Differences in amino acid frequency in CagA and VacA sequences of Helicobacter pylori distinguish gastric cancer from gastric MALT lymphoma

Hashinaga, Masahiko; Suzuki, Rumiko; Akada, Junko; Matsumoto, Takashi; Kido, Yasutoshi; Kodama, Masaaki; Murakami, Kazunari; Yamaoka, Yoshio

doi:10.1186/s13099-016-0137-x

Cited by 15 publications

(10 citation statements)

References 41 publications

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“…(39-41) This finding is partially in agreement with the result obtained by Masahiko et al ., that the Amino acid frequency of gastritis samples seems to be intermediate between gastric cancer and MALT lymphoma samples. (42) In contrast, two Japanese strains (NCTC11637 and NCTC11638) isolated from patients with gastritis do not have any mutations in this region (amino acid residues 428-510) except N467G which was found in all our sequences in regardless to gastroduodenal diseases. (43)…”

Section: Discussionmentioning

confidence: 76%

Genetic Diversity of thecagAgene ofHelicobacter pyloristrains from Sudanese Patients with Different Gastroduodenal Diseases

Hassan

Idris

Hassan³

et al. 2019

Preprint

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Background: There is an increase in the prevalence of Helicobacter pylori infection in Sudan, accompanied by a high incidence of upper gastrointestinal malignancy. The cytotoxin-associated gene cagA gene is a marker of a pathogenicity island (PAI) in H. pylori and plays a crucial role in determining the clinical outcome of Helicobacter infections.Objective: This study aimed to determine the frequency and heterogeneity of the cagA gene of H. pylori and correlate the presence of cagA gene with clinical outcomes. Materials and methods:Fifty endoscopy biopsies were collected from Fedail and Soba hospitals in Khartoum state. DNA was extracted using the Guanidine chloride method followed by PCR to amplify 16S rRNA and cagA gene of H. pylori using specific primers. DNA amplicons of cagA gene were purified and sequenced. Bioinformatics and statistical analysis were done to characterize and to test the association between cagA gene and gastric complications. Results:CagA gene was detected in 20/37(54%) of the samples that were found positive for H.pylori. There was no association between endoscopy finding and the presence of the cagA gene (p = 0.225). Specific amino acid variations were found at seven loci related to strains from a patient with duodenitis, gastric ulcer, and gastric atrophy (R448H, T457K, S460L, IT463-464VA, D470E, A482Q, KNV490-491-492TKT) while mutations in cancerous strain were A439P, T457P, and H500Y. Conclusion:Disease-specific variations of cagA of H. pylori strains, in the region of amino acid residues 428-510, were evident among Sudanese patients with different gastroduodenal diseases.A novel mutation (K458N) was detected in a patient with duodenitis, which affects the positive electrostatic surface of cagA. Phylogenetic analysis showed a high level of diversity of cagA from Sudanese H. pylori strains.

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Section: Discussionmentioning

confidence: 76%

Genetic Diversity of thecagAgene ofHelicobacter pyloristrains from Sudanese Patients with Different Gastroduodenal Diseases

Hassan

Idris

Hassan³

et al. 2019

Preprint

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“…Characteristics of selected studies A total of 153 articles were collected in the initial search, and nally 10 eligible articles met our criteria and were included in the current analysis [32][33][34][35][36][37][38][39][40][41] . A owchart of the article search strategy and study selection is presented in Fig.…”

Section: Reultsmentioning

confidence: 99%

Helicobacter pylori cagA Status and Gastric Mucosa-associated Lymphoid Tissue Lymphoma: a Systematic Review and Meta-analysis

Karbaalei

Sahebkar

Yamaoka

et al. 2021

Preprint

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Background: Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is estimated that approximately 0.1% of people infected with H. pylori develop gastric MALT. However, the role of the CagA antigen, the highest causative agent of H. pylori, in increasing the risk of gastric MALT remains unclear and controversial. A systematic review and meta-analysis were conducted to evaluate the effect of cagA status on the development of gastric MALT.Methods: All articles evaluating the status of the cagA gene in the development of gastric MALT were collected using systematic searches in online databases, including PubMed, Scopus, Embase, and Google Scholar, regardless of publication date. The association between cagA and gastric MALT was assessed using the odds ratio (OR) summary. In addition, a random-effects model was used in cases with significant heterogeneity.Results: A total of 10 studies met our inclusion criteria, among which 1,860 patients participated. We observed a meaningful association between cagA status and gastric MALT, especially in Western countries (OR: 1.30; 0.90–1.87 with 95% CIs). However, the heterogeneity was significant; therefore, the results should be interpreted with caution. Surprisingly, a strong positive association was observed between cagA status and high-grade lymphomas (OR: 6.43; 2.45–16.84 with 95% CIs). In addition, no study has evaluated the correlation between cagA and vacA, but we observed an inverse association between vacA and gastric MALT risk (OR: 0.92; 0.57–1.50 with 95% CIs). Conclusion: CagA may not play a significant role in the early stages of gastric MALT, but it can be translocated to B cells and affect the development of high-grade lymphomas.

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“…However, the detailed mechanisms of CagA-mediated pathogenicity still remain unknown. In a recent study, we reported the dominant presence of asparagine (N), serine (S), valine (V), and serine (S) at CagA site 314, 594, 684, and 1077, respectively, in strains isolated from gastric cancer when compared with the presence of amino acids in strain 26695, whereas serine (S), leucine (L), valine (V), and threonine (T) were in the majority of strains isolated from MALT lymphoma patients [ 36 ].…”

Section: Cytotoxin-associated Gene a (Caga)mentioning

confidence: 99%

Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

Ansari

Yamaoka

2020

IJMS

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Helicobacter pylori causes persistent infection in the gastric epithelium of more than half of the world’s population, leading to the development of severe complications such as peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Several virulence factors, including cytotoxin-associated gene A (CagA), which is translocated into the gastric epithelium via the type 4 secretory system (T4SS), have been indicated to play a vital role in disease development. Although infection with strains harboring the East Asian type of CagA possessing the EPIYA-A, -B, and -D sequences has been found to potentiate cell proliferation and disease pathogenicity, the exact mechanism of CagA involvement in disease severity still remains to be elucidated. Therefore, we discuss the possible role of CagA in gastric pathogenicity.

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Differences in amino acid frequency in CagA and VacA sequences of Helicobacter pylori distinguish gastric cancer from gastric MALT lymphoma

Cited by 15 publications

References 41 publications

Genetic Diversity of thecagAgene ofHelicobacter pyloristrains from Sudanese Patients with Different Gastroduodenal Diseases

Genetic Diversity of thecagAgene ofHelicobacter pyloristrains from Sudanese Patients with Different Gastroduodenal Diseases

Helicobacter pylori cagA Status and Gastric Mucosa-associated Lymphoid Tissue Lymphoma: a Systematic Review and Meta-analysis

Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

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