Helicobacter pylori and gastric cancer

BACKGROUND: Helicobacter pylori (H. pylori) is classified as a Group 1 carcinogen, because H. pylori infection considerably increases the risk of gastric cancer development. METHODS: The study involved a total of 191 patients divided into two groups. The first group comprised 117 patients who underwent endoscopy. A total of 203 biopsy specimens of the gastric mucosa were taken and analyzed using microbiological and histopathological methods. The second group comprised 74 patients with gastric cancer, who were examined for the gastric cancer type, the presence of H. pylori infection and the cancer localization. The presence of H. pylori infection in the tissue was con?firmed by staining pathohistological sections according to the method of Warthin-Starry. The microbilogical diagnosis involved the staining of direct tissue smears according to the method of Gram, as well as the cultivation of the specimens. To test the hypothesis for possible differences in H. pylori positive findings between the treatment groups, x2 test with Yates correction or Fisher exact test were used. RESULTS: The first treatment group comprised 117 patients with various clinical diagnoses. Gastric cancer was diagnosed in 8 patients, and of these 87.50% were found to have H. pylori. No statistically significant difference in H. pylori positive tests was detected between the patients with gastric ulcer and the patients with gastric cancer (Fisher exact test: p=1.00; p>0.05) nor was it established between the patients with duodenal ulcer and those with gastric cancer (Fisher exact test: p= 1.00; p>0.05). The second treatment group comprised 74 patients, of whom 52 (70.27%) had intestinal-type gastric cancer and 22 (29.72%) had diffuse-type gastric cancer. No statistically significant difference in the positive tests for H. pylori was registered between the patients with intestinal-type and those with diffuse-type gastric cancer (x2=0.07; p=0.798; p>0.05). The most frequent localization of the cancer was the antrum. CONCLUSION: The results are supportive of the hypothesis on a correlation between H. pylori infection and gastric adenocarcinoma development, but no differences between the intestinal and diffuse type of adenocarcinoma have been revealed with respect to the malignant process.

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Characteristics of Helicobacter pylori infection in a National Referral Hospital in Bhutan

Bhutan Health Journal ◽

10.47811/bhj.93 ◽

2020 ◽

Vol 6 (1) ◽

pp. 6-10

Author(s):

Chhabi Lal Adhikari ◽

Guru Prasad Dhakal ◽

Nongluck Suwisith ◽

Sonam Dargay ◽

Krishna P Sharma

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Age Groups ◽

Referral Hospital ◽

Upper Gastrointestinal Endoscopy ◽

Age Group ◽

Exact Test ◽

Significant Difference ◽

H Pylori ◽

National Referral Hospital

Introduction: Helicobacter pylori (H. pylori) is a bacterium causing chronic gastric infection and may cause gastric cancer. It was necessary to see the trend of infection, especially in symptomatic patients. This retrospective descriptive study was aimed to describe the characteristics of H. pylori infection in Bhutanese patients referred for an endoscopy to the National Referral Hospital, Thimphu. Methods: The sample of the study was randomized 380 medical records of the patients who underwent upper gastrointestinal endoscopy and Rapid Urea Test for symptomatic dyspepsia and peptic ulcer. Data was collected using a survey form designed by the researchers. Data analysis was done using descriptive statistics and either Chi-square or Fisher’s exact test. Results: The prevalence of H. pylori infection was very high (76.6%). The mean age of the infection was 42 with a range from 15 to 84 years. The highest prevalence of infection was observed in the age group 20-29 years (82.7%) and lowest in the oldest age group 70-84 years (66.7%). The analysis showed no significant difference in infection amongst age groups, gender, and endoscopic findings to the positive results at 5% significant level except for monthly prevalence (p<0.001). Gastritis was the commonest endoscopy finding (153/380) and gastro-duodenitis had the highest positivity rate (88.9%). Conclusion: The prevalence of infection was relatively high compared with previous studies. Young and middle-aged adults had a high prevalence and this group needs to be given priority for screening and eradication treatment considering limited resources to prevent associated gastric cancer in Bhutan.

