Figure 1 - uploaded by Elroy Patrick Weledji
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Photograph of gastric intestinal metaplasia (4). (A) Complete type with well-defined goblet cells alternating with eosinophilic enterocytes displaying well-developed brush border (inset) and paneth cells (arrow); (B) Incomplete type resembles a colonic epithelium phenotype, showing multiple intracytoplasmic mucin droplets of varying sizes and absence of a brush border. (Haematoxylin and eosin; original magnification ×400).
Source publication
Intestinal metaplasia (IM) of the stomach has been shown to increase the relative risk of gastric cancer. Endoscopic surveillance has been proposed and advocated for populations at risk. Those patients who had undergone surgery for gastric malignancy exhibited precancerous lesions such as atrophic gastritis and IM, and the possibility of anastomoti...
Context in source publication
Context 1
... IM resembles colonic epithelium with multiple, irregular mucin droplets of variable size in the cytoplasm and absence of a brush border. Complete IM resembles small intestinal epithelium with eosinophilic enterocytes, a brush border, goblet cells, and variable Paneth cells (Figure 1). H. pylori colonization can be patchy in complete IM type (21)(22)(23). ...
Citations
... As a precancerous lesion of the stomach, gastric intestinal metaplasia (GIM) has attracted much attention in recent years [4, 5]. In GIM, normal gastric epithelium cells are replaced with intestinal cell types [6, 7]. One study suggested that the incidence of GIM advancing to gastric cancer was 1.8% in a separate cohort of patients followed up for 1 to 10 years [8]. ...
Background
hTERT has been reported involved in the proliferation and metastasis of gastric cancer, but the role of hTERT in gastric intestinal metaplasia, a premalignant lesion of the gastric mucosa was unknown. The aim of the present study was to investigate the role of hTERT in GIM and the effect of hTERT on CDX2 expression in gastric cells.
Results
Experiments showed that expression of hTERT was significantly higher in GIM than in normal gastric mucosa. Moreover, hTERT increased the KLF4 level via NF-κB during GIM. Furthermore, KLF4 is involved in the up-regulation of CDX2 induced by hTERT, and hTERT can interact with p50, thereby increasing the level of CDX2.
Materials and Methods
Immunohistochemistry was used to detect the expression of hTERT in gastric intestinal metaplasia tissue. Then, effect of hTERT on the expression of CDX2 was detected by qRT-PCR, WB and dual luciferase experiment. The role of p65 and p50 in the regulation of CDX2 were further detected by WB, CO-IP and ChIP.
Conclusions
We may conclude that hTERT promotes GIM by up-regulating CDX2 via NF-κB signaling pathway.
... The gastric mucosa of the patients who underwent gastric surgery for malignancy tends to develop recurrent cancer, less than 10 years after surgery at the anastomosis site and new cancers at the nonanastomosis site. Those patients with initially benign disease may develop cancer but more than 10 years after at the anastomosis site [56]. By attenuating the chronic gastritis-metaplasia-dysplasiacarcinoma sequence, there is a role for H. pylori eradication therapy in preventing anastomotic recurrence or a new primary [27,56]. ...
... Those patients with initially benign disease may develop cancer but more than 10 years after at the anastomosis site [56]. By attenuating the chronic gastritis-metaplasia-dysplasiacarcinoma sequence, there is a role for H. pylori eradication therapy in preventing anastomotic recurrence or a new primary [27,56]. ...
Gastric bypass surgery is indicated for several clinical reasons including benign and malignant upper gastrointestinal
tract pathologies. Any gastric resection or bypass procedure interferes with gastric emptying
and the aim of reconstruction is to minimize the disturbance to the upper gastrointestinal physiology.
Gastric bypass procedures induce early satiety, with or without concomitant impaired absorption of nutrients,
and offer the best solution for morbid obesity. The long-term health benefits of gastric bypass
surgery for morbid obesity must be found to outweigh the operative risks and side-effects of gastric bypass
and thus patient selection is fundamental. The aim of the study was to review the indications, complications,
sequelae and outcome of gastric bypass procedures.
... The gastric mucosa of the patients who underwent gastric surgery for malignancy tends to develop recurrent cancer, less than 10 years after surgery at the anastomosis site and new cancers at the non-anastomosis site. Those patients with initially benign disease may develop cancer but more than 10 years after, at the anastomosis site [57]. ...
... By attenuating the chronic gastritis-metaplasia-dysplasia-carcinoma sequence, there is a role for H.pylori eradication therapy in preventing anastomotic recurrence or a new primary [27,57]. ...
Gastric bypass surgery is indicated for several clinical reasons including benign and malignant upper gastrointestinal tract pathologies. Any gastric resection or bypass procedure interferes with gastric emptying and the aim of reconstruction is to minimize the disturbance to the upper gastrointestinal physiology. Gastric bypass procedures induce early satiety, with or without concomitant impaired absorption of nutrients, and offers the best solution for morbid obesity. The long-term health benefits of gastric bypass surgery for morbid obesity must be found to outweigh the operative risks and side-effects of gastric bypass and thus patient selection is fundamental. The aim of the study was to review the indications, complications, sequelae and outcome of gastric bypass procedures.
Keywords: gastric bypass; indications; complications; sequelae
