Immune checkpoint B7-H3 is a potential therapeutic target in prostate cancer.

High expression of immune checkpoint molecule B7-H3 (CD276) in many cancer types makes it a promising immunotherapeutic target. Both coinhibitory and costimulatory effects of B7-H3 in tumors have been demonstrated, but the mechanism of B7-H3 immune response under dual effects is open to question. B7-H3 is crucially involved in the migration and invasion, angiogenesis, metabolism and chemotherapy resistance of prostate cancer.

Crosstalk between CD180-overexpression macrophages and glioma cells worsens patient survival through malignant phenotype promotion and immunosuppressive regulation.

Background: Understanding the molecular mechanisms in immunosuppressive regulation is crucial for improving immunotherapeutic strategies. Macrophages, the major immune cells in tumor microenvironment (TME), play a dual role in tumor progression. CD180, primarily expressed in macrophages, remains unclear and requires further investigation.

Cancer immunotherapeutic challenges from autophagy-immune checkpoint reciprocal regulation.

Multiple strategies have been clinically employed as combination partners to enhance the therapeutic efficacy of immune checkpoint inhibitors (ICIs). Although these combinations have demonstrated improved effectiveness in some instances, each presents its own limitations. Autophagy-targeting therapy offers several advantages when combined with ICIs, including enhanced tumor immunogenicity, reduced side effects, and broader applicability to diverse patient populations.

Guselkumab in patients with moderately to severely active ulcerative colitis (QUASAR): phase 3 double-blind, randomised, placebo-controlled induction and maintenance studies.

Background: Interleukin-23 inhibition is effective in treating ulcerative colitis. Guselkumab is a dual-acting, human IgG1, interleukin-23p19 subunit inhibitor that potently neutralises interleukin-23 and can bind to CD64. We aimed to evaluate the efficacy and safety of guselkumab as induction and maintenance therapy in patients with ulcerative colitis.

Immunotherapeutic strategies beyond the PD-1/PD-L1 pathway in head and neck squamous cell carcinoma - A scoping review on current developments in agents targeting TIM-3, TIGIT, LAG-3, and VISTA.

Head and neck squamous cell carcinoma (HNSCC) poses a considerable challenge due to its high incidence and mortality rates. Immunotherapy targeting PD-(L)1 emerges as a promising approach for HNSCC, as it has the potential to trigger a broad and long-lasting anti-tumor response. Nevertheless, the effectiveness of immunotherapy encounters hurdles, and only a small proportion of patients benefit, with many eventually experiencing relapse.

The Landmark Series: Cancer Vaccines for Solid Tumors.

Immunotherapy has become an integral part of the treatment for solid tumors. Cancer vaccines represent a potentially powerful class of immunotherapeutic agents to drive antitumor immunity. Cancer vaccine development involves selecting immunogenic target antigens expressed by tumor cells that can be effectively delivered for uptake by antigen-presenting cells to generate a robust adaptive immune response against tumor.

Targeted nanoparticle delivery unleashes synergistic photothermal and immunotherapeutic effects against hepatocellular carcinoma.

The substantial mortality and morbidity of hepatocellular carcinoma, representing 90% of liver cancers, poses a significant health burden. The effectiveness of traditional hepatocellular carcinoma treatments such as surgical resection, radiotherapy, and chemotherapy is limited, underscoring the need for innovative therapeutic strategies. To this end, we synthesized phthalyl-pullulan nanoparticles encapsulating IR780 (an NIR-responsive heptamethine cyanine dye) and R848 (resiquimod; a TLR7/8 agonist) (PIR NPs).

Zinc-based radioenhancers to activate tumor radioimmunotherapy by PD-L1 and cGAS-STING pathway.

Radiotherapy and immunotherapy have already become the primary form of treatment for non-small-cell lung cancer (NSCLC), but are limited by high radiotherapy dose and low immune response rate. Herein, a multi-pronged strategy using a radio-immuno-enhancer (ZnO-Au@mSiO) is developed by inducing tumor cells apoptosis and reprograming the immunosuppressive tumor microenvironment (TME). The radio-immuno-enhancer employed Au as a radiosensitizer, transition Zn ions as immune activators, which not only tremendously enhances the anti-proliferative activity of radiotherapy toward cancer cells, but also activates the immune response with multi-targets to let "exhausted" T cells "back to life" by triggering immunogenic cell death (ICD), immune checkpoint blockade (ICB) that target PD-1/PD-L1 and cGAS-STING under X-ray irradiation with a low dosage.