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A study on the effect of Helicobacter pylori infection on p53 expression in gastric cancer and gastritis tissues

The Journal of Infection in Developing Countries ◽

10.3855/jidc.2993 ◽

2013 ◽

Vol 7 (09) ◽

pp. 651-657 ◽

Cited By ~ 9

Author(s):

Barik A Salih ◽

Zuhal Gucin ◽

Nizamettin Bayyurt

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

P53 Protein ◽

Immunohistochemical Analysis ◽

Intestinal Type ◽

Diffuse Type ◽

P53 Expression ◽

Normal Tissues ◽

Genotype Frequencies ◽

H Pylori

Introduction: Helicobacter pylori cause damage to gastric epithelial cells and alterations in the p53 gene that lead to cancer development. This study aimed to determine the correlation of p53 expression with H. pylori using immunohistochemistry, RFLP-PCR, and histopathology. Methodology: Gastric biopsy samples from gastric cancer (GC) (n = 54) and gastritis (n = 31) patients were examined for histopathological changes and expression of p53 protein by immunohistochemistry. Results: Immunohistochemical analysis of p53 protein expression in H. pylori-positive GC sections showed an average of 44.3% positive cells in tumors and 6.9% in normal tissues, as compared to 16.4% and 4.4% in H. pylori-negative sections. P53 expression showed significant association with H. pylori (P = 0.005), invasion depth (P = 0.029) and inflammation reaction (P = 0.008). In gastritis sections, no difference in the average p53 staining in H. pylori-positive or -negative sections was seen. PCR-RFLP results also showed no difference in genotype frequencies of p53 in H. pylori-positive or -negative gastritis sections. Histopathology study of H. pylori-positive GC sections showed that 97.2% were the intestinal type and 2.8% the diffuse type, while in H. pylori-negative sections 35.2% were the intestinal type and 64.8% the diffuse type. Biopsy sections from H. pylori-positive gastritis patients revealed more severe inflammation than those of H. pylori-negative patients. Conclusion: Our results show that H. pylori infection affects p53 expression in GC. The average p53 expression was significantly higher in tumor than in normal tissues. In gastritis sections p53 expression was significantly associated with H. pylori.

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Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication

Journal of Gastroenterology ◽

10.1007/s00535-019-01639-w ◽

2019 ◽

Vol 55 (3) ◽

pp. 281-288 ◽

Cited By ~ 10

Author(s):

Susumu Take ◽

Motowo Mizuno ◽

Kuniharu Ishiki ◽

Chiaki Kusumoto ◽

Takayuki Imada ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Incidence Rate Ratio ◽

Gastric Atrophy ◽

Diffuse Type ◽

Gastric Cancer Risk ◽

Helicobacter Pylori Eradication ◽

H Pylori ◽

Diffuse Type Gastric Cancer

Abstract Background and aims Eradication of Helicobacter pylori reduces the risk of gastric cancer. In this study, we investigated the risk beyond 10 years after eradication of H. pylori. Methods We conducted a retrospective cohort study of 2737 patients who had yearly endoscopic follow-up after cure of H. pylori infection. For comparison of gastric cancer risk in the second decade of follow-up with that in the first decade, we calculated standardized incidence ratios (SIRs) by dividing the number of observed cases of gastric cancer in the second decade of follow-up by that of expected cases which was estimated using the incidence rate ratio of age in the first decade. Results During the follow-up for as long as 21.4 years (mean 7.1 years), gastric cancer developed in 68 patients (0.35% per year). The SIRs for diffuse-type gastric cancer was infinity (0 expected case and 4 observed cases) in patients with mild gastric mucosal atrophy and 10.9 (95% confidence interval 4.53–26.1) with moderate atrophy, whereas no significant increase of SIRs was observed in intestinal-type cancer regardless of the grade of baseline gastric atrophy or in diffuse-type cancer in patients with severe atrophy even though who had the highest risk. Conclusions The longer the follow-up, the greater the risk of developing diffuse-type gastric cancer becomes in patients with mild-to-moderate gastric atrophy at baseline. Endoscopic surveillance should be continued beyond 10 years after cure of H. pylori irrespective of the severity of gastric atrophy.

