Background: The efficacy of CD22 or CD19 chimeric antigen receptor T (CAR‐T) cells in the management of acute lymphoblastic leukemia (ALL) and non‐Hodgkin lymphoma (NHL) was observed. Because antigen loss and lack of CAR‐T‐cell persistence are the leading causes of progressive disease following single‐antigen targeting, we evaluated CD22/CD19 dual‐targeting CAR‐T‐cell therapy efficacy and safety in relapsed/refractory B‐cell malignancies.Methods: The Web of Science, PubMed, Cochrane, and Embase databases were searched until July 2022. Patients confirmed with any relapsed/refractory B‐cell hematological malignancies were included regardless of age, gender, or ethnicity, receiving CD22 and CD19‐dual‐targeting CAR‐T‐cell therapy. The studies conducted on patients with coexisting other cancer were excluded. We used random‐effect models to explore the outcome, and heterogeneity was investigated by subgroup analysis.Results: Fourteen studies (405 patients) were included. The pooled overall response (OR) and complete remission (CR) were 97% and 93%, respectively, for ALL patients. The 1‐year proportions of overall survival (OS) and progression‐free survival (PFS) were 70% and 49%, respectively. For NHL, OR occurred in 85% of patients, and 57% experienced CR. The results illustrated that the 1‐year OS and 1‐year PFS were 77% and 65%, respectively. The subgroup analysis showed that the dual‐targeting modality achieved higher CR in the following cases: coadministration of CD22/CD19‐CAR‐T cells and third‐generation CAR‐T cells combined with ASCT and BEAM pretreatment. The ALL and NHL groups seemed similar in treatment‐related toxicity: all grade cytokine release syndrome (CRS), severe CRS, and neurotoxicity occurred in 86%, 7%, and 12% of patients, respectively.Conclusions: Our meta‐analysis demonstrated that the CD22/CD19 dual‐targeting CAR‐T‐cell strategy has high efficiency with tolerable adverse effects in B‐cell malignancies.

The effectiveness and safety of combination treatments such as chemoimmunotherapies in chronic lymphocytic leukemia and small lymphocytic lymphoma (CLL/SLL) remain controversial. Bruton tyrosine kinase inhibitors (BTKis) are an effective therapy for CLL/SLL patients. This meta-analysis aimed to compare the efficacy and safety of BTKis versus combination therapy in CLL/SLL patients. We searched the PubMed, Cochrane, Medline, and Embase databases through February 2023 for relevant randomized controlled trials (RCTs). Four RCTs (including 1510 patients) were found and met the inclusion criteria. Progression-free survival (PFS) was significantly improved with BTKis when compared to the combination therapy (hazard ratio (HR), 0.30; 95% confidence interval (CI), 0.22–0.40), while a pooled analysis of overall survival did not favor single-agent BTKis over the combination therapy (HR, 0.87; 95% CI, 0.67–1.15). We observed consistent benefits for PFS among patients with high-risk disease characteristics. Although there was no difference in complete response between the two arms (risk ratio (RR), 0.54; 95% CI, 0.20–1.46), BTKi use was related to a better overall response rate (RR, 1.10; 95% CI, 1.04–1.16). The risk of grade ≥3 adverse events (AEs) was comparable between the two arms (RR, 0.82; 95% CI, 0.55–1.23). However, the risk of grade ≥3 AEs was significantly lower in the second-generation BTKi group than in the combination therapy group (RR, 0.73; 95% CI, 0.54–0.98). Overall, BTKis have superior efficacy compared to the combination regimens in patients with untreated or treated CLL/SLL without excess toxicity. Further studies are needed to confirm these results and determine the optimal therapy for managing patients with CLL/SLL.

Glycogen synthase kinase-3 (GSK-3), a serine/threonine kinase, is a vital glycogen synthase regulator controlling glycogen synthesis, glucose metabolism, and insulin signaling. GSK-3 is widely expressed in different types of cells, and its abundant roles in cellular bioregulation have been speculated. Abnormal GSK-3 activation and inactivation may affect its original bioactivity. Moreover, active and inactive GSK-3 can regulate several cytosolic factors and modulate their diverse cellular functional roles. Studies in experimental liver disease models have illustrated the possible pathological role of GSK-3 in facilitating acute hepatic injury. Pharmacologically targeting GSK-3 is therefore suggested as a therapeutic strategy for liver protection. Furthermore, while the signaling transduction of GSK-3 facilitates proinflammatory interferon (IFN)-γ in vitro and in vivo, the blockade of GSK-3 can be protective, as shown by an IFN-γ-induced immune hepatitis model. In this study, we explored the possible regulation of GSK-3 and the potential relevance of GSK-3 blockade in IFN-γ-mediated immune hepatitis.

