Explore the vast range of titles available.

Immune checkpoint blockade has vastly changed the landscape of cancer treatment and showed a promising prognosis for cancer patients. However, there is still a large portion of patients who have no response to this therapy. Therefore, it's essential to investigate biomarkers to predict the efficacy of immune checkpoint inhibitors. This article summarizes the predictive value of established biomarkers, including programmed cell death ligand 1(PD-L1) expression level, tumor mutational burden, tumor-infiltrating lymphocytes, and mismatch repair deficiency. It also addresses the predictive value of tumorous mutations, circulation factors, immune-related factors, and gut microbiome with immunotherapy treatment. Furthermore, some of the emerging novel biomarkers, and potential markers for hyper progressive disease are discussed, which should be validated in clinical trials in the future.

Background Vitreoretinal lymphoma (VRL) is regarded as a subtype of primary central nervous system lymphoma (PCNSL). Hence, extending progression‐free survival (PFS) is crucial for enhancing the prognosis of VRL patients. Nevertheless, a lack of standard treatment options currently exists for VRL. This systematic review aims to explore the most optimal treatment strategy. Methods The methods for this systematic review and meta‐analysis adhered to PRISMA guidelines and followed a protocol registered on the PROSPERO registry. A search was conducted on PubMed, Embase, and Scopus up to October 14, 2023, using predefined search terms. Primary endpoints included overall response rate (ORR) and complete response rate (CRR), while secondary endpoints comprised overall survival (OS) and progression‐free survival (PFS). Results Thirty‐seven studies comprising 801 patients were included in the meta‐analysis. The pooled CRR was 85%, and the ORR was 93%. The pooled 1‐year PFS was 83%, and the 2‐year PFS was 58%. The 1‐year OS was 92%, and the 2‐year OS was 80%. The combined median PFS was 22.87 months, and the median OS was 51.19 months. Survival analysis of the extracted data showed significant associations between PFS and OS with systemic therapy (p = 0.00098 and p = 0.0091) and multi‐strategy combination therapy (p = 0.0081 and p = 0.007); however, age, gender, and bilateral involvement exhibited no significant relationship (p > 0.05). Conclusions In conclusion, while existing treatment strategies have led to higher remission rates and longer OS for VRL patients, PFS remains suboptimal. The primary focus of future clinical and basic research will be to explore effective treatment strategies for controlling disease recurrence or progression. Trial Registration: This meta‐analysis was registered in the international prospective register of systematic reviews (PROSPERO) (CRD42023400305).

Asparaginase (ASP) is the cornerstone drug in the treatment of extranodal NK/T-cell lymphoma (ENKTCL), and the mechanisms of resistance to ASP remain largely unknown. Long non-coding RNAs play important roles in chemotherapy resistance in various cancers. However, the expression of BCYRN1 and its role in ENKTCL still remain unidentified. Lentivirus-mediated BCYRN1 overexpression and knockdown were performed in SNK-6 cells. Cell autophagy was analyzed by adenovirus expressing GFP-LC3B fusion protein. RNA pull-down and RNA Binding Protein Immunoprecipitation Assay were performed to investigate the relationship between BCYRN1 and p53. Western blot analysis was performed to assess the effect of BCYRN1 on different autophagy pathways. Finally, in vivo xenograft tumor model was constructed to analyze the effect of BCYRN1 on tumor growth and ASP resistance. BCYRN1 was overexpressed in ENKTCL than normal NK cells, and patients with higher expression had significantly inferior progression-free survival (PFS). The IC50 value of ASP was significantly increased in BCYRN1-overexpressed SNK-6 cells and BCYRN1 overexpression could resist the inhibitory effect of ASP on proliferation. ASP could induce concurrent apoptosis and autophagy in ENKTCL, and the latter process was enhanced by overexpression of BCYRN1, mainly through affecting both PI3K/AKT/mTOR and p53/mTOR pathways. BCYRN1 could induce the degradation of p53 via ubiquitination, thus resulting in enhancement of autophagy and ASP resistance, which could be reversed by drug-induced autophagy inhibition. The effect of BCYRN1 on tumor growth and autophagy were confirmed in vivo xenograft model. It was found that BCYRN1 was a valuable prognostic biomarker in ENKTCL. BCYRN1 could promote resistance to ASP by inducing autophagy, which could be reversed by inhibition of autophagy. Our findings highlight the feasibility of combining autophagy inhibition and ASP in the treatment of ENKTCL.

