. Interestingly, genome-stable IM lesions had higher γH2AX levels underscoring a protective anti-cancer role for DDR signalling. In contrast, genome-unstable IM lesions with higher mutational burden/CNAs had lower γH2AX levels, elevated CD44v9 expression and modest promoter hypermethylation of DNA repair genes WRN, MLH1 and RAD52. Conclusions Our data suggest that IM lesions with active DDR will likely experience a longer latency at the premalignant state until additional hits that override DDR signalling clonally expand and promote progression. These observations provide insights on the factors governing IM progression.


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