Abstract
Despite medical advances, gastric-cancer (GC) mortality remains high in Europe. Bacterial infection with Helicobacter pylori (H. pylori) and viral infection with the Epstein–Barr virus (EBV) are associated with the development of both distal and proximal gastric cancer. Therefore, the detection of these infections and the prediction of further cancer development could be clinically significant. To this end, microRNAs (miRNAs) could serve as promising new tools. MiRNAs are highly conserved noncoding RNAs that play an important role in gene silencing, mainly acting via translational repression and the degradation of mRNA targets. Recent reports demonstrate the downregulation of numerous miRNAs in GC, especially miR-22, miR-145, miR-206, miR-375, and miR-490, and these changes seem to promote cancer-cell invasion and tumor spreading. The dysregulation of miR-106b, miR-146a, miR-155, and the Let-7b/c complex seems to be of particular importance during H. pylori infection or gastric carcinogenesis. In contrast, many reports describe changes in host miRNA expression and outline the effects of bamHI-A region rightward transcript (BART) miRNA in EBV-infected tissue. The differential regulation of these miRNA, acting alone or in close interaction when both infections coexist, may therefore enable us to detect cancer earlier. In this review, we focus on the two different etiologies of gastric cancer and outline the molecular pathways through which H. pylori- or EBV-induced changes might synergistically act via miR-155 dysregulation to potentiate cancer risk. The three markers, namely, H. pylori presence, EBV infection, and miR-155 expression, may be checked in routine biopsies to evaluate the risk of developing gastric cancer.
Highlights
Gastric-cancer (GC) outcomes remain poor despite therapeutic advances
Numerous factors contribute to these poor outcomes, including poor detection during endoscopies, limited surgical experience, and aspects of chemotherapy
The majority of tumors are detected in the advanced stages, resulting in poor prognoses and outcomes since GC is generally not highly sensitive to chemotherapy, a treatment that is only successful in certain patient subgroups
Summary
Gastric-cancer (GC) outcomes remain poor despite therapeutic advances. In Europe in 2012, an estimated 139,600 GC cases were diagnosed, with an incidence rate of 13.7/100,000 person years (age-standardized rate), and approximately 107,000 deaths, with a mortality rate of 10.3 per 100,000 person years [1]. The Medical Research Council Adjuvant Gastric Chemotherapy (MAGIC) trial demonstrated a clear benefit of perioperative and postoperative chemotherapy [4]. This protocol is a current treatment standard, the overall survival rate of patients treated under this regimen in Europe remains only at around 40–45%. An evaluation of the clinical response to chemotherapy revealed that not all patients benefit from neoadjuvant, perioperative, and postoperative regimens. It is, of enormous clinical value to identify markers from biopsies that could predict the chemotherapy response in patients with or without subsequent surgery. We focus on the two different etiologies of GC and outline the molecular pathways through which both agents might act synergistically to potentiate cancer risk
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