Shenhong Qu

The treatment response to immunotherapy for nasopharyngeal carcinoma (NPC) exhibits significant interindividual variability. As a biomarker closely associated with NPC, Epstein-Barr virus (EBV) DNA holds substantial importance in this research context. However, there is still an insufficient comprehensive assessment of the current research status and development trends of EBV DNA as a biomarker for NPC immunotherapy in the existing literature. In this study, we conducted a bibliometric analysis of 164 original English articles and reviews on EBV DNA as a biomarker in NPC immunotherapy, utilizing the WoSCC database along with CiteSpace and Bibliometrix software tools. The analysis and visualization were performed from the following aspects: publication trends, country/region distribution, keyword co-occurrence networks, patterns of co-authorship and co-citation, and the evolution of cited journals and themes. Since 2017, research in this area has developed rapidly, with China and the United States being the two main contributors. The primary research hotspots include PD-1 inhibitors, antitumor activity, and exploration of molecular mechanisms. The field showed a clear shift from traditional themes centered on tumor burden, recurrence, radiotherapy, and prognosis toward immunotherapy-related themes, including PD-1, clinical trials, and dynamic monitoring. EBV DNA is increasingly viewed as a dynamic biomarker that integrates viral biology, tumor burden, and treatment response in NPC. Plasma EBV DNA is mainly derived from apoptotic or necrotic EBV-positive tumor cells, making its baseline level a surrogate of systemic tumor burden. Its kinetic changes during immunotherapy indicate tumor control, while fluctuations or elevations reflect combined effects of tumor destruction, viral reactivation and host immunity. Its value in prognostic stratification and dynamic monitoring has been relatively well established. Broader clinical use will require assay standardization and prospective validation.

Background: Non‐small cell lung cancer ( NSCLC ) is the leading cause of cancer‐related death worldwide. Cyclin‐dependent kinase 4 ( CDK4 ) is a well‐validated oncogenic driver in NSCLC , yet current CDK4 inhibitors—predominantly based on the aminopyrimidine scaffold—are limited by structural homogeneity and the rapid emergence of acquired resistance, underscoring the need for novel chemotypes. Methods: We employed a HuProt human proteome microarray to screen for direct cellular targets of artesunate, an FDA ‐approved artemisinin derivative. Candidate interactions were validated by molecular docking, surface plasmon resonance ( SPR ), and in vitro kinase assays. Functional effects were assessed in A549 and H1299 NSCLC cell lines using flow cytometry and Western blotting. Results: Artesunate was identified as a direct binder of CDK4 , with molecular docking revealing a strong binding affinity (−7.069 kcal/mol). SPR analysis confirmed this interaction with a K _d of 488 μM , and in vitro kinase assays demonstrated potent inhibition of CDK4 /Cyclin D3 activity ( IC ₅₀ = 0.2943 μM ). Treatment with artesunate induced significant G0 / G1 cell cycle arrest in both A549 and H1299 cells. This effect was mediated through inhibition of the CDK4 –Rb– E2F axis, as evidenced by dose‐dependent suppression of Rb phosphorylation at Ser780 and Ser795. Conclusion: Our findings establish artesunate as a structurally distinct, non‐aminopyrimidine CDK4 inhibitor with potent biochemical and cellular activity in NSCLC models. This work provides a promising therapeutic strategy to circumvent resistance associated with current CDK4 inhibitors and supports the repurposing of artesunate for CDK4 ‐driven cancers.

Background: The relationship between changes in alcohol consumption and hepatic steatosis among alcohol consumers remains poorly understood. This study aimed to evaluate the association between changes in alcohol consumption and hepatic steatosis in a large population-based cohort of alcohol consumers.Methods: This study included 33,427 participants with reported alcohol consumption, categorized as mild, moderate, or heavy at baseline and imaging visits. Hepatic steatosis was assessed via magnetic resonance (MR) imaging during the imaging visit.Results: 9,131 (27.3%) participants were diagnosed with hepatic steatosis at imaging visit. After adjusting for confounders, mild drinkers who progressed to moderate (aOR 1.26, 95% CI 1.10–1.44) or heavy drinking (aOR 1.70, 95% CI 1.12–2.57) had elevated odds of hepatic steatosis compared to stable mild drinkers. Moderate drinkers who maintained moderate drinking (aOR 1.36, 95% CI 1.21–1.53) or progressed to heavy drinking (aOR 2.27, 95% CI 1.84–2.79) also showed increased risk compared to those who transitioned to mild drinking. Conversely, heavy drinkers who transitioned to moderate (aOR 0.58, 95% CI 0.47–0.72) or mild drinking (aOR 0.34, 95% CI 0.25–0.45) had significantly lower odds compared to stable heavy drinkers. Stratified analyses revealed that males, individuals under 65 years, those with higher BMI, and hypertensive patients were more susceptible to hepatic steatosis with increased alcohol consumption.Conclusion: Increasing alcohol intake raises the odds of hepatic steatosis, while reducing intake lowers the odds. Public health strategies should focus on decreasing alcohol consumption to alleviate the burden of hepatic steatosis.

Observational studies have suggested associations among the gut microbiome, immune cells, and the risk of malignant neoplasms of nasopharynx. However, the causality of these relationships remains unclear. Thus, we conducted multiple Mendelian Randomization analyses to estimate the causal association of gut microbiota with the risk of malignant neoplasms of nasopharynx and to evaluate the mediating effect of immune cells on this causal pathway. Genetic variants extracted from genome-wide association studies of human gut microbiota compositions (n = 211), immune cell traits (n = 731) and malignant neoplasms of nasopharynx served as instrumental variables for calculating causal associations and mediating effects. Four gut microbiota compositions and eight immune cell traits exhibited detrimental causal effects, while three gut microbiota compositions and fifteen immune cell traits demonstrated protective effects. Interestingly, the causal association of genus Candidatus Soleaferrea id.11350 was no longer significant after adjusting for two established immune cell traits (HLA DR + + monocyte %leukocyte and HLA DR + + monocyte % monocyte). Moreover, HLA DR + + monocyte %leukocyte exhibited a mediating effect (OR 0.75, 95% CI 0.59–0.96) on the causal pathway of genus Candidatus Soleaferrea id.11350–malignant neoplasms of nasopharynx, with a mediating proportion of 21.59%. To our knowledge, this study is the first to identify potential therapeutic targets and elucidate mechanistic insights for malignant neoplasms of nasopharynx interventions involving gut microbiota and immune cell traits; however, these findings warrant further validation through adequately powered randomized clinical trials (RCTs).