Background. Diffuse large B cell lymphoma (DLBCL) is a life-threatening malignant tumor characterized by heterogeneous clinical, phenotypic, and molecular manifestations. Given the association between immunity and tumors, identifying a suitable immune biomarker could improve DLBCL diagnosis. Methods. We systematically searched for DLBCL gene expression microarray datasets from the GEO database. Immune-related genes (IRGs) were obtained from the ImmPort database, and 318 transcription factor (TF) targets in cancer were retrieved from the Cistrome Cancer database. An immune-related classifier for DLBCL prognosis was constructed using Cox regression and LASSO analysis. To assess differences in overall survival between the low- and high-risk groups, we analyzed the tumor microenvironment (TME) and immune infiltration in DLBCL using the ESTIMATE and CIBERSORT algorithms. WGCNA was applied to study the molecular mechanisms explaining the clinical significance of our immune-related classifier and TFs. Results. Eighteen IRGs were selected to construct the classifier. The multi-IRG classifier showed powerful predictive ability. Patients with a high-risk score had poor survival. Based on the AUC for three- and five-year survival, the classifier exhibited better predictive power than clinical data. Discrepancies in overall survival between the low- and high-risk score groups might be explained by differences in immune infiltration, TME, and transcriptional regulation. Conclusions. Our study describes a novel prognostic IRG classifier with strong predictive power in DLBCL. Our findings provide valuable guidance for further analysis of DLBCL pathogenesis and clinical treatment.

The technology of using light-emitting diodes as light source for visible communication is one of the hot spots in the field of optical wireless communication. This paper analyses the characteristics of visible communication technology, focuses on the key technologies needed for the realization of visible communication system in a specific room, and studies the feasibility and application prospects of indoor visible communication combined with the development status at home and abroad.

Dichloroacetate (DCA) is an inhibitor of pyruvate dehydrogenase kinase, which promotes the flux of carbohydrates into mitochondria and enhances the aerobic oxidation of glucose. DCA has previously been demonstrated to exhibit antitumor properties. The present study revealed that treatment with DCA induced increased levels of autophagy-associated proteins in esophageal squamous carcinoma cells while minimally affecting apoptosis. The present study examined the localization of light chain (LC)-3 by adenovirus infection with a green fluorescent protein (FP)-red FP-LC3 reporter construction and confirmed that DCA treatment induced significant autophagy. Furthermore, the inhibition of DCA-induced autophagy facilitated cell apoptosis and improved the drug sensitivity of esophageal squamous carcinoma cells to DCA and 5-FU (5-fluorouracil). The proliferation of TE-1 cells was markedly inhibited at low concentrations of DCA and 5-FU treatment when subjected to Atg5 mRNA interference, indicating that autophagy performed a protective role in cell survival upon DCA treatment. To determine the underlying mechanism of DCA-induced autophagy, the present study measured alterations in autophagy-associated signaling pathways. Notably, the protein kinase B (Akt)-mechanistic target of rapamycin (mTOR) signaling pathway, an important negative regulator of autophagy, was demonstrated to be suppressed by DCA treatment. These results may direct the development of novel strategies for the treatment of esophageal squamous carcinoma based on the combined use of DCA and autophagy inhibitors.

