Transforming growth factor beta 1 (TGF-β1) modulates Epstein-Barr virus reactivation in absence of Helicobacter pylori infection in patients with gastric cancer

Shukla, Sanket K.; Khatoon, Jahanarah; Prasad, Kashi Nath; Prakash, Ravi; Singh, Amrita; Kumar, Sushil; Ghoshal, Uday C; Krishnani, Narendra

doi:10.1016/j.cyto.2015.07.023

Cited by 15 publications

(17 citation statements)

References 25 publications

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“…The expression of miR-21 in gastric tissues activates the COX-2, which is a key enzyme responsible for conversion of arachidonic acid into prostaglandins (PGE-2). Upregulated expression of COX-2 was noticed in H. pylori infected colon and stomach [46]. PGE-2 transforms the enterocytes into metaplasia and pre neoplastic gastric lesions, these lesions were resistance to apoptosis and express broad spectrum of growth factors and cytokines.…”

Section: Mir-21-induced Expression By H Pylori Infection In Gastric mentioning

confidence: 96%

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Significance of microRNA 21 in gastric cancer

Sekar

Ravindran

Thirugnanasambantham

et al. 2016

Clinics and Research in Hepatology and Gastroenterology

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Section: Mir-21-induced Expression By H Pylori Infection In Gastric mentioning

confidence: 96%

“…Role of H. pylori infection induced miR-21and cascade of gene activation in gastric cancer progressions[2,28,45,46].…”

mentioning

confidence: 99%

Significance of microRNA 21 in gastric cancer

Sekar

Ravindran

Thirugnanasambantham

et al. 2016

Clinics and Research in Hepatology and Gastroenterology

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“…Interestingly, presence of EBV has been shown to increase the oncogenic potential of the H. pylori protein, CagA [1]. Conversely, a study by Shukla et al suggested that H. pylori might prevent EBVaGC by attenuating TGF-β expression, which is required for EBV reactivation [66]. …”

Section: Ebv and Helicobacter Pylorimentioning

confidence: 99%

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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“…H. pylori positive patients show increased anti-EBV IgG titre which suggests H. pylori role in augmenting EBV DNA load and higher immune responses [291]. However, some study is also available which suggested that H. pylori attenuated TGF- β expression which reactivates EBV lytic phase and might play a role in preventing EBV lytic reactivation and preventing GC [292]. Therefore, the mechanism of coexistence for H. pylori and EBV must be studied to find the probable and potential pathogenic roles for both pathogens.…”

Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Singh

Jha

2017

Journal of Oncology

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Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.

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Transforming growth factor beta 1 (TGF-β1) modulates Epstein-Barr virus reactivation in absence of Helicobacter pylori infection in patients with gastric cancer

Cited by 15 publications

References 25 publications

Significance of microRNA 21 in gastric cancer

Significance of microRNA 21 in gastric cancer

Outlooks on Epstein-Barr virus associated gastric cancer

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

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