THE ASSOCIATION OF THE COMBINATION OF TP53 GENE CODON 72 POLYMORPHISM AND HELICOBACTER PYLORI INFECTION WITH GASTRIC CANCER

2017 ◽  
pp. 47-52
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Tp53 Gene ◽  
Codon 72 ◽  
Codon 72 Polymorphism ◽  
Pcr Rflp ◽  
Two Factors ◽  
Risk Patients ◽  
H Pylori

Background: The interaction of environment factor and host factor plays the important role in the pathogenesis of gastric cancer (GC). This study aimed to evaluate the association of the combination of TP53 gene codon 72 polymorphism and the H. pylori infection with GC risk. Patients and methods: 112 patients with GC and 136 patients without GC were extracted DNA from specimens of gastric mucosa, then were determined TP53 gene codon 72 polymorphism by PCR-RFLP and diagnosed H. pylori infection by PCR with ureC gene-specific primers. Results: There was no significant association between TP53 gene codon 72 polymorphism and GC risk, as well as between H. pylori infection and GC risk. The combination of two factors (TP53 gene codon 72 polymorphism and H. pylori infection) was found to be associated with GC risk: The combination of Pro/Pro genotype and H. pylori (+) was the GC risk factor, OR = 2.62 (95%CI: 1.20–5.71) as compared to other combinations. In the group of H. pylori-positive patients, Pro/Pro genotype was the GC risk factor, OR = 2.42 (95%CI: 1.05 – 5.59) as compared to (Arg/Arg + Arg/Pro) group, and OR = 3.48 (95%CI: 1.23 – 9.78) as compared to Arg/Arg genotype. Conclusion: The factors of TP53 gene codon 72 polymorphism and H. pylori infection were not associated with GC risk as assessed separately, but they had the interaction associated with GC risk. Key words: TP53 gene codon 72 polymorphism, Helicobacter pylori, gastric cancer

scholarly journals Association of TP53 gene codon 72 polymorphism with Helicobacter pylori-positive non-cardia gastric cancer in Vietnam

2019 ◽  
Vol 13 (11) ◽  
pp. 984-991
Author(s):  
Thi Minh Thi Ha ◽  
Thanh Nha Uyen Le ◽  
Viet Nhan Nguyen ◽  
Van Huy Tran
Keyword(s):  
Gastric Cancer ◽  
Control Group ◽  
Rapid Urease Test ◽  
Genotype Distribution ◽  
Codon 72 ◽  
Codon 72 Polymorphism ◽  
Urease Test ◽  
Significant Difference ◽  
Tp53 Codon 72 Polymorphism ◽  
H Pylori

Introduction: This research aimed to determine the association of the combination of H. pylori infection and TP53 codon 72 polymorphism with non-cardia gastric cancer (GC) in Vietnam. Methodology: A total of 164 patients with non-cardia GC and 164 patients with peptic ulcer disease or functional dyspepsia in controls matched by sex and age were enrolled. H. pylori infection was diagnosed by rapid urease test and polymerase chain reaction (PCR). The cagA gene-positivity and vacA sm subtypes were determined by multiplex PCR. Genotypes of TP53 codon 72 polymorphism were determined by PCR-restriction fragment length polymorphism. Results: The prevalence of H. pylori infection in GC and control group were 61.6% and 55.4%, respectively. The rates of cagA-positive strains in the two H. pylori-positive groups were 80.2% and 71.4%, respectively. There was no statistically significant difference in TP53 codon 72 genotype distribution between GC group (frequencies of Arg/Arg, Arg/Pro and Pro/Pro genotypes were 31.1%, 43.3% and 25.6%, respectively) and controls (29.3%, 52.4% and 18.3%, respectively), p = 0.172. The significant difference in genotype distribution was observed in recessive model (Pro/Pro vs Arg/Arg + Arg/Pro) when stratifying by H. pylori infection (OR = 2.02, 95% CI 1.03–3.96, p = 0.041) and by cagA-positivity (OR = 2.33, 95% CI 1.07–5.07, p = 0.032). Conclusions: This study suggests a synergistic interaction between H. pylori infection, especially cagA-positive H. pylori, and Pro/Pro genotype of TP53 codon 72 polymorphism might play a significant role in the pathogenesis of GC in the Vietnamese population.

scholarly journals Detection of Early Gastric Cancer after Helicobacter pylori Eradication

