Assessment of p21, p53 expression, and Ki-67 proliferative activities in the gastric mucosa of children with Helicobacter pylori gastritis

2015 ◽  
Vol 27 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Coskun Saf ◽  
Enver Mahir Gulcan ◽  
Ferda Ozkan ◽  
Seyhan Perihan Cobanoglu Saf ◽  
Ayca Vitrinel
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Ki 67 ◽  
P53 Expression ◽  
Helicobacter Pylori Gastritis

scholarly journals Gastric foveolar-type adenomas endoscopically showing a raspberry-like appearance in the Helicobacter pylori-uninfected stomach

2019 ◽  
Vol 07 (06) ◽  
pp. E784-E791 ◽  
Author(s):  
Kotaro Shibagaki ◽  
Chika Fukuyama ◽  
Hironobu Mikami ◽  
Daisuke Izumi ◽  
Noritsugu Yamashita ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Narrow Band Imaging ◽  
Past History ◽  
Clinicopathological Characteristics ◽  
Igg Antibody ◽  
Ki 67 ◽  
Mucin Phenotype ◽  
White Light Endoscopy ◽  
Japanese Classification

Abstract Background and study aims Foveolar-type adenoma is described as a very rare tumor that occurs in individuals without Helicobacter pylori (HP) infection and diagnosed as adenocarcinoma in the Japanese Classification of Gastric Carcinoma (JCGC). However, we have frequently encountered patients with foveolar-type adenoma that endoscopically resembles a hyperplastic polyp, suggesting that it has just been overlooked to date. Here, we analyzed clinicopathological characteristics of a special subtype of foveolar-type adenoma showing specific endoscopic findings. Patients and methods From a total of 212 patients with gastric cancer resected during a 22-month period, we enrolled 14 (6.6 %) diagnosed with foveolar-type adenoma (adenocarcinoma in JCGC). HP infection status was determined by eradication history, HP serum IgG antibody level, urea breath test, and endoscopic and histological findings. All lesions were observed using white-light endoscopy and narrow-band imaging with magnification endoscopy (NBIME). Endoscopically resected lesions were histologically examined. Results None of 14 patients had a current or past history of HP infection. All lesions were visualized on non-atrophic gastric mucosa as small reddish protrusions with fine granular surface, showing a raspberry-like appearance. NBIME showed papillary or gyrus-like microstructures with irregular capillary. Lesions were histologically diagnosed as foveolar-type adenoma showing MUC5AC-positive gastric mucin phenotype. Ki-67 was overexpressed (median labeling index 69.9 %, range 28.4 – 92.1 %), though all lesions were an intraepithelial tumor without stromal invasion. p53 over-staining was not seen in any. Conclusions Raspberry-like lesions on non-atrophic gastric mucosa in HP-uninfected individuals should be evaluated for the possibility of a special subtype of foveolar-type adenoma.

Histopathology and expression of Ki-67 and cyclooxygenase-2 in childhood Helicobacter pylori gastritis

2004 ◽  
Vol 39 (3) ◽  
pp. 231-237 ◽  
Author(s):  
Kyung Mo Kim ◽  
Young Lyun Oh ◽  
Jae Sung Ko ◽  
Yon Ho Choe ◽  
Jeong Kee Seo
Keyword(s):  
Helicobacter Pylori ◽  
Cyclooxygenase 2 ◽  
Ki 67 ◽  
Helicobacter Pylori Gastritis

Acute Inflammation of the Proliferative Zone of Gastric Mucosa in Helicobacter pylori Gastritis

1999 ◽  
Vol 195 (10) ◽  
pp. 689-697 ◽  
Author(s):  
Eunsil Yu ◽  
Hun Kyung Lee ◽  
Hae Ryun Kim ◽  
Moo-Song Lee ◽  
Inchul Lee
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Acute Inflammation ◽  
Proliferative Zone ◽  
Helicobacter Pylori Gastritis

scholarly journals Diminution of pp60c-sarc Thyrosine Kinase in the Gastric Mucosa of Children With Helicobacter Pylori Gastritis. † 481

1997 ◽  
Vol 41 ◽  
pp. 83-83
Author(s):  
Yoram Elitsur ◽  
Jeffrey A. Moshier ◽  
Julie Dosescu ◽  
Johnny Tureaud ◽  
Adib P.N. Majumdar
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Helicobacter Pylori Gastritis

scholarly journals Non-invasive laboratory markers assessing efficacy of Helicobacter pylori eradication therapy