Head and neck squamous cancer (HNSC) is a prevalent malignancy with a complex genetic profile. Tumor Mutational Burden (TMB) is an emerging biomarker associated with prognostic and therapeutic implications. In this study, we aimed to develop machine-learning models for predicting TMB and patient survival using RNA sequencing data and clinical features. Methods: We collected RNA sequencing data and clinical information of HNSC patients from Gene Expression Omnibus (GEO) (GSE142083) and The Cancer Genome Atlas (TCGA) databases. Machine learning models, including Random Forest, Support Vector Machine (SVM), k-Nearest Neighbors (kNN), and Logistic Regression, were built to predict TMB levels based on patient gene expression profiles. The top 100 important features (genes) were selected from these models to create a survival prediction model. Results: Among the tested models, Random Forest showed the highest accuracy (0.8011), followed by SVM (0.796), kNN (0.777), and logistic regression (0.704). Using the top 100 important genes, we developed a model to predict HNSC patient survival (under 3 years, 3--5 years, and over 5 years). Random forest achieved an accuracy of 0.70, while SVM and kNN reached 0.65. We identified five genes (KRT14, KRT6B, COL1A1, FN1, KRT6C) most closely related to TMB and patient survival. Through KEGG pathway analysis and neural network approaches, we discovered that these genes play a significant role in three pathways: PI3K-Akt signaling pathway, Human papillomavirus infection, and Bacterial invasion of epithelial cells. In Conclusion, our study highlights the potential of machine learning in integrating bioinformatics for predicting TMB and patient survival in HNSC. The identified genes (KRT14, KRT6B, COL1A1, FN1, KRT6C) and related pathways may serve as potential biomarkers and therapeutic targets in HNSC treatment and prognosis.

Background: Diffuse Large B-Cell Lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. While R-CHOP is the standard of care, treatment failure remains a challenge. Pretreatment anemia is a common paraneoplastic manifestation, yet its prognostic utility in Vietnamese patients remains under-investigated. Materials and Methods: A combined prospective and retrospective study was conducted on 106 patients with CD20-positive DLBCL treated with first-line R-CHOP at Hue University of Medicine and Pharmacy Hospital, Hue Central Hospital and Da Nang Oncology Hospital from December 2022 to August 2025. Pretreatment anemia was classified according to NCI-CTCAE v5.0. Clinicopathological features, toxicity, treatment response, and survival were analyzed. Results: The prevalence of pretreatment anemia was 32.1%, with the majority being Grade 1 (26.4%). Anemia was significantly associated with B symptoms (p=0.034) and older age (p=0.039). Regarding efficacy, non-anemic patients had approximately 12 times higher odds of responding (Odds Ratios = 11.897; 95% CI: 1.33–106.34, p = 0.014). Toxicity analysis showed a 3.8% treatment-related mortality rate due to severe infections. There was no statistically significant difference in overall survival or progression-free survival (p > 0.05). Conclusion: Pretreatment anemia is a robust and easily accessible predictor of poor early treatment response in Vietnamese patients with DLBCL treated with R-CHOP. Anemic patients have significantly lower odds of achieving remission. While long-term survival benefits were obscured by treatment-related toxicity in this cohort, the strong link between hemoglobin levels and therapeutic efficacy suggests that anemia should be integrated into risk stratification.

Dengue fever is highly prevalent in tropical and subtropical regions, where it is caused by dengue virus (DENV) and transmitted by arthropods. While DENV infection manifests with a spectrum of clinical symptoms, severe cases can lead to hemorrhagic fever and shock syndrome. Increasing evidence over the past decade has highlighted the neurological complications associated with DENV; however, the underlying mechanisms remain poorly understood. Despite this knowledge gap, various central nervous system (CNS)–targeted drugs have shown promise in mitigating DENV‐induced neurological impairment. In this review, we provide an overview of the neurotropic features of DENV and summarize current evidence on the antiviral effects of selected nervous system‐acting compounds. We also explore the potential mechanisms by which these agents may reduce DENV infection. Given the urgent need for effective dengue therapeutics, repurposing CNS‐targeting drugs represents a promising strategy. Finally, we examine the potential and underlying mechanisms for employing neuropharmaceutical agents as one of the antiviral therapies for DENV infection.