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NOD1 rs2075820 (p.E266K) polymorphism is associated with gastric cancer among individuals infected with cagPAI-positive H. pylori

Biological Research ◽

10.1186/s40659-021-00336-4 ◽

2021 ◽

Vol 54 (1) ◽

Author(s):

Patricio Gonzalez-Hormazabal ◽

Diana Pelaez ◽

Maher Musleh ◽

Marco Bustamante ◽

Juan Stambuk ◽

...

Keyword(s):

Gastric Cancer ◽

Intestinal Type ◽

Diffuse Type ◽

Pathogen Recognition Receptors ◽

H Pylori ◽

Gastric Cancer Patients ◽

Diffuse Type Gastric Cancer ◽

Allele Model ◽

Control Study ◽

Oligomerization Domain

Abstract Background Helicobacter pylori is detected by pathogen recognition receptors including toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors, eliciting an innate immune response against this bacteria. The aim of this study was to assess if polymorphisms of TLR2, TLR4, TLR5, NOD1 and NOD2 genes are associated with gastric cancer, in particular in individuals infected with H. pylori. Results A case-control study of 297 gastric cancer patients and 300 controls was performed to assess the association of 17 polymorphisms. Analyses performed under the allele model did not find association with gastric cancer. However, NOD1 rs2075820 (p.E266K) showed association with intestinal-type gastric cancer among H. pylori infected subjects (OR = 2.69, 95% CI 1.41–5.13, p = 0.0026). The association was not statistically significant in diffuse-type gastric cancer cases (OR = 1.26, 95% CI 0.63–2.52, p = 0.51). When the analyses were performed in patients carrying H. pylori strains harboring the cag pathogenicity island (cagPAI), we noticed significant association with NOD1 rs2075820 (OR = 4.90, 95% CI 1.80–3.36, p = 0.0019), in particular for intestinal-type gastric cancer cases (OR = 7.16, 95% CI 2.40–21.33, p = 4.1 × 10− 4) but not among diffuse-type gastric cancer cases (OR = 3.39, 95% CI 1.13–0.10, p = 0.03). Conclusions NOD1 rs2075820 increases the risk of intestinal-type gastric cancer among individuals infected with H. pylori, particularly in those harboring the cagPAI.

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Diffuse Gastric Cancer: A Summary of Analogous Contributing Factors for Its Molecular Pathogenicity

International Journal of Molecular Sciences ◽

10.3390/ijms19082424 ◽

2018 ◽

Vol 19 (8) ◽

pp. 2424 ◽

Cited By ~ 16

Author(s):

Shamshul Ansari ◽

Boldbaatar Gantuya ◽

Vo Tuan ◽

Yoshio Yamaoka

Keyword(s):

Gastric Cancer ◽

Diffuse Gastric Cancer ◽

Cell Integrity ◽

Diffuse Type ◽

Asian Countries ◽

Contributing Factors ◽

Incidence And Mortality ◽

Genetic Abnormalities ◽

H Pylori ◽

Diffuse Type Gastric Cancer

Gastric cancer is the third leading cause of cancer-related deaths and ranks as the fifth most common cancer worldwide. Incidence and mortality differ depending on the geographical region and gastric cancer ranks first in East Asian countries. Although genetic factors, gastric environment, and Helicobacter pylori infection have been associated with the pathogenicity and development of intestinal-type gastric cancer that follows the Correa’s cascade, the pathogenicity of diffuse-type gastric cancer remains mostly unknown and undefined. However, genetic abnormalities in the cell adherence factors, such as E-cadherin and cellular activities that cause impaired cell integrity and physiology, have been documented as contributing factors. In recent years, H. pylori infection has been also associated with the development of diffuse-type gastric cancer. Therefore, in this report, we discuss the host factors as well as the bacterial factors that have been reported as associated factors contributing to the development of diffuse-type gastric cancer.