Digestion ◽  
2021 ◽  
pp. 1-8
Author(s):  
Satoki Shichijo ◽  
Noriya Uedo ◽  
Tomoki Michida
Keyword(s):  
Risk Factors ◽  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Early Gastric Cancer ◽  
Eradication Therapy ◽  
Low Grade ◽  
Gastric Cancers ◽  
Risk Patients ◽  
Linked Color Imaging ◽  
H Pylori

<b><i>Background:</i></b> Based on evidence that <i>Helicobacter pylori</i> eradication reduces the development of gastric cancer and other diseases such as peptic ulcer, eradication therapy has prevailed. However, gastric cancer can develop even after successful eradication. <b><i>Summary:</i></b> In this review article, we searched for studies that identified the characteristics of primary and metachronous gastric cancers after <i>H. pylori</i> eradication, the risk factors for the development of these cancers after successful <i>H. pylori</i> eradication, and whether image-enhanced endoscopy is useful for diagnosing gastric cancer after eradication. A gastritis-like appearance is seen as a characteristic endoscopic finding, which corresponds to an epithelium with low-grade atypia – also known as nonneoplastic epithelium – covering the surface of the cancerous glands. This finding may make endoscopic detection of early gastric cancer difficult after <i>H. pylori</i> eradication. Similar risk factors, such as the male sex, endoscopic atrophy, histologic intestinal metaplasia, and late eradication, have been reported as predictors for the development of both primary and metachronous gastric cancers. Image-enhanced endoscopy, such as linked color imaging, may be useful for the detection and risk stratification of gastric cancer after eradication. <b><i>Key Messages:</i></b> Based on these findings, we believe that effective surveillance of high-risk patients leads to early detection of gastric cancer in the era of <i>H. pylori</i> eradication.

scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication: A Retrospective Study

2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Retrospective Study ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
H Pylori

Abstract Background: Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods: Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of no to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results: Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected in the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). Submucosal ECGs in the H. pylori-EG were more likely to be seen in the no to mild atrophic mucosa subgroup (4/6, 67%) compared with the moderate to severe atrophic gastric mucosa subgroup (1/23, 4%) (P = 0.003). Conclusions: Careful follow-up endoscopies are necessary after H. pylori eradication.

scholarly journals Evaluating the presence of Mycoplasma hyorhinis, Fusobacterium nucleatum, and Helicobacter pylori in biopsies of patients with gastric cancer

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Camila do Nascimento Araujo ◽  
Aline Teixeira Amorim ◽  
Maysa Santos Barbosa ◽  
Julieta Canjimba Porto Lucas Alexandre ◽  
Guilherme Barreto Campos ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Cancer Risk ◽  
Fusobacterium Nucleatum ◽  
Control Group ◽  
Cancer Risk Factor ◽  
Mycoplasma Hyorhinis ◽  
H Pylori ◽  
And Control

Abstract Background Gastric cancer is the third leading cause of cancer-related deaths worldwide and has been associated with infections that may promote tumour progression. Accordingly, we analysed the presence of Mollicutes, Mycoplasma hyorhinis, Fusobacterium nucleatum and Helicobacter pylori in gastric cancer tissues and evaluated their correlation with clinicopathological factors. Methods Using a commercial kit, DNA were extracted from 120 gastric samples embedded in paraffin: 80 from patients with gastric cancer and 40 from cancer free patients, dating from 2006 to 2016. Mollicutes and H. pylori were detected by PCR; F. nucleatum and M. hyorhinis were detected by qPCR, together with immunohistochemistry for the latter bacteria. Results Mollicutes were detected in the case and control groups (12% and 2.5%) and correlated with the papillary histologic pattern (P = 0.003), likely due to cell transformation promoted by Mollicutes. M. hyorhinis was detected in the case and control group but was not considered a cancer risk factor. H. pylori was detected at higher loads in the case compared to the control group (8% and 22%, P = 0.008) and correlated with metastasis (P = 0.024), lymphatic invasion (P = 0.033), tumour of diffused type (P = 0.028), and histopathological grading G1/G2 (P = 0.008). F. nucleatum was the most abundant bacteria in the case group, but was also detected in the control group (26% and 2.5%). It increased the cancer risk factor (P = 0.045, OR = 10.562, CI95% = 1.057–105.521), and correlated with old age (P = 0.030) and tumour size (P = 0.053). Bacterial abundance was significantly different between groups (P = 0.001). Conclusion Our findings could improve the control and promote our understanding of opportunistic bacteria and their relevance to malignant phenotypes.

scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication

2021 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
Careful Patient ◽  
H Pylori

Abstract Background. Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods. Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of none to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results. Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected on the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). As for submucosal ECGs in the H. pylori-EG, it was more likely to be seen in the none to mild atrophic mucosa subgroup compared to the moderate to severe atrophic gastric mucosa subgroup (P = 0.003). Conclusions. EGCs after H. pylori eradication were characterized as small and of the depressed type. Submucosal invasive EGCs developed more frequently in the none to mild atrophic mucosa after H. pylori eradication. Therefore, careful patient follow-up is important after H. pylori eradication.

scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication: A Retrospective Study

2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
Careful Patient ◽  
H Pylori

Abstract Background: Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods: Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of none to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results: Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected on the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). As for submucosal ECGs in the H. pylori-EG, it was more likely to be seen in the mild atrophic mucosa subgroup (4/6, 67%) compared to the moderate to severe atrophic gastric mucosa subgroup (1/23, 4%) (P = 0.003).Conclusions: EGCs after H. pylori eradication were characterized as small and of the depressed type. Submucosal invasive EGCs developed more frequently in the none to mild atrophic mucosa after H. pylori eradication. Therefore, careful patient follow-up is important after H. pylori eradication.

DETERMINATION OF P53 GENE CODON 72 POLYMORPHISMS IN PATIENTS WITH GASTRIC CANCER

2013 ◽  
pp. 11-17
Author(s):  
Thi Tuy Ha Nguyen ◽  
Thi Minh Thi Ha
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
P53 Gene ◽  
Diffuse Gastric Cancer ◽  
Codon 72 ◽  
Cancer Group ◽  
Pcr Rflp ◽  
Gastric Cancer Patients ◽  
The Relationship

Background: The role of p53 gene in the gastric cancer is still controversial. This study is aimed at determining the rate of the p53 gene codon 72 polymorphisms in gastric cancer patients and evaluating the relationship between these polymorphisms and endoscopic and histopathological features of gastric cancer. Patients and methods: Sixty eight patients with gastric cancer (cases) and one hundred and thirty six patients without gastric cancer (controls) were enrolled. p53 gene codon 72 polymorphisms were determined by PCR-RFLP technique with DNA extracted from samples of gastric tissue. Results: In the group of gastric cancer, Arginine/Argnine, Arginine/Proline and Proline/Proline genotypes were found in 29.4%, 42.7% and 27.9%, respectively. The differences of rates were not statistically significant between cases and controls (p > 0,05). In males, the Proline/Proline genotype was found in 38.1% in patients with gastric cancer and more frequent in patients without gastric cancer (15.7%, p = 0,01). An analysis of ROC curve showed that the cut-off was the age of 52 in the Proline/Proline genotype, but it was 65 years old in the Arginine/Proline genotype. The Proline/Proline genotype was found in 41.9% in Borrmann III/IV gastric cancer, this rate was higher than Borrmann I/II gastric cancer (16.2%, p = 0.037) and also higher than controls (18.4%, p = 0,01). The rate of Proline/Proline genotype was 41.7% in the diffuse gastric cancer, it was higher than in controls (p = 0,023). Conclusion: No significative difference of rate was found in genotypes between gastric cancer group and controls. However, there was the relationship between Proline/Proline genotype and gastric cancer in males, Borrmann types of gastric cancer, the diffuse gastric cancer. Key words: polymorphism, codon 72, p53 gene, PCR - RFLP, gastric cancer.

Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

2020 ◽  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Helicobacter Pylori ◽  
Cancer Stem Cells ◽  
Histopathological Examination ◽  
Physiological Saline ◽  
Rrna Gene ◽  
Peptic Ulcers ◽  
Gastric Cancer Stem Cells ◽  
H Pylori

Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.

scholarly journals The correlation between lncRNAs and Helicobacter pylori in gastric cancer

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Molecular Mechanisms ◽  
Gastrointestinal Diseases ◽  
Mechanisms Of Action ◽  
Molecular Pathways ◽  
Gastric Diseases ◽  
Non Coding Rnas ◽  
H Pylori ◽  
The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

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