Gastric adenocarcinoma: bioinformatic analysis and its relationship to perineural invasion

This article aims to evaluate some important molecular aspects of gastric adenocarcinoma (STAD), and to evaluate its relationship with Schwann cells and other factors associated with perineural invasion. It is an analysis of open access genomic and proteomic data. Our study allowed us to identify differentially expressed genes in STAD, 1382 increased genes and 1490 decreased genes. These genes are associated with a total of 66 altered pathways, of which we selected 7 for further analysis (“PI3K-Akt”, “cytochrome P450 drug metabolism”, “renin secretion”, “renin-angiotensin system”, “PPAR”, “circadian entrainment”, and “neuroactive ligand-receptor interaction”). Of these pathways, 58 genes with an impact on survival were identified, with a negative impact on survival: COL1A1, COL1A2, COL3A1, COL4A1, COL5A1, COL5A2, COL5A3, COL6A3, ITGA11, ALDH3A1 and ALDH3B2. Other genes were also evaluated for survival and mutations. We identified frequent alterations in the SMAD4, CDH1 and MSH6 genes associated with some syndromes that have an increased risk for the development of gastric cancer. The evaluation of Schwann and STAD cells identified 47 increased and 85 decreased. These genes resulted in 3 significantly altered pathways, however with a small number of genes involved. We identified some genes related to perineural invasion that were reported in the literature, such as the NTN1 and SLIT2 genes, which revealed little evidence of perineural invasion, but evidence of dedifferentiation of Schwann cells in STAD.