Gastric cancer (GC) is a leading cause of cancer death, associated with environmental and genetic factors, with increasing incidence in young patients. Recently, as part of the Cancer Genome Atlas (TCGA) project, a comprehensive molecular characterization of gastric adenocarcinoma revealed unique molecular and genetic patterns that were classified GC into four subtypes among which is the Epstein-Barr Virus (EBV)-associated subtype. The EBV-associated subtype is positive for the virus, displays unique genomic landscape and represents 8.7% of the cohort of the TCGA. Since most of the young-onset GC is sporadic and non-hereditary upon former studies, environmental factors may play a role in the pathogenesis of GC among young patients. We hypothesized that the prevalence of EBV-subtype may be higher in young-onset GC than in the average-onset.
Tissue tumor samples of matched cohorts of young-onset (60y) were retrospectively retrieved, DNA was extracted and analyzed by quantitative PCR (qPCR) for EBV using two different EBNA primers to validate the detection of the virus. Clinical data among which patient demographics, tumor location and family history were extracted from medical records and correlated to age.
Twenty-nine young-onset GC patients and 34 average-onset GC patients were enrolled into the study. Median age for the young-onset was 34y (range 21-45) and for the average-onset 69y (60-90). Thirty-six percent of the young-onset were male, compared with 57% in the average-onset. Family history was more prevalent in the average-onset cohort (37% vs. 29%). The distribution of the tumor location differed between the two groups – whereas in the young-onset 36% of the tumors were in the body of the stomach compared with 46% of the average-onset that were in the antrum. EBV was significantly more prevalent in the young-onset cohort (32.1% compared with 11.4% in the average-onset).
Our study indicate that EBV may play a key role in the pathogenesis of young-onset GC. Since young-onset GC is not predominated by hereditary factors, environmental and microbial factors should be further studied as essential contributors, what may potentially govern early detection in high risk populations.
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All authors have declared no conflicts of interest.