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S1609 Clinical Evaluation of Helicobacter pylori Tyrosine-Phosphorylated CagA in Diffuse-Type Gastric Cancer Patients: A Case-Control Study

Gastroenterology ◽

10.1016/s0016-5085(08)61080-x ◽

2008 ◽

Vol 134 (4) ◽

pp. A-234

Author(s):

Yoshihiro Wada ◽

Masanori Ito ◽

Shunsuke Takata ◽

Shosuke Kitamura ◽

Akemi Takamura ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Cancer Patients ◽

Clinical Evaluation ◽

Case Control Study ◽

Case Control ◽

Diffuse Type ◽

Gastric Cancer Patients ◽

Diffuse Type Gastric Cancer ◽

Control Study

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ANALYSIS OF GENE MUTATION IN EARLY SPORADIC DIFFUSE-TYPE GASTRIC CANCER BASED ON HELICOBACTER PYLORI INFECTION STATUS THROUGH WHOLE-EXOME SEQUENCING

10.1055/s-0040-1704859 ◽

2020 ◽

Author(s):

K Namikawa ◽

J Fujisaki ◽

S Mori

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Exome Sequencing ◽

Gene Mutation ◽

Whole Exome Sequencing ◽

Helicobacter Pylori Infection ◽

Infection Status ◽

Diffuse Type ◽

Whole Exome ◽

Diffuse Type Gastric Cancer

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Does Helicobacter pylori infection induce diffuse-type gastric cancer?

Gastroenterology ◽

10.1016/s0016-5085(00)80875-6 ◽

2000 ◽

Vol 118 (4) ◽

pp. A1257

Author(s):

Fumiaki Kitahara ◽

Tadashi Sato ◽

Yuichiro Kojima ◽

Toshiya Nakamura ◽

Atsuro Morozumi ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Helicobacter Pylori Infection ◽

Diffuse Type ◽

Diffuse Type Gastric Cancer

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Asporin Expression on Stromal Cells and/or Cancer Cells Might Be A Useful Prognostic Marker in Patients with Diffuse-Type Gastric Cancer

European Surgical Research ◽

10.1159/000515458 ◽

2021 ◽

pp. 1-8

Author(s):

Masakazu Yashiro ◽

Tsuyoshi Hasegawa ◽

Yurie Yamamoto ◽

Gen Tsujio ◽

Sadaaki Nishimura ◽

...

Keyword(s):

Gastric Cancer ◽

Overall Survival ◽

Cancer Cells ◽

Prognostic Marker ◽

Cancer Progression ◽

Stromal Cells ◽

Intestinal Type ◽

Human Gastric Cancer ◽

Diffuse Type ◽

Diffuse Type Gastric Cancer

Background: Asporin (ASPN), a member of the proteoglycan family, has been shown to have a close correlation with cancer progression. It is not known whether ASPN is an oncogenic driver or a tumor suppressor in human gastric cancer. We sought herein to determine the relationship between ASPN expression and clinicopathological features of gastric cancer. Patients and Methods: A total of 296 gastric cancer patients (diffuse type, n = 144; intestinal type, n = 152) were enrolled. The ASPN expression level in each case was analyzed by immunohistochemistry. Results: ASPN was mainly found on stromal cells, especially on fibroblasts in tumor stroma, i.e., cancer-associated fibroblasts. The ASPN expression on either cancer cells or stromal cells was significantly high in macroscopic scirrhous-type tumors (p < 0.001) and histologically abundant stroma-type tumors (p < 0.001). Interestingly, a Kaplan-Meier survival curve of the 144 cases of diffuse-type gastric cancer revealed a significantly poorer prognosis in patients with ASPN-positive expression (p = 0.043; log rank) compared to those with ASPN-negative expression, but the prognoses were not significantly different in these subgroups of the 152 cases of intestinal-type gastric cancer. A multivariate analysis with respect to overall survival showed that ASPN expression on stromal cells and/or cancer cells was significantly correlated with overall survival in patients with diffuse-type gastric cancer (p = 0.041). Conclusion: In gastric cancer, ASPN was expressed mainly on stromal cells and partially on cancer cells. ASPN expression on stromal cells and/or cancer cells might be a useful prognostic marker in patients with diffuse-type gastric cancer.

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