Chimeric antigen receptor T (CAR-T) cell therapy has demonstrated remarkable efficacy in relapsed/refractory large B-cell lymphoma (R/R LBCL), yet nearly 40-60% of patients fail to achieve durable responses. The mechanisms underlying interpatient variability in CAR-T expansion and persistence remain incompletely understood. In this exploratory study, we preliminarily investigated the associations between baseline peripheral blood immune subsets, CAR-T expansion kinetics, and clinical outcomes. We retrospectively analyzed 33 patients with R/R LBCL who received CD19/CD22 bispecific chimeric antigen receptor T-cell therapy (CAR2219) at our center. Peripheral blood samples were analyzed by flow cytometry. CAR-T cell expansion was monitored longitudinally, and group-based trajectory modeling (GBTM) classified patients into expansion patterns. Associations with progression-free survival (PFS) and overall survival (OS) were evaluated using Kaplan-Meier analysis and Cox regression. Twenty-two patients received tislelizumab (a PD-1 inhibitor) as maintenance therapy (200 mg intravenously every 3 weeks) starting on day 28 after CAR-T infusion. This regimen was not used as prior therapy, bridging therapy, or co-infusion, rather, it was designed to potentially enhance CAR-T persistence after the initial expansion phase. Given the small sample size (n = 33) and the exploratory nature of the analyses, all findings are hypothesis-generating only and require validation in large prospective cohorts. Two distinct CAR-T expansion trajectories were identified: a low-expansion group (Group 1, n = 18) and a high-expansion group (Group 2, n = 15). Compared to Group 1, Group 2 exhibited higher peak expansion (Cmax, p < 0.001), greater total exposure (area under the curve (AUC), p < 0.001), and delayed time to peak (Tmax, 14 days vs. 10 days). Group 2 had higher baseline naive T cells (FDR-adjusted p = 0.024), helper T cells (FDR-adjusted p = 0.006), and CD4/CD8 ratio (FDR-adjusted p = 0.049), and fewer activated regulatory T cells (Tregs) (FDR-adjusted p = 0.018). Higher CD4/CD8 ratio associated with longer PFS (HR 0.41, 95% CI 0.17-0.73, p = 0.047). In exploratory subgroup analyses, a directional trend toward longer PFS was noted among patients with high baseline PD-1 expression who received PD-1 inhibitor maintenance therapy, whereas no such trend was observed in those without maintenance. These hypothesis-generating observations require validation in larger prospective cohorts. Baseline immune cell composition may associate with CAR-T expansion and outcomes in R/R LBCL. Exploratory subgroup analyses suggested that the direction of association between baseline PD-1 expression and PFS may differ according to receipt of PD-1 inhibitor maintenance therapy (initiated on day 28 post-infusion), though no statistical significance was reached in either subgroup. Current evidence does not support the clinical use of baseline PD-1 expression as a predictive biomarker, and further validation in prospective studies is warranted.

Background： Congenital heart disease （CHD） is the most common congenital malformations with high mortality and morbidity. The prevalence of CHD reported previously ranged from 4 per 1000 live births to 50 per 1000 live births. In this cross-sectional study, we aimed to document the prevalence of CHD in Langfang district of Hebei Province, China by analyzing data collected by hospitals located in 11 the counties of the district, as supported by a public health campaign. Methods： A total of 67,718 consecutive 3-month-old infants were included from July 19,2012 to July 18, 2014. Structural abnormalities were diagnosed based on echocardiography findings, including two-dimensional and color Doppler echocardiography results. Results： Of the 67,718 infants, 1554 were found to have cardiac structural abnormalities. The total prevalence of CHD was 22.9 per 1000 live births, a value significantly higher than the previously reported prevalence of 8 cases per 1000 live births. The top five most common cardiac abnormalities were as follows： atrial septal defect （ASD, 605 cases, 8.93‰）; ventricular septal defect （550 cases, 8.12‰）; patent ductus arteriosus （228 cases, 3.37‰）; pulmonary stenosis （66 cases, 0.97‰）; and tetralogy of Fallot （32 cases, 0.47‰）. The CHD prevalence differed by gender in this study （x^2 = 23.498, P 〈 0.001）, and the majority of ASD cases were females. Regional differences in prevalence were also found （x^2 = 24.602, P 〈 0.001）; a higher prevalence was found in urban areas （32.2 cases per 1000 live births） than in rural areas （21. 1 cases per 1000 live births）. There was a significant difference in the prevalence of CHD in preterm versus full-term infants （x^2 - 133.443, P 〈 0.001 ）. Prevalence of CHD in infants of maternal aged 35 years or over was significantly higher （x^2 86.917, P 〈 0.001）. Conclusions： The prevalence of CHD in Langfang district was within the range reported using echocardiography. Echocardiography can be used to early diagnose the CHD.