Prevalence of multiple infections and the risk of gastric adenocarcinoma development at earlier age

Fattahi, Sadegh; Nikbakhsh, Novin; Taheri, Hassan; Ghadami, Elham; Kosari-Monfared, Mohadeseh; Amirbozorgi, Galia; Asouri, Mohsen; Pilehchian-Langroudi, Maryam; Ranaee, Mohammad; Samadani, Ali Akbar; Paryan, Mahdi; Akhavan‐Niaki, Haleh

doi:10.1016/j.diagmicrobio.2018.04.015

Cited by 32 publications

(31 citation statements)

References 41 publications

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“…The 7 studies that investigated the relationship between HBV and GC involved 53,396 patients with GC and 325,458 any controls ( 26 , 27 , 35 , 47 , 52 , 55 , 56 ). The pooled HBV prevalence in GC was 7.6% (95% CI 4.6%–10.6%, random model, heterogeneity P < 0.001).…”

Section: Resultsmentioning

confidence: 99%

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Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Wang

Chen

et al. 2020

Clinical and Translational Gastroenterology

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INTRODUCTION: Besides Helicobacter pylori and Epstein-Barr virus, other viruses might play potential roles in gastric carcinogenesis. This systematic review and meta-analysis was conducted to compare the prevalence of the viruses between gastric cancer (GC) and any controls. METHODS: Comprehensive literature was searched up to January 25, 2019, and search was updated on April 6, 2020. The studies that compared the prevalence of viruses other than Epstein-Barr virus between GC and healthy or nonmalignant controls were eligible. Stata 12.0 software was used for heterogeneity tests and meta-analyses. Meanwhile, subgroup analysis, sensitivity analysis, and publication bias evaluation were performed where applicable. The power (1–β) was estimated by the PASS 11 software for each individual study. RESULTS: A total of 41 eligible studies were included, concerning 11 kinds of viruses. Prevalence were significantly higher in GC for hepatitis B virus (odds ratio [OR] = 1.39, 95% confidence interval [CI] 1.11–1.75), human cytomegalovirus (OR = 2.25, 95% CI 1.14–4.43), human papillomavirus (HPV) (OR = 1.63, 95% CI 1.05–2.54), and John Cunningham virus (OR = 2.52, 95% CI 1.26–5.04). In subgroup analyses, HPV-16 infection was significantly associated with GC (OR = 2.42, 95% CI 1.00–5.83). DISCUSSION: This study demonstrated that hepatitis B virus, human cytomegalovirus, HPV, and John Cunningham virus were more prevalent in GC. However, the causal relationship between their infection and risk of GC remains inconclusive, and further investigations are required.

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Section: Resultsmentioning

confidence: 99%

“…Five studies sought to detect HCMV in GC with 682 samples (265 for cases with GC, 417 for noncancer controls) ( 10 , 26 , 30 , 37 , 51 ). The pooled HCMV prevalence in GC was 43.1% (95% CI 14.2%–72.0%, random model, heterogeneity P < 0.001).…”

Section: Resultsmentioning

confidence: 99%

Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Wang

Chen

et al. 2020

Clinical and Translational Gastroenterology

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“…Epigenetics consist of DNA methylation, histone modification, histone acetylation, histone phosphorylation and also RNA remodeling which DNA methylation is the most important element [6][7][8][9][10][11][12]. Meanwhile, alongside with the investigation of epigenetics fluctuation in GI cancers, gene expression study must be added in order to have a better comparison and result [13][14][15][16][17][18][19][20].…”

Section: Epigenetic and Cancermentioning

confidence: 99%

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Babaei¹,

Khaksar²,

Zeinali³

et al. 2019

BioMedicine

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Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

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“…In particular, TGFβ1 molecule produced by stromal cells can impart an important role in regulating microenvironmental bystander effects. [65][66][67][68][69] The role of this molecule in three processes of maintaining tissue stability, responding to radiation, and developing bystander effect further confirms a link between the bystander effect and the microenvironmental response to radiation.…”

Section: Radiation Microenvironment and Carcinogenesismentioning

confidence: 65%

The Role of Ionizing Radiation in Cellular Signaling Pathways, Mutagenesis, and Carcinogenesis

rezaiekahkhaie

Keikhaie

2019

Int J Basic Sci Med

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One of the negative effects of ionizing radiation is the alteration of cellular signaling pathways which lead to carcinogenesis and tumorigenesis. In this review, we discussed the impacts of ionizing radiation on cells and cellular signaling pathways. In this regard, exposure to radiation can directly or indirectly alter cellular signaling pathways. Remarkably, irradiated cells release special mediators into cellular matrix, aberrating cell-cell and cell-environment interactions. Most notably, these mediators include nitric oxide (NO), reactive oxygen species (ROS), and cell growth factors which contribute to cellular interactions between irradiated cells and their neighbor cells, a phenomenon known as radiation-induced bystander effect. DNA molecule is the most important cellular compartment damaged by ionizing radiation. On the other hand, the ability of irradiated cells to repair the damaged DNA is very low. Therefore, DNA alternations are passed to the next generations, and ultimately lead to carcinogenesis. The study of ionizing radiations and their impacts on biological systems is of remarkable importance to divulge their impacts on cellular signaling pathways.

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Prevalence of multiple infections and the risk of gastric adenocarcinoma development at earlier age

Cited by 32 publications

References 41 publications

Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

The Role of Ionizing Radiation in Cellular Signaling Pathways, Mutagenesis, and Carcinogenesis

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