Background Tumor is a new organism formed by abnormal hyperplasia of local tissue cells under the action of various tumorigenic factors. Inflammation plays a decisive role in inducing tumorigenesis, promoting tumor development, invasion and migration. More and more evidence indicate that exosomes are involved in regulating the formation of tumor microenvironment in the process of proinflammatory carcinogenesis, leading to the stimulation of anti-tumor immune response or systemic immunosuppression, and exosomes play a crucial role in the development of tumor. Methods The articles on tumor-derived exosomes and inflammatory responses from January 2005 to January 2024 were collected through Web of Science (WOS), and the inclusion criteria were “Article”, “Review Article” and “Early Access”. Articles obtained after excluding “Book Chapters”, “Editorial Material”, “Proceeding Paper”, “Meeting Abstract” and “Retracted Publication”. Bibliometrics and visualization analysis were carried out on the obtained articles using CiteSpace6.2.R6 and VOSviewer1.6.20. Results Total of 703 articles were included. The number of published documents showed a fluctuating growth trend year by year. A total of 61 countries have participated in the research on the effects of exosomes and inflammatory responses on tumors, among which China and the United States have the largest influence in this field. The obtained articles have been published in 60 journals around the world, among which PLOS ONE and NAT REV IMMUNOL are the journals with the most published articles and the highest co-citations respectively. The article from French author THERY C was cited the most (202 times). As a major researcher on the basic function of exosomes, THERY C established the gold standard for extraction, separation and identification of exosomes, and found that exosomes promote tumor metastasis through direct regulation of miRNA. Her research has had a huge impact on the field. Keyword co-occurrence analysis indicate that extracellular vesicles, inflammation, cancer, miRNAs, mesenchymal stem cells, drug delivery, gastric cancer and circulating endothelial microparticles are the research hotspot at present stage. The main keywords of the cluster analysis show that extracellular vesicles, human papilloma virus, myeloid cells, tumor macro-environment are the current research hotspots and frontier. The research hotspots have developed over time from the time chart of keywords and clustering, especially after 2016, exosomes have established extensive links with drug delivery, cancer treatment, inflammatory response and other fields. Tumor-derived exosomes stimulate receptor cells to secrete pro-inflammatory cytokines and growth factors, enabling immune and inflammatory cells to perceive the intracellular environment of cancer cells even when cancer cells do not express any tumor-specific antigens. For example, in anoxic environment, cancer cells can secrete exosomes containing pro-inflammatory factors to promote the invasion and metastasis of cancer cells. In the complex tumor microenvironment, both tumor cells and various stromal cells will secrete specific exosomes, and promote the development of tumors through various ways, so that tumor cells have drug resistance, and bring adverse effects on the clinical treatment of tumor patients. MicroRNAs and long noncoding RNA as hot keywords play important roles in regulating and mediating tumor development, and their specificity makes them important biomarkers for cancer prediction and diagnosis. Highlighting word analysis shows that microRNAs secreted by leukemia patients can effectively promote the proliferation of malignant cells and the development of cardiovascular diseases. At the same time, exosomes can induce the secretion of some microRNAs in patients, leading to cardiac repair and regeneration. Therefore, the detection and screening of microRNAs plays a crucial role in predicting the incidence of cardiovascular diseases in patients. Conclusion Exosomes have attracted increasing attention due to their significant heterogeneity and ability to regulate the tumor immune microenvironment. However, tumor cell-derived exosomes accelerate tumor progression by enhancing immunosuppression and inflammation, increasing oxidative stress, and promoting angiogenesis, which may lead to poor prognosis. Graphical abstract

Background/Aims: To investigate the etiology of esophageal cancer (EC) related with human papillomavirus (HPV) infection. Materials and Methods: Fresh surgically resected tissue samples and clinical information were obtained from 189 patients. Genomic DNA was extracted, and HPV was detected using polymerase chain reaction (PCR) with HPV L1 gene primers of MY09/11; HPV16 was detected using HPV16 E6 type-specific primer sets. Copies of HPV16 E2, E6, and the human housekeeping gene β-actin were tested using quantitative PCR to analyze the relationship between HPV16 integration and esophageal squamous cell carcinoma and the relationship between the HPV16 integration status and clinical information of patients. Results: Of the 189 samples, 168 HPV-positive samples were detected, of which 76 were HPV16 positive. Among the HPV16 positive samples, 2 cases (E2/E6 ratio>1) were 2.6% (2/76) purely episomal, 65 (E2/E6 ratio between 0 and 1) were 85.6% (65/76) mixture of integrated and episomal, and 9 (E2/E6 ratio=0) were 11.8% (9/76) purely integrated. The results indicate that integration of HPV16 was more common in the host genome than in the episome genome. The prevalence rate of HPV16 integration is increasing with the pathological stage progression of esophageal carcinoma (EC). Conclusion: A high prevalence of HPV16 suggested that HPV16 has an etiological effect on the progress of EC. Integration of HPV16 is more common than episome genome in the host cells, indicating that continuous HPV infection is the key to esophageal epithelial cell malignant conversion and canceration. Cite this article as: Li S, Shen H, Li J, Hou X, Zhang K, Li J. Prevalence of Human papillomavirus 16 integration status in esophageal carcinoma samples. Turk J Gastroenterol 2018; 29: 157-63.

Esophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This study investigated the etiological relationship between HPV infection and the occurrence of esophageal carcinoma at Tangshan City of the Hebei province in China. 189 samples of esophageal carcinoma patients were collected. DNA and RNA were isolated from samples, HPV DNA was detected by polymerase chain reaction (PCR) using My09/11 for HPV L1, and HPV16 was determined using type-specific primer sets for HPV16 E6. The HPV16 integration site was verified by amplification of papillomavirus oncogene transcripts, and HPV16 oncogene transcript products were ligated to the pMD-18 T vector and sequenced to confirm the physical location of HPV16 integration. 168 HPV-positive samples were detected in 189 samples, and among them 76 specimens were HPV16 positive. Approximately 600 bp of the HPV16 oncogene transcript were detected in nine esophageal cancer samples. Sequence analysis revealed that HPV16 E7 integrated into human chromosome 2 in three samples, into human chromosome 5 in one sample, into human chromosome 6 in one sample, into human chromosome 8 in two samples, and into human chromosome 17 in two samples. The results verified that the integrated HPV16 E7 in five samples harbored one mutation of viral DNA compared with the HPV16 sequence provided in GenBank (K02718). The high prevalence of HPV16 suggests that HPV16 may play an etiological role in the development of esophageal cancer. The integration of HPV16 into host cell chromosomes suggests that persistent HPV infection is key for esophageal epithelial cell malignant transformation and carcinogenesis.

Objective: To investigate the epidemiological characteristics and genetic profile of human bocavirus (HBoV) among patients with acute respiratory infection (ARI) in Yucheng, Henan, China.Methods: A total of 1,153 throat swabs were collected from ARI patients between March and June 2023. These samples were tested for 18 pathogens using quantitative chain reaction (qPCR). The VP1 gene were amplified and sequenced from HBoV-positive samples. The viral genetic characterization was analyzed by comparing the HBoV1 sequences with reference sequences.Results: Of the 1,153 samples, the detection rate of HBoV positive was 6.85%, primarily detected in May 2023. The majority of HBoV positive cases were found in children under 5 years old. Clinical manifestations in HBoV-positive patients predominantly were fever and cough, with a clinical diagnosis of lower respiratory tract infection. Other viruses were also detected in 20% of HBoV-positive samples. All HBoV sequences identified in this study belonged to HBoV1, with the Ib sublineage being the predominant strain circulating in Yucheng during March–June 2023.Conclusion: After the implementation of the optimized COVID-19 prevention and control strategy in December 2022, HBoV infection was prevalent in Yucheng, Henan in May-June 2023, mainly among children younger than 5 years old, especially those under 2 years old. The Ib sublineage of HBoV was the dominant circulating strain in Yucheng, Henan during March–June 2023.

Background/Aims: The study aimed to explore the effects of Epstein-Barr virus–-encoded BARF1 in human gastric epithelial cells (GES-1). Materials and Methods: A eukaryotic expression vector carrying BARF1 gene (pcDNA3.1-BARF1) was constructed. The pcDNA3.1-BARF1 was transfected into GES-1 cells, and they were selected by G418. The GES-1 cells lines that expressed BARF1 (GES-1-BARF1) were obtained. The cycle of GES-1-pcDNA3.1 cells (GES-1 cells transfected with empty vector), GES-1-BARF1 cells (GES-1 cells transfected with BARF1), and TPA-GES-1-BARF1(GES-1-BARF1 cells stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) were analyzed by flow cytometry. Colony formation in soft agar and tumorigenicity of the transfected cells in mice with severe combined immunodeficiency (SCID) were also observed. Results: The morphology of GES-1-BARF1 cells were changed from the original shuttle to round, the adhesion between the cells and bottle wall was weakened, and the cells showed overlapping growth. The proliferation rate of GES-1-BARF1 and TPA-GES-1-BARF1 cells were faster than GES-1 and GES-1-pcDNA3.1 cells; the S phase was significantly prolonged for GES-1-BARF1 and TPA-GES-1-BARF1. GES-1-BARF1 and TPA-GES-1-BARF1 cells formed colonies in soft agar, with a cloning rate of 24.2% (58/240) and 40.0% (96/240), respectively; GES-1 and GES-1-pcDNA3.1 cells did not form colonies in soft agar. Tumors were formed in mice with SCID after injecting TPA-GES-1-BARF1 cell groups. Tumor formation did not occur in mice with SCID after injecting GES-1 and GES-1-pcDNA3.1 cell groups, but nodules were formed in the mice with SCID after injecting GES-1-BARF1 cell groups. Conclusion: GES-1-BARF1 cells malignant transformation was induced by transfected BARF1 gene and TPA stimulation. This result indicated that tumor formation not only require oncogenes, but also the stimulation of cancer-promoting substance.

Esophageal carcinoma (EC) is the sixth most deadly of all cancers. It is among the most malignant cancers due to its highly aggressive nature and low survival rate. The incidence of EC is high in Asia, particularly in Southern areas including China, Iran and Japan. There is a large body of evidence to suggest an association between the melanoma antigen gene (MAGE) family and the initiation of cancer; however, there is no clear evidence to suggest an association between EC and MAGE. Discovery of the chemical and physiological processes relevant to the occurrence of EC is vital for clinicians to diagnose and treat this highly aggressive cancer. The present study focused on the association of EC with the expression of MAGE family member A6 (MAGEA6) at the mRNA and protein levels using gene chip, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and immunohistochemistry. The expression of MAGEA6 in human esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) tissue samples were compared with those in paracancerous tissue. The result of the gene chip assay revealed that as the generation grew, there was a significant increase in MAGEA6 transcription in the esophageal epithelial cell line, SHEE Different ESC cell lines also exhibited a significantly higher transcription of MAGEA6 compared with the HaCaT cell line, as determined via reverse transcription‑quantitative PCR. An higher positive rate of MAGEA6 expression in ESCC and EAC tissues was also revealed when compared with paracancerous tissues, as determined via immunohistochemistry. The results indicated that MAGEA6 is highly transcribed and expressed in the development of EC and may therefore serve as a novel biomarker for the diagnosis or treatment of EC.