Advancing the next generation of cancer treatment with circular RNAs in CAR-T cell therapy.

Chimeric Antigen Receptor T-cell (CAR-T) therapy has revolutionized the treatment of hematological malignancies. However, its effectiveness against solid tumors remains constrained by challenges such as T-cell exhaustion, limited persistence, and off-target effects. These challenges highlight critical gaps in current CAR-T cell therapeutic strategies, particularly for solid tumor applications.

Cytokine modulation and immunoregulation of uterine NK cells in pregnancy disorders.

Uterine natural killer (uNK) cells play a pivotal role in promoting placental development and supporting maternal-fetal immune tolerance, primarily through cytokine regulation and growth factor production. While the importance of uNK cells in pregnancy is well-established, the mechanisms of their interactions with trophoblasts and contributions to various pregnancy complications remain incompletely understood. This review highlights recent advancements in understanding uNK cell functions, with a focus on cytokine production, growth factor secretion, and receptor-ligand interactions, particularly involving killer immunoglobulin-like receptors (KIR) and human leukocyte antigen-C (HLA-C).

Exploring the therapeutic potential of precision T-Cell Receptors (TCRs) in targeting KRAS G12D cancer through development.

Objectives: The Kirsten rat sarcoma virus (KRAS) G12D oncogenic mutation poses a significant challenge in treating solid tumors due to the lack of specific and effective therapeutic interventions. This study aims to explore innovative approaches in T cell receptor (TCR) engineering and characterization to target the KRAS G12D mutation, providing potential strategies for overcoming this therapeutic challenge.

Methods: In this innovative study, we engineered and characterized two T cell receptors (TCRs), KDA11-01 and KDA11-02 with high affinity for the KRAS G12D mutation.

Redefining the tumor microenvironment with emerging therapeutic strategies.

The environment surrounding a tumor, known as the tumor microenvironment (TME), plays a role in how cancer progresses and responds to treatment. It poses both challenges and opportunities for improving cancer therapy. Recent progress in understanding the TME complexity and diversity has led to approaches for treating cancer.

Role of LECT2 in exacerbating atopic dermatitis: insight from and models via NF-κB signaling pathway.

Leukocyte cell-derived chemotaxin 2 (LECT2) is linked to various immune diseases. Previously, we reported that serum LECT2 levels correlate with disease severity in atopic dermatitis (AD) patients. To investigate the role of LECT2 in AD and elucidate its potential mechanisms, we used LECT2 to treat an AD mouse model induced by 1-Chloro-2,4-dinitrobenzene (DNCB) in LECT2 knockout (KO) and wild-type (WT) mice, and an AD cell model using TNF-α/IFN-γ-induced HaCaT cells.

Biomarker discovery in hepatocellular carcinoma (HCC) for personalized treatment and enhanced prognosis.

Hepatocellular carcinoma (HCC) is a leading contributor to cancer-related deaths worldwide and presents significant challenges in diagnosis and treatment due to its heterogeneous nature. The discovery of biomarkers has become crucial in addressing these challenges, promising early detection, precise diagnosis, and personalized treatment plans. Key biomarkers, such as alpha fetoprotein (AFP) glypican 3 (GPC3) and des gamma carboxy prothrombin (DCP) have shown potential in improving clinical results.

Unleashing the potential of CD39-targeted cancer therapy: Breaking new ground and future prospects.

The review article titled CD39 Transforming Cancer Therapy by Modulating Tumor Microenvironment published in June 2024 in Cancer Letters provides a comprehensive overview of CD39's multifaceted roles in cancer, particularly its influence on immunoregulation, angiogenesis, and metabolic reprogramming within the tumor microenvironment (TME). This commentary builds on that foundation by incorporating recent advancements in CD39 research, highlighting unresolved issues, and proposing future research directions. We delve into the therapeutic potential of targeting CD39, addressing clinical translation challenges, and exploring the integration of CD39-based strategies into precision oncology.

The next frontier in immunotherapy: potential and challenges of CAR-macrophages.

Chimeric antigen receptor macrophage (CAR-MΦ) represents a significant advancement in immunotherapy, especially for treating solid tumors where traditional CAR-T therapies face limitations. CAR-MΦ offers a promising approach to target and eradicate tumor cells by utilizing macrophages' phagocytic and antigen-presenting abilities. However, challenges such as the complex tumor microenvironment (TME), variability in antigen expression, and immune suppression limit their efficacy.

CD39 transforming cancer therapy by modulating tumor microenvironment.

CD39 is a pivotal enzyme in cancer, regulating immune response and tumor progression via extracellular ATP and adenosine in the tumor microenvironment (TME). Beyond its established immunoregulatory function, CD39 influences cancer cell angiogenesis and metabolism, opening new frontiers for therapeutic interventions. Current research faces gaps in understanding CD39's full impact across cancer types, with ongoing debates about its potential beyond modulating immune evasion.

BDE-47-induced damage prevented by melatonin in grass carp hepatocytes (L8824).

Polybrominated diphenyl ethers (PBDEs) are toxic to organisms with melatonin (MT) providing protection for tissues and cells against these. This study investigates the mechanism of damage of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) and the cellular protection of MT on grass carp hepatocytes. Grass carp hepatocytes were exposed to 25 μmol/L BDE-47 and/or 40 μmol/L MT for 24 h before testing.

Cytokines and soluble mediators as architects of tumor microenvironment reprogramming in cancer therapy.

