We analyzed mutations and gene copy number changes in nontumor, IEN, and ESCC samples, collected from 70 patients. IEN and ESCCs each had similar mutations and markers of genomic instability, including apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like. Genomic changes observed in precancerous lesions might be used to identify patients at risk for ESCC.

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Background and Aim Nowadays, anti‐inflammation treatment is a promising approach for preventing tumorigenesis, and human microflora is closely related to inflammation. This study aimed to investigate the gastric cardiac microbiome and identify inflammation‐related microorganisms for gastric cardiac inflammation. Methods We performed 16S rRNA sequencing on a total of 11 healthy individuals and 89 individuals with different degree of gastric cardiac inflammation. Immunohistochemistry was used for verifying candidate bacteria. Phylogenetic reconstruction of unobserved states (picrust) was used for predicting the pathways involved by cardiac microflora. Results The resident phyla in normal were Proteobacteria, Firmicutes, Bacteroides, and Actinobacteria, and the dominant genus in normal were Halomonas, shewanella, and Comamonas. In the progression of gastric cardiac inflammation, the diversity of cardiac microflora did not change (P > 0.05). However, the composition structure of cardiac microflora varied between healthy and inflamed tissues (P < 0.05). Meanwhile, there were 64 species parallel increased with inflammation degree, especially Helicobacter pylori, Lactobacillus spp. Additionally, inflammation‐related species were detected (P < 0.05), including H. pylori, Acinetobacter ursingii, and Streptococcus agalactiae. Higher H. pylori colonization was positively related to the progression of cardiac inflammation (γ coefficient = 0.678, P < 0.001), and it also influenced the cardiac microbial community structure. Cardiac microflora also participated in DNA repair pathways and is affected by the relative abundance of H. pylori (P < 0.0001). Conclusions Cardiac microflora dysbiosis, especially the increasing of the relevant abundance of H. pylori, promotes the progression of cardiac inflammation.

Although the pathogenic operations of cancer–nerve crosstalk (e.g., neuritogenesis, neoneurogensis, and perineural invasion—PNI) in the peripheral nervous system (PNS) during tumorigenesis, as well as the progression of all cancer types is continuing to emerge as an area of unique scientific interest and study, extensive, wide-ranging, and multidisciplinary investigations still remain fragmented and unsystematic. This is especially so in regard to the roles played by extracellular vesicles (EVs), which are lipid bilayer-enclosed nano- to microsized particles that carry multiple-function molecular cargos, facilitate intercellular communication in diverse processes. Accordingly, the biological significance of EVs has been greatly elevated in recent years, as there is strong evidence that they could contribute to important and possibly groundbreaking diagnostic and therapeutic innovations. This can be achieved and the pace of discoveries accelerated through cross-pollination from existing knowledge and studies regarding nervous system physiology and pathology, as well as thoroughgoing collaborations between oncologists, neurobiologists, pathologists, clinicians, and researchers. This article offers an overview of current and recent past investigations on the roles of EVs in cancer–nerve crosstalk, as well as in neural development, physiology, inflammation, injury, and regeneration in the PNS. By highlighting the mechanisms involved in physiological and noncancerous pathological cellular crosstalk, we provide hints that may inspire additional translational studies on cancer–nerve interplay.