Status of Epstein-Barr Virus Coinfection with<i>Helicobacter pylori</i>in Gastric Cancer

Singh, Shyam; Jha, Hem Chandra

doi:10.1155/2017/3456264

Cited by 53 publications

(45 citation statements)

References 269 publications

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“…Certain co-infections could also increase one’s risk, such as HIV and H pylori [1]. Kayamba et al reported EBVaGC among 60% of HIV patients in Zambia, suggesting HIV increases risk for EBV related gastric cancers [47].…”

Section: Epidemiology Of Ebvagcmentioning

confidence: 99%

“…Until the late 1930s, gastric cancer was the leading cause of cancer death in the United States [1]. Today, it is the third most common cause of cancer-related mortality and the fifth most common cancer worldwide [2].…”

Section: Introductionmentioning

confidence: 99%

“…Today, it is the third most common cause of cancer-related mortality and the fifth most common cancer worldwide [2]. In the United States, it is the 14 th most common cause of cancer, with approximately 10,960 deaths per year [1]. Gastric cancer has a significant socioeconomic, ethnic and geographic disparity, with highest rates in Eastern Asia, followed by Central and Eastern Europe, and lowest in North America and Western Africa [3].…”

Section: Introductionmentioning

confidence: 99%

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Outlooks on Epstein-Barr virus associated gastric cancer

Naseem

Barzi

Brezden-Masley

et al. 2018

Cancer Treatment Reviews

166

143

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Epstein-Barr virus associated gastric cancer (EBVaGC) comprises approximately 10% of gastric carcinomas. Multiple factors contribute to tumorigenesis, including EBV driven hypermethylation of tumor suppressor genes, inflammatory changes in gastric mucosa, host immune evasion by EBV and changes in cell cycle pathways. The unique molecular characteristics of EBVaGC, such as programmed death ligand 1 (PD-L1) overexpression, highlight the potential for using EBV as a biomarker for response to immunotherapy. Few studies have reported benefit from immunotherapy in EBV positive cancers, and clinical trials investigating the impact of checkpoint inhibitors in EBVaGC are currently underway. This review provides the most recent updates on molecular pathophysiology, epidemiology, clinical features and treatment advances pertaining to EBVaGC.

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Section: Epidemiology Of Ebvagcmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Outlooks on Epstein-Barr virus associated gastric cancer

Naseem

Barzi

Brezden-Masley

et al. 2018

Cancer Treatment Reviews

166

143

View full text Add to dashboard Cite

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“…Recientemente se describe que VEB puede en asociación con el Helicobacter pylori generar un sinergismo en la carcinogénesis de esta entidad 22 .…”

Section: Epstein Barr Virusunclassified

Role of Epstein Barr Virus and Gastric Carcinoma

Beltrán-Gárate¹,

Cruz-Vargas²

2018

RFMH

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RESUMENEl cáncer gástrico (CG) es uno de las neoplasias más frecuentes en Perú. Recientemente se ha tipificado los subtipos moleculares en CG. Un subtipo molecular es el asociado al virus Epstein Barr. Esta entidad se presenta con una frecuencia del 10%, en una región no cardial, en pacientes varones y con el subtipo histológico difuso. El pronóstico es mejor comparado a los otros tipos de CG. Presenta sus propias alteraciones moleculares que en el futuro podrían ser susceptibles a terapias target o inmunoterapia. ABSTRACTGastric cancer (CG) is one of the most common neoplasms in Peru. Recently the molecular subtypes have been typified in CG. A molecular subtype is associated with the Epstein Barr virus. This entity presents with a frequency of 10%, in a non-cardiac region, in male patients and with the diffuse histological subtype. The prognosis is better compared to the other types of CG. It presents its own molecular alterations that in the future could be susceptible to target therapies or immunotherapy.

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“…Lipopolysaccharide (LPS) binds to external receptors and activates cellular signal pathways, promoting the occurrence and development of GC [6]. In addition, EBV infection can also promote development of GC [7,8]. Therefore, GC is considered an inflammation-related cancer [2,9].…”

Section: Introductionmentioning

confidence: 99%

Induction of Pro-Inflammatory Response via Activated Macrophage-Mediated NF-κB and STAT3 Pathways in Gastric Cancer Cells

Zhou

Xia

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic inflammation plays an important role in the initiation and progression of gastric cancer (GC). However, the role and relationship of activated macrophages with gastric mucous epithelium cells in initiating and maintaining the inflammatory process during gastric carcinogenesis remains unclear. Methods: The tumour associated macrophages (TAMs) density of gastric cancer was characterized by immunohistochemistry, and the relationship between macrophages and gastric epithelium cells was analysed using an in vitro culture system that imitates the inflammatory microenvironment. The production of pro-inflammatory cytokines was detected by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time PCR (qRT-PCR). MTT assays, Western blotting, qRT-PCR, and luciferase reporter assays were used to detect the effects of cell proliferation, as well as the NF-κB and STAT3 signalling pathways. Results: TAMs infiltrated with a high intensity in GC and were significantly correlated with histology grade (P = 0.012), metastasis (P = 0.001), TNM stage (P = 0.002), and poor prognosis in patients (PFS, P = 0.005; OS, P = 0.028). In addition, IL-6 and IL-8 were elevated in the serum of GC patients and significantly promoted the growth of GC. The exposure of BGC823 gastric cancer cells to a conditioned medium from LPS-treated D-THP-1 cells significantly induced the production of TNF-α, IL-6, IL-1β and IL-8 (P< 0.01). LPS and LPS-treated D-THP-1-conditioned media promoted gastric cancer cell proliferation and triggered the significant activation of NF-κB and STAT3 with a concomitant degradation of IκBα and an increase in JAK2 phosphorylation (P < 0.05). Moreover, gastric cancer cells markedly expressed cell membrane LPS receptors, such as TLR1, TLR4, TLR6, CD14 and MD2. Conclusions: TAMs are closely associated with the growth of GC and prognosis in GC patients. GC cells may directly sustain and amplify the local pro-inflammatory response upon encountering activated macrophages and LPS via NF-κB and STAT3 signalling pathways, thereby promoting tumour progression.

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Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Cited by 53 publications

References 269 publications

Outlooks on Epstein-Barr virus associated gastric cancer

Outlooks on Epstein-Barr virus associated gastric cancer

Role of Epstein Barr Virus and Gastric Carcinoma

Induction of Pro-Inflammatory Response via Activated Macrophage-Mediated NF-κB and STAT3 Pathways in Gastric Cancer Cells

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