Type I interferons (IFN-I) play pivotal roles in tumor therapy for three decades, underscoring the critical importance of maintaining the integrity of the IFN-1 signaling pathway in radiotherapy, chemotherapy, targeted therapy, and immunotherapy. However, the specific mechanism by which IFN-I contributes to these therapies, particularly in terms of activating dendritic cells (DCs), remains unclear. Based on recent studies, aberrant DNA in the cytoplasm activates the cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling pathway, which in turn produces IFN-I, which is essential for antiviral and anticancer immunity. Notably, STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. These research advancements contribute to our comprehension of the distinctions between IFN-I drugs and STING agonists in the context of oncology therapy and shed light on the challenges involved in developing STING agonist drugs. Thus, we aimed to summarize the novel mechanisms underlying cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle in this review.

Oncolytic viruses (OVs) have emerged as effective gene therapy and immunotherapy drugs. As an important gene delivery platform, the integration of exogenous genes into OVs has become a novel path for the advancement of OV therapy, while the herpes simplex virus type 1 (HSV-1) is the most commonly used. However, the current mode of administration of HSV-1 oncolytic virus is mainly based on the tumor in situ injection, which limits the application of such OV drugs to a certain extent. Intravenous administration offers a solution to the systemic distribution of OV drugs but is ambiguous in terms of efficacy and safety. The main reason is the synergistic role of innate and adaptive immunity of the immune system in the response against the HSV-1 oncolytic virus, which is rapidly cleared by the body’s immune system before it reaches the tumor, a process that is accompanied by side effects. This article reviews different administration methods of HSV-1 oncolytic virus in the process of tumor treatment, especially the research progress in intravenous administration. It also discusses immune constraints and solutions of intravenous administration with the intent to provide new insights into HSV-1 delivery for OV therapy.

Cyclic GMP-AMP synthase (cGAS) recognizes double-stranded DNA (dsDNA) derived from invading pathogens and induces an interferon responseviaactivation of the key downstream adaptor protein stimulator of interferon genes (STING). This is the most classic biological function of the cGAS-STING signaling pathway and is critical for preventing pathogenic microorganism invasion. In addition, cGAS can interact with various types of nucleic acids, including cDNA, DNA : RNA hybrids, and circular RNA, to contribute to a diverse set of biological functions. An increasing number of studies have revealed an important relationship between the cGAS-STING signaling pathway and autophagy, cellular senescence, antitumor immunity, inflammation, and autoimmune diseases. This review details the mechanism of action of cGAS as it interacts with different types of nucleic acids, its rich biological functions, and the potential for targeting this pathway to treat various diseases.

Porcine epidemic diarrhea virus (PEDV), a member of the Alpha-coronavirus genus in the Coronaviridae family, induces acute diarrhea, vomiting, and dehydration in neonatal piglets. This study aimed to investigate the genetic dependencies of PEDV and identify potential therapeutic targets by using a single-guide RNA (sgRNA) lentiviral library to screen host factors required for PEDV infection. Protein kinase C θ (PKCθ), a calcium-independent member of the PKC family localized in the cell membrane, was found to be a crucial host factor in PEDV infection. The investigation of PEDV infection was limited in Vero and porcine epithelial cell-jejunum 2 (IPEC-J2) due to defective interferon production in Vero and the poor replication of PEDV in IPEC-J2. Therefore, identifying suitable cells for PEDV investigation is crucial. The findings of this study reveal that human embryonic kidney (HEK) 293T and L929 cells, but not Vero and IPEC-J2 cells, were suitable for investigating PEDV infection. PKCθ played a significant role in endocytosis and the replication of PEDV, and PEDV regulated the expression and phosphorylation of PKCθ. Apoptosis was found to be involved in PEDV replication, as the virus activated the PKCθ-B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) axis in HEK293T and L929 cells to increase viral endocytosis and replication via mitochondrial apoptosis. This study demonstrated the suitability of HEK293T and L929 cells for investigating PEDV infection and identified PKCθ as a host factor essential for PEDV infection. These findings provide valuable insights for the development of strategies and drug targets for PEDV infection.

Chimeric antigen receptor T (CAR-T)-cell therapy has revolutionized the treatment of hematological malignancies, yet long-term efficacy remains constrained by antigen escape and T-cell dysfunction. Recent advances have rapidly elucidated the molecular underpinnings of antigen escape mechanisms and intrinsic T-cell dysfunction, revealing novel vulnerabilities in current CAR-T paradigms. In this review, we discuss the limitations of CAR-T-cell therapy in hematological malignancies, particularly regarding antigen escape mechanisms and T-cell dysfunction. It is noteworthy that in recent years, multi-targeted CAR-T and engineered CAR-T cells have demonstrated promising clinical efficacy in overcoming drug resistance and relapse in hematological malignancies. Here, we also discuss emerging approaches to enhance the efficacy of CAR-T-cell therapy, including advanced CAR-T-cell engineering techniques, the identification of novel therapeutic targets, and the development of multi-targeted CAR-T-cell strategies.

Introduction: Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype associated with poor prognosis and limited treatment options. This study utilized the SEER database to investigate clinicopathologic characteristics and prognostic factors in TNBC patients.Methods: Machine learning algorithms specifically Gradient Boosting Machines (XGBoost) and Random Forest classifiers were applied to develop survival prediction models and identify key prognostic markers.Results: Results indicated significant predictors of survival, including tumor size, lymph node involvement, and distant metastases. Our proposed work showed better predictive performance, with a C-index of 0.8544 and AUC-ROC values of 0.9008 and 0.8344 for one year and three year overall survival predictions. Major predictors of survival comprises tumor size, HR is 3.657 for T4, lymph node involvement, HR is 3.018 for N3, distant metastases, HR is 1.743 for M1, and prior treatments includes surgery, HR is 0.298, chemotherapy, HR is 0.442, and radiotherapy, HR is 0.607.Discussion: The findings emphasize the clinical utility of AI-driven models in improving TNBC prognosis and guiding personalized treatment strategies. This study provides novel insights into the survival dynamics of TNBC patients and underscores the potential of predictive analytics in oncology.