Navigating the intricate landscape of the tumor microenvironment (TME) unveils a pivotal arena for cancer therapeutics, where cytokines and soluble mediators emerge as double-edged swords in the fight against cancer. This review ventures beyond traditional perspectives, illuminating the nuanced interplay of these elements as both allies and adversaries in cancer dynamics. It critically evaluates the evolving paradigms of TME reprogramming, spotlighting innovative strategies that target the sophisticated network of cytokines and mediators.

Corrigendum: Targeting HER3 to overcome RGFR TKI resistance in NSCLC.

[This corrects the article DOI: 10.3389/fimmu.2023.

Malignant A-to-I RNA editing by ADAR1 drives T cell acute lymphoblastic leukemia relapse via attenuating dsRNA sensing.

Leukemia-initiating cells (LICs) are regarded as the origin of leukemia relapse and therapeutic resistance. Identifying direct stemness determinants that fuel LIC self-renewal is critical for developing targeted approaches. Here, we show that the RNA-editing enzyme ADAR1 is a crucial stemness factor that promotes LIC self-renewal by attenuating aberrant double-stranded RNA (dsRNA) sensing.

Targeting HER3 to overcome EGFR TKI resistance in NSCLC.

Receptor tyrosine kinases (RTKs) play a crucial role in cellular signaling and oncogenic progression. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) have become the standard treatment for advanced non-small cell lung cancer (NSCLC) patients with EGFR-sensitizing mutations, but resistance frequently emerges between 10 to 14 months. A significant factor in this resistance is the role of human EGFR 3 (HER3), an EGFR family member.

Opportunities and challenges of CD47-targeted therapy in cancer immunotherapy.

Cancer immunotherapy has emerged as a promising strategy for the treatment of cancer, with the tumor microenvironment (TME) playing a pivotal role in modulating the immune response. CD47, a cell surface protein, has been identified as a crucial regulator of the TME and a potential therapeutic target for cancer therapy. However, the precise functions and implications of CD47 in the TME during immunotherapy for cancer patients remain incompletely understood.

Game-changing insights on vertebral skeletal stem cells in bone metastasis and therapeutic horizons.

Greenblatt and his team have unveiled vertebral skeletal stem cells (vSSCs) as a critical player in the landscape of bone metastasis. This commentary delves into the transformative discoveries surrounding vSSCs, emphasizing their distinct role in bone metastasis compared to other stem cell lineages. We illuminate the unique properties and functions of vSSCs, which may account for the elevated susceptibility of vertebral bones to metastatic invasion.

Navigating the Immune Maze: Pioneering Strategies for Unshackling Cancer Immunotherapy Resistance.

Cancer immunotherapy has ushered in a transformative era in oncology, offering unprecedented promise and opportunities. Despite its remarkable breakthroughs, the field continues to grapple with the persistent challenge of treatment resistance. This resistance not only undermines the widespread efficacy of these pioneering treatments, but also underscores the pressing need for further research.

Unraveling the enigma of tumor-associated macrophages: challenges, innovations, and the path to therapeutic breakthroughs.

Tumor-associated macrophages (TAMs) are integral to the tumor microenvironment (TME), influencing cancer progression significantly. Attracted by cancer cell signals, TAMs exhibit unparalleled adaptability, aligning with the dynamic tumor milieu. Their roles span from promoting tumor growth and angiogenesis to modulating metastasis.

Decoding TROP2 in breast cancer: significance, clinical implications, and therapeutic advancements.

Breast cancer is a heterogeneous disease characterized by distinct molecular subtypes, varied prognoses, and differential treatment responses. Understanding the molecular landscape and identifying therapeutic targets, such as trophoblast cell-surface antigen 2 (TROP2), is vital. TROP2 is notably overexpressed in breast cancer, playing a significant role in tumor growth, invasion, metastasis, and treatment resistance.

Role of Txnrd3 in NiCl-induced kidney cell apoptosis in mice: Potential therapeutic effect of melatonin.

Nickel (Ni) exposure is a significant risk factor for kidney dysfunction and oxidative stress injury in humans. Thioredoxin reductase 3 (Txnrd3), an important enzyme in animals, plays a role in maintaining cellular homeostasis and regulating oxidative stress. However, its protective effect against kidney injury has been determined.

Txnrd3 knockout enhancement of lung injury induced by Ni exposure via the VEGF-VEGFR-2 axis and alleviation of this effect by melatonin.

Ni exposure leads to respiratory diseases in mice. Txnrd3 has been shown to have a protective effect on the body, but there is a paucity of empirical research focusing specifically on lung tissue. Melatonin possesses potent antioxidant, anti-inflammatory, and anti-fibrotic effects.

Exploring the Toxic Effects of ZEA on IPEC-J2 Cells from the Inflammatory Response and Apoptosis.

Zearalenone (ZEA) is the most common fungal toxin contaminating livestock and poultry feeding, especially in pigs, causing severe toxic effects and economic losses. However, the mechanism of ZEA damage to the intestine is unknown. We constructed an in vitro model of ZEA toxicity in a porcine small intestinal epithelial cell (IPEC-J2) line.

Malignant A-to-I RNA editing by ADAR1 drives T-cell acute lymphoblastic leukemia relapse via attenuating dsRNA sensing.

Leukemia initiating cells (LICs) are regarded as the origin of leukemia relapse and therapeutic resistance. Identifying direct stemness determinants that fuel LIC self-renewal is critical for developing targeted approaches to eliminate LICs and prevent relapse. Here, we show that the RNA editing enzyme ADAR1 is a crucial stemness factor that promotes LIC self-renewal by attenuating aberrant double-stranded RNA (dsRNA) sensing.