Molecular profiling of high-risk neuroblastoma: clinical and therapeutic implications

Age-associated regulation of chondrocyte hypertrophy in osteoarthritis: Mechanisms, therapeutic implications, and cartilage fate reprogramming.

Cellular senescence in neurodegenerative diseases: A bibliometric analysis and mechanistic synthesis linking translational pathways to therapeutic implications.

Mitofusin 2 in central nervous system disorders: Roles in mitochondrial dynamics and therapeutic Implications.

Targeting STAT3 in Alzheimer's disease: Potential mechanisms and therapeutic implications.

The dual role of formyl peptide receptor 1 (FPR1) in gastrointestinal inflammation and carcinogenesis: mechanisms and therapeutic implications.

Role of pyroptosis in lung cancer: Molecular mechanisms and therapeutic implications.

Autoimmune myelitis represents a heterogeneous group of disorders whose classification has evolved substantially over the past decade. Advances in antibody diagnostics and the widespread use of immune checkpoint inhibitors (ICIs) in oncology have reshaped current concepts, revealing mechanistic and clinical overlaps between antibody-mediated, paraneoplastic, and treatment-induced myelopathies. Antibody-associated myelitis, including myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), aquaporin-4 (AQP4)-immunoglobulin G (IgG)-positive NMOSD and glial fibrillary acidic protein (GFAP) astrocytopathies, accounts for many cases previously labeled idiopathic. Paraneoplastic myelitis is rare but severe, possibly overlapping with NMOSD or GFAP astrocytopathies. In parallel, ICIs have emerged as a novel trigger of immune-mediated myelitis, capable of inducing de novo inflammatory spinal cord syndromes or unmasking latent autoimmune diseases, including AQP4-IgG-positive NMOSD and GFAP astrocytopathies but not MOGAD. Autoimmune myelitis is best conceptualized within an etiological and context-dependent framework integrating antibody status, oncological evaluation, and exposure to immunotherapies. The expanding interface between astrocytopathies, paraneoplastic syndromes, and ICI-associated myelitis has important diagnostic and therapeutic implications, underscoring the need for systematic antibody testing and cancer screening in patients with inflammatory myelopathy.

Oncogenicity and Therapeutic Implications of Molecular Biomarkers in Colorectal Carcinoma.

Immune-metabolic plasticity in AML: Prognostic roles of aCTLs (activated Cytotoxic T Cells) and Kynurenine.

Homologous recombination deficiency (HRD) plays a central role in the pathogenesis and therapeutic vulnerability of epithelial ovarian cancer (EOC), particularly in high-grade serous subtypes. HRD reflects the inability of tumor cells to accurately repair DNA double-strand breaks, rendering them sensitive to platinum-based chemotherapy and poly(ADP-ribose) polymerase (PARP) inhibitors. Several genomic assays have been developed to identify HRD status through the detection of genomic instability patterns, with varying degrees of clinical validation and regulatory approval. Beyond widely adopted assays such as Myriad myChoice® CDx and FoundationFocus™ CDx BRCA LOH, innovative approaches including the Leuven PARPi Benefit Test, circulating tumor DNA-based methods, and artificial intelligence-driven computational pathology are reshaping the diagnostic landscape. Nevertheless, important challenges remain, including the static nature of genomic scar assays, the impact of tumor heterogeneity, and the emergence of resistance through reversion mutations. Functional assays and integrative strategies may provide more dynamic insights into real-time DNA repair capacity, thereby supporting more accurate patient selection and treatment monitoring. Cost-effectiveness analyses further support the integration of HRD testing at diagnosis, highlighting its role in guiding optimal use of PARP inhibitors and improving healthcare resource allocation. This review summarizes the biological rationale, diagnostic methods, therapeutic implications, and economic considerations of HRD in EOC, with a focus on first-line maintenance strategies and future directions in precision oncology.

Understanding antiphospholipid syndrome clinical phenotypes with the guidance of antiphospholipid antibody-related pathogenic mechanisms.

Saposin C (Sap C) deficiency (GDSAPC, OMIM #610539, ORPHA:309252) is an ultra-rare autosomal recessive disorder caused by mutations in the PSAP gene. Sap C functions as an essential activating cofactor of glucosylceramidase (GCase) and facilitates the degradation of glucosylceramide in the lysosome. In the absence of its activator, GCase is structurally intact but its function is impaired, leading to pathological accumulation of glucosylceramide in the lysosome. Sap C deficiency resembles another rare autosomal recessive disorder, Gaucher disease (GD), in which pathogenic variants in the GBA1 gene result in GCase deficiency and accumulation of glucosylceramide within the lysosomal compartment of the mononuclear phagocyte system. Despite the overlapping clinical features of Sap C and GD, the therapeutic implication is utterly different. To date, no specific therapy is approved for Sap C deficiency. Enzyme replacement therapy (ERT), highly effective in GD is biologically implausible in Sap C deficiency, where the GCase structure is normal but lacks its essential activator for its functions. In GD, substrate reduction therapy (SRT) is an alternative to ERT by limiting the synthesis of glucosylceramide through inhibition of glucosylceramide synthase. Given that substrate accumulation is the common pathological consequence in both GD and Sap C deficiency, we hypothesized that SRT with Eliglustat, a potent glucosylceramide synthase inhibitor, could also benefit patients with Sap C deficiency. We describe the first documented therapeutic attempt using eliglustat in Sap C deficiency. A 47-year-old patient with PSAP mutations causing Sap C deficiency who presented with features similar to those seen in GD, has received Eliglustat over the course of 9years, demonstrating an improvement in her hepatosplenomegaly, haematological parameters, biomarkers and bone density, providing proof-of-concept that Eliglustat can be of benefit when the GCase cofactor is deficient. However, no improvement was observed in the patient's seizure activity where future brain penetrant molecules may be of benefit.

Tau phosphorylation homeostasis: Mechanisms, targets, and therapeutic implications in Alzheimer's disease.

Eco-sustainable fabrication of copper oxide nanoparticles from Barleria longiflora: Implications for water treatment and cancer therapeutics

Addition of high-sensitivity troponin to the T-Amylo score for the diagnosis of transthyretin cardiac amyloidosis in acute heart failure: TnT-Amylo.

Furanocoumarin derivatives inhibit MRGPRX2-mediated pseudo-allergy.

Research progress on histone epigenetic modifications in placental trophoblast syncytialization.

Colon cancer with a peritumoural abscess: Real-world evidence on prognostic and therapeutic implications of a disregarded entity.

Chimeric antigen receptor T cell therapy for glioblastoma: overcoming current barriers and strategies to enhance efficacy for therapeutic implications.