FTO activates PD-L1 promotes immunosuppression in breast cancer via the m6A/YTHDF3/PDK1 axis under hypoxic conditions.

Introduction: Altered epigenetic reprogramming enables breast cancer cells to adapt to hypoxic stress. Hypoxic microenvironment can alter immune cell infiltration and function, limiting the effectiveness of immunotherapy.

Objectives: The study aimed to identify how fat mass and obesity-associated protein (FTO) helps breast cancer cells cope with the hypoxic microenvironment and the mechanisms behind breast cancer cell resistance to tumor immunity.

Bacterial ghosts: A breakthrough approach to cancer vaccination.

Cancer is a devastating disease worldwide with high mortality rates and is a foremost concern for society. Immunotherapy has emerged as a promising strategy for treating cancer, harnessing the power of immune system to recognize and kill tumor cells. Bacterial ghosts (BGs), a novel platform in cancer vaccination, are suitable for personalized and effective immunotherapeutic interventions.

Akkermansia muciniphila activates natural killer cells by suppressing the TGF-β signaling pathway in lung adenocarcinoma cells.

Lung adenocarcinoma (LUAD) stands out as a prevalent malignant tumor necessitating innovative strategies to enhance therapeutic outcomes. Akkermansia muciniphila (AKK) has emerged as intricately linked to tumor immunotherapy, yet its impact on natural killer (NK) cells, which play a crucial role in immunotherapy, remains unclear. This study aims to investigate the effects of AKK outer membrane proteins on NK cells in LUAD and elucidate potential associated molecular mechanisms.

Comprehensive analysis of PDE2A: a novel biomarker for prognostic value and immunotherapeutic potential in human cancers.

Phosphodiesterase 2A (PDE2A) plays a pivotal role in modulating cyclic nucleotide metabolism. Recent studies have shown that PDE2A is associated with some tumors, but its expression profiles, prognostic significance, and immunological roles in diverse cancer types remain unclear. Utilizing advanced bioinformatics tools, we performed a comprehensive analysis of PDE2A gene expression in multiple human cancers.

Bioinformatics analysis reveals 's prognostic significance in head and neck squamous cell carcinoma and its association with immune cell infiltration.

Background: Head and neck squamous cell carcinoma (HNSCC) has a poor prognosis due to late diagnosis and complex molecular mechanisms. Vascular endothelial growth factor C (VEGFC) is associated with angiogenesis and lymphangiogenesis. This study aimed to investigate 's prognostic value in HNSCC and its correlation with immune cell infiltration.

Immunotherapy for locally advanced and metastatic basal cell carcinoma: a narrative review.

Background And Objective: Basal cell carcinoma (BCC) is the most common malignancy of humankind, characterized by its low propensity for metastasis and its high recurrence rate. Surgical intervention is the predominant therapeutic approach. However, for cases of locally advanced BCC (laBCC) and metastatic BCC (mBCC), systematic therapy may be the first option.

mutation-related immune checkpoint molecule absent in melanoma 2 () contributes to immune infiltration in pediatric and adult acute myeloid leukemia: evidence from bioinformatics analysis.

Background: The use of FMS-like tyrosine kinase 3 () as a crucial target for kinase inhibitors is well established, but its association with immune infiltration remains unclear. This study aimed to explore the relationship between mutations and immune checkpoint molecules (ICMs) in patients with acute myeloid leukemia (AML).

Methods: The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases were used to identify the ICMs associated with mutations.

SON-1010: an albumin-binding IL-12 fusion protein that improves cytokine half-life, targets tumors, and enhances therapeutic efficacy.

Background: Cytokines have been promising cancer immunotherapeutics for decades, yet only two are licensed to date. Interleukin-12 (IL-12) is a potent regulator of cell-mediated immunity that activates NK cells and interferon-γ (IFNγ) production. It plays a central role in multiple pathways that can enhance cancer cell death and modify the tumor microenvironment (TME).

Siglec15 in blood system diseases: from bench to bedside.

Inhibiting the PD-1/PD-L1 pathway using immunomodulators has demonstrated promising outcomes in clinics. Immunomodulators can effectively target immune checkpoints with a strong preference for the tumor microenvironment (TME). Besides, immunomodulators specifically target the recently discovered inhibitory immune checkpoint, sialic acid-binding immunoglobulin-like lectin (Siglec-15).