2019 ◽  
Vol 9 (3-4) ◽  
pp. 523-530
Author(s):  
L. B. Drygina ◽  
V. N. Ellenidi ◽  
N. A. Bardysheva ◽  
M. M. Bogoslovskiy
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Eradication Therapy ◽  
Helicobacter Pylori Infection ◽  
Igg Antibodies ◽  
Ki 67 ◽  
Helicobacter Pylori Eradication ◽  
Pepsinogen I ◽  
Non Invasive ◽  
Pepsinogen Ii

Effective eradication of Helicobacter pylori infection is an important means to reduce the risk of precancerous changes in the gastric mucosa and prevention of gastric cancer. A search for non-invasive diagnostic tools for Helicobacter pylori infection, evaluation of the effectiveness of eradication remains of high importance.The aim of the study was to assess an informative value of detecting pepsinogen I and II as well as serum antibodies to Helicobacter pylori while assessing an efficacy of treated chronic Helicobacter gastritis and identifying preneoplastic changes in the stomach mucosa. There enrolled 113 male patients with chronic gastritis aged 41 to 76, average age- (56.7±0.7) years. Examination of patients was carried out at admission to the clinic, as well as at 2 and 12 months after administering a standard eradication therapy. It was found that Helicobacter pylori infection was detected in 101 (89.4%) patients. Groups of patients with effective eradication therapy were noted. A time-dependent level of antibodies to Helicobacter pylori, as well as measured concentration of pepsinogen I and II after the onset of eradication treatment were determined. Which were analyzed in connection with the results of histology examination of gastric mucosa biopsy specimens and expression of oncoproteins Ki-67, Bcl-2, c-erbB-2, p16 in the gastric mucosa depending on efficacy of eradication therapy. It is shown that effective eradication therapy was characterized by significantly decreased serum level of IgG antibodies to Helicobacter pylori 2 months after the onset of treatment. Moreover, a significantly decreased pepsinogen II and serum IgG antibodies to Helicobacter pylori during eradication therapy were accompanied by a significant decrease in Ki-67 expression in the gastric epithelium. Decreased concentration of pepsinogen II within the first year after Helicobacter pylori eradication therapy was due to a greater decrease in activity of inflammatory changes in the gastric mucosa than to dynamic changes in gastric atrophy and metaplasia. An inverse relation between the serum level of pepsinogen I and atrophy as well as intestinal metaplasia within the gastric mucosa were found.

scholarly journals Prostaglandin E2 in gastric mucosa of children with Helicobacter pylori gastritis: relation to thickness of mucus gel layer.

1993 ◽  
Vol 46 (9) ◽  
pp. 836-839 ◽  
Author(s):  
G Oderda ◽  
M D'Alessandro ◽  
P Mariani ◽  
P Lionetti ◽  
M Bonamico ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Prostaglandin E2 ◽  
Gel Layer ◽  
Mucus Gel ◽  
Helicobacter Pylori Gastritis

p53 Expression in the Gastric Mucosa Before and After Eradication of Helicobacter pylori

Helicobacter ◽  
2001 ◽  
Vol 6 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Kiichi Satoh ◽  
Ken Kihira ◽  
Hiroshi Kawata ◽  
Kenkichi Tokumaru ◽  
Yasuhisa Kumakura ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
P53 Expression ◽  
Before And After

scholarly journals Dynamic characterization of intestinal metaplasia in the gastric corpus mucosa of Atp4a-deficient mice

2020 ◽  
Vol 40 (2) ◽  
Author(s):  
Wei Liu ◽  
Liang-jun Yang ◽  
Yuan-liang Liu ◽  
Dong-sheng Yuan ◽  
Zi-ming Zhao ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Secretory Activity ◽  
Membrane System ◽  
Parietal Cells ◽  
Ki 67 ◽  
Α Subunit ◽  
P53 Expression

