1. IFGRNS score is a novel prognostic biomarker upregulated in myeloid lineage cells.
2. IFGRNS score correlates with survival outcomes across multiple cancer types.
3. IFGRNS score is associated with tumour pathology and immune microenvironment.
4. IFGRNS score predicts immunotherapy response, with potential for clinical application.

• Spink7, which originates from differentiated epidermal granular keratinocytes of proliferative phase, plays a crucial role during skin wound healing.

• Spink7 promotes inflammation resolution by suppressing multiple proteases activities including uPA, MMP2/9, and KLK5/7 during skin wound healing.

• Spink7 promotes the transition from inflammation to proliferation through inhibiting production of cytokines/chemokines and modulating M2 polarization of macrophage.

• Modulating Spink7 levels by siRNAs in wounds of radiation combined injury facilitates healing by enhancing inflammation.

Virtually all CML patients in blast crisis display SETD2 loss of function

SETD2 loss seems to be accomplished at the posttranslational level rather than being the result of genetic/genomic hits or transcriptional repression

Phosphorylation by Aurora kinase A and ubiquitination by MDM2 contribute to SETD2 proteasome-mediated degradation in blast crisis CML patients

Loss of SETD2 results in increased DNA damage

Graphical abstract of the CKD sendotype discovery pipeline demonstrating the use of multiple omic datasets from patient plasma, patient biopsies and kidney organoid models for both clustering and validation.

Spatial omics, by facilitating visualised precision medicine and accomplishing the spatial localisation of microscopic substances, is poised to emerge as a crucial tool in future research areas, including the exploration of molecular pathways, the implementation of precision targeted therapies and the refinement of disease diagnostic techniques.

1. PCIF1 promotes OSCC progression via m6Am methylation at the MTF2 mRNA 5′ cap.
2. m6Am methylation suppresses MTF2 translation, enhancing tumour cell proliferation and invasion.
3. Targeting PCIF1 holds therapeutic potential for OSCC treatment.

• NSUN2 is upregulated in CRC and associated with poor prognosis of CRC patients.
• NSUN2 promotes CRC malignancy independently of its m5C-enzymatic activity, a mechanism that has not been previously reported.
• The non-m5C carcinogenic roles of NSUN2 may be mediated through interactions with CUL4B, thereby activating the ErbB-STAT3 signalling pathway.
• NSUN2-mediated upregulation of ErbB-STAT3 pathway enhances the sensitivity of CRC to lapatinib treatment.

• Metabolites such as lactate, succinate, and itaconate modulate immune functions through specific sensors.
• AARS1 and AARS2 are identified as key lactate sensors, regulating immune responses via lactylation of cGAS.
• Targeting metabolite sensors holds potential for improving cancer immunotherapies and treating autoimmune diseases.

1. Single-cell analysis identifies transitional CXCL14⁺ myofibroblastic cancer-associated fibroblasts (myCAFs) predominantly exist in the advanced-stage lung adenocarcinoma (LUAD).
2. Transitional CXCL14⁺ myCAFs fuel metastasis by promoting epithelial–mesenchymal transition (EMT) and angiogenesis on the spatial level.
3. CXCL14 is a potential diagnostic marker for LUAD patients and predict the occurrence of metastasis.
4. Transitional CXCL14⁺ myCAFs induce the resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) and JAK1 inhibitor, filgotinib could reverse the effect.

1. ATG16L1-deficient macrophages exhibited impaired LC3B lipidation and accumulation of ROS, resulting in the activation of the NLRP3 inflammasome.

2. Overactivated ATG16L1-deficient macrophages aggravated the damage of alveolar epithelial cells, and increased the release of dsDNA.

3. Released dsDNA activated the STING‒NLRP3 signalling pathway, leading to positive feedback activation of macrophage NLRP3 signalling in macrophages.

• Probe-Capture Metagenome had a significantly higher positive rate than blood culture (51.6% vs. 17.4%, p < .001).

• Combining blood culture and RT-PCR results, Probe-Capture Metagenome achieved a consistency rate of 91.8%.

• Antibiotics were adjusted in 34.8% of patients based on Probe-Capture Metagenome results, and 22.3% of patients experienced a more than 2-point decrease in SOFA score.

Nebulised miR-146a-engineered hucMSC-EVs reduce lung IRI in transplantation by inhibiting NLRP3 inflammasome activation through the IRAK1/TRAF6/NF-κB pathway, improving graft function and reducing inflammation.

We summarised the role of cancer-associated fibroblasts (CAFs) in urological tumours, including their origin, exosomes and extracellular matrix (ECM). CAFs are derived from various precursor cells and can communicate with other cells to form a hypoxic and immunosuppressive microenvironment. Additionally, CAFs can interact with tumour cells through various exosomes and exert a tumour-promoting effect .

1. In theory, CAR-engineering therapy can achieve therapeutic effects by targeting cells expressing specific antigens and thereby eliminating or regulating disease-related cell subpopulations.

2. Although CAR-engineering therapy is currently only approved for the treatment of cancer, it has also shown potential in non-tumour diseases.

3. Immune cells from different sources expand the potential applications of CAR-engineering therapy.

• Primary prostate cancer (PCa) tumours from patients pathologically diagnosed as N0 (pN0) or N1 (pN1) were dually assessed for microRNA (miRs) and mRNA levels using an NGS-based assay.
• A four-mRNA and an eight-miRNA signatures were found.
• The mRNA signatures were further validated using two datasets.
• The combination of serum prostate-specific antigen (PSA) levels or Grade Group with the miR/mRNA signatures separate pN1 from pN0 PCa patients.

Ad-E6/7-HR activates HPV16-specific CD8⁺ T cells in the blood and spleen with enhanced IFN-γ/TNF-α secretion. Ad-E6/7-HR provides both preventative and therapeutic effects for HPV-associated cancers. Ad-E6/7-HR reprograms TME via increased CD8⁺ T-cell infiltration and reduced immunosuppressive MDSCs and M2 macrophages.

1. Response-adapted zanubrutinib plus tislelizumab potentially enhances the efficacy of CAR T-cell therapy for R/R LBCL with acceptable safety profile.

2. This regimen functions independently of genetic subtypes, rendering it more applicable for clinical practice with CAR T-cell therapy.

3. This regimen effectively abrogates T-cell exhaustion, but fails to overcome the immunosuppressive effects of M2 macrophages, providing a rationale for remodelling TME to optimise CAR T-cell therapy.

Inflammation reduces transcriptional inhibition on EEPD1 by lowering KLF4 levels. Elevated EEPD1 subsequently activates ERK phosphorylation. This process exacerbates endothelial inflammation and apoptosis, thus accelerating atherosclerosis development .

• Angiogenesis plays a key role in tumour progression, invasion and metastasis, so strategies targeting angiogenesis are gradually becoming an important direction in cancer therapy.
• Interactions between endothelial cells and stromal cells and immune cells in the tumour microenvironment are significant in angiogenesis.
• The application of antiangiogenic immunotherapy and nanotechnology in antiangiogenic therapy provides a vital strategy for prolonging the survival of cancer patients.

• Antisense oligonucleotide (ASO) treatment in a mouse model of Pompe disease achieves robust knockdown of glycogen synthase (GYS1).

• ASO treatment reduces glycogen content in skeletal muscle.

• Combination of ASO and enzyme replacement therapy (ERT) further improves motor performance compared to ASO alone in a mouse model of Pompe disease.