Updates in novel immunotherapeutic strategies for relapsed/refractory AML.

Acute myeloid leukemia (AML) is a severe hematological malignancy with poor outcomes, particularly in older adults. Traditional treatment options like high-dose chemotherapy often lead to refractory or relapsed AML, with even worse outcomes. New therapies for relapsed and refractory AML are needed, and this review explores the most recent advancements in immunotherapy in AML.

EBV-induced upregulation of CD55 reduces the efficacy of cetuximab treatment in nasopharyngeal carcinoma.

Cetuximab, an anti-epidermal growth factor receptor (EGFR) antibody, has been shown to improve survival in nasopharyngeal carcinoma (NPC) patients. However, a correlation between the expression of EGFR and the response to cetuximab has not been observed, indicating that the mechanism underlying the effects of cetuximab needs to be further elucidated. The antitumour response involves immunotherapeutic mechanisms that target tumour-associated antigens, including complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC), act either alone or, more often, in combination.

Structure-activity relationship studies and design of a PTPN22 inhibitor with enhanced isozyme selectivity and cellular efficacy.

Protein tyrosine phosphatase non-receptor type 22 (PTPN22) lies downstream of the T cell receptor (TCR) and attenuates T cell signaling by dephosphorylating key effector proteins such as LCK, Zap70, and the intracellular region of the TCR. Recent evidence implicates PTPN22 as an exciting target for enabling immunotherapeutic efficacy against cancer. We carried out structural optimization of a benzofuran salicylic acid-based orthosteric PTPN22 inhibitor 8b, using a combination of crystal structure analysis, synthesis, matched molecular pairs analysis, and biochemical and cell-based assays.

Tumor infiltrating T-cells and loss of expression of SWI/SNF genes in varying stages of clear cell renal cell carcinoma.

Background: Patients with clear cell renal cell carcinoma (ccRCC) metastases face poor prognoses, even with adjuvant therapies. Tumor-infiltrating T-cells and macrophages are critical in targeting tumor cells within the renal microenvironment. Beyond VHL mutations, loss-of-function mutations in SWI/SNF complex genes, including PBRM1, BAP1, ARID1A, SETD2, SMARCA4 (BRG1), and SMARCA2 (BRM), have been implicated in ccRCC progression.

Understanding rare genetic variants within the terminal pathway of complement system in preeclampsia.

Preeclampsia is a common multifactorial disease of pregnancy. Dysregulation of complement activation is among emerging candidates responsible for disease pathogenesis. In a targeted exomic sequencing study of 609 women with preeclampsia and 2092 non-preeclamptic controls, we identified 14 variants within nine genes coding for components of the membrane attack complex (MAC, C5b-9) that are associated with preeclampsia.

Exploring Shared Targets in Cancer Immunotherapy and Cancer-Induced Bone Pain: Insights from Preclinical Studies.

Cancer casts a profound shadow on global health, with pain emerging as one of the dominant and severe complications, particularly in advanced stages. The effective management of cancer-induced pain remains an unmet need. Emerging preclinical evidence suggests that targets related to tumor immunotherapy may also modulate cancer-related pain pathways, thus offering a promising therapeutic direction.

Identification of immunogenic cell death gene-related subtypes and risk model predicts prognosis and response to immunotherapy in ovarian cancer.

Background: Immunogenic cell death (ICD) has been associated with enhanced anti-tumor immunotherapy by stimulating adaptive immune responses and remodeling the immune microenvironment in tumors. Nevertheless, the role of ICD-related genes in ovarian cancer (OC) and tumor microenvironment remains unexplored.

Methods: In this study, high-throughput transcriptomic data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases as training and validation sets separately were obtained and proceeded to explore ICD-related clusters, and an ICD-related risk signature was conducted based on the least absolute shrinkage and selection operator (LASSO) Cox regression model by iteration.

Hepcidin Is a Valuable Therapeutic Target for Colorectal Cancer.

Colorectal cancer (CRC) is one of the most frequent neoplasms and a major cause of cancer death worldwide. Despite recent advances in treatment approaches, the prognosis of advanced CRC remains poor, thus indicating the necessity of more effective treatments for CRC patients. CRC cells produce high levels of hepcidin, a peptide hormone that binds to the membrane-bound ferroportin and promotes its internalization and degradation, thus sequestering iron into the cancer cells with the downstream effect of enhancing tumor growth.