Abstract Parietal cells of the gastric mucosa contain a complex and extensive secretory membrane system that harbors gastric H+, K+-adenosine triphosphatase (ATPase), the enzyme primarily responsible for gastric lumen acidification. Here, we describe the characterization of mice deficient in the H+, K+-ATPase α subunit (Atp4a−/−) to determine the role of this protein in the biosynthesis of this membrane system and the biology of the gastric mucosa. Atp4a−/− mice were produced by gene targeting. Wild-type (WT) and Atp4a−/− mice, paired for age, were examined at 10, 12, 14 and 16 weeks for histopathology, and the expression of mucin 2 (MUC2), α-methylacyl-CoA racemase (AMACR), Ki-67 and p53 proteins was analyzed by immunohistochemistry. For further information, phosphoinositide 3-kinase (PI3K), phosphorylated-protein kinase B (p-AKT), mechanistic target of rapamycin (mTOR), hypoxia-inducible factor 1α (HIF-1α), lactate dehydrogenase A (LDHA) and sirtuin 6 (SIRT6) were detected by Western blotting. Compared with the WT mice, hypochlorhydric Atp4a−/− mice developed parietal cell atrophy and significant antral inflammation (lymphocyte infiltration) and intestinal metaplasia (IM) with elevated MUC2 expression. Areas of dysplasia in the Atp4a−/− mouse stomach showed increased AMACR and Ki-67 expression. Consistent with elevated antral proliferation, tissue isolated from Atp4a−/− mice showed elevated p53 expression. Next, we examined the mechanism by which the deficiency of the H+, K+-ATPase α subunit has an effect on the gastric mucosa. We found that the expression of phosphorylated-PI3K, p-AKT, phosphorylated-mTOR, HIF-1α, LDHA and SIRT6 was significantly higher in tissue from the Atp4a−/− mice compared with the WT mice (P<0.05). The H+, K+-ATPase α subunit is required for acid-secretory activity of parietal cells in vivo, the normal development and cellular homeostasis of the gastric mucosa, and attainment of the normal structure of the secretory membranes. Chronic achlorhydria and hypergastrinemia in aged Atp4a−/− mice produced progressive hyperplasia and mucolytic and IM, and activated the Warburg effect via PI3K/AKT/mTOR signaling.

scholarly journals Prognostic aspects of immunohistochemical assessment of cellular renewal and transcription factor SOX2 with precancerous changes in the gastric mucosa depending on the genotype of Helicobacter pylori in patients with various types of chronic gastritis

2018 ◽  
Vol 22 (4) ◽  
pp. 674-681
Author(s):  
D. Sukhan ◽  
S. Vernigorodskiy
Keyword(s):  
Transcription Factor ◽  
Gastric Mucosa ◽  
Cyclin D1 ◽  
Chronic Gastritis ◽  
Caspase 3 ◽  
Severe Dysplasia ◽  
Cell Renewal ◽  
Ki 67 ◽  
P53 Expression ◽  
H Pylori

The precancerous potential of chronic gastritis (CG) associated with H. pylori is discussed in numerous writings, and today, CG is central to precancerous conditions of the stomach. A convincing theoretical basis for such an assessment of chronic gastritis is its characteristic feature — an interruption of cell renewal with the proliferation phase predominating over the differentiation phase. However, the determination of the degree of proliferative activity and impaired differentiation of the epithelium of the gastric mucosa (GM) remains not fully understood. The goal of our study was the immunohistochemical evaluation of the expression of Ki-67, Cyclin D1, p53, CPP32, HER2 and the Sox2 transcription factor in GM epithelial cells in patients with H. pylori-associated chronic gastritis.. To accomplish this goal, histological, cytological, immunohistochemical, molecular genetic, morphometric and statistical research methods were used. We found that in chronic H. pylori-associated non-atrophic gastritis (CNG) compared with H. pylori (-), the GM epithelium renewal rate increased, characterized by a significant increase in the expression of caspase-3 and Ki-67 proliferation markers, cyclin D1 (p <0.001) with expansion of the proliferative compartment and apoptosis zones. Ki-67, Cyclin D1, and p53 expression in severe dysplasia (SD) of GM was significantly (p <0.05) higher than the mild in patients with chronic non-atrophic and atrophic H. pylori-associated gastritis, despite a decrease in the expression of the transcription factor Sox2 and caspase-3 in cases of SD. The most specific marker for determining SD in patients with H. pylori-associated chronic gastritis was marker p53 (sensitivity 98.73%; specificity 83.38%, confidence interval 95%, p <0.05). Considering the immunohistochemical markers of H. pylori, a screening system has been developed for the early diagnosis of precancerous changes in the GM that will help optimize the treatment tactics of patients with chronic gastritis and increase the efficiency of detecting dysplastic and atrophic changes in the GM at their early stages of development.

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