Developmental Cell, Journal Year: 2025, Volume and Issue: unknown
Published: May 1, 2025
Language: Английский
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 9, 2025
Inorganic dietary nanoparticles (IDNPs) are frequently utilized as food additives and in packaging, resulting their exposure becoming a substantial yet often overlooked concern for patients with inflammatory bowel disease (IBD). Considering that impaired intestinal barrier function plays central role the pathogenesis of IBD, this review concentrates on roles mechanisms IDNPs (physical, chemical, biological, immune barriers) IBD patients. Previous studies have shown different types varying effects animals diverse states. In context, factors such source, size, shape, dosage, duration action nanoparticles, well species, gender, habits, age animals, significantly influence research outcomes. Future should undertake more comprehensive explorations into sources properties
Language: Английский
Citations
0
Cellular Oncology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 26, 2025
Immune checkpoint plus tyrosine kinase inhibition (IO + TKI) has emerged as the first-line therapy in metastatic renal cell carcinoma (RCC), but no biomarker can predict its efficacy. Thymidine 1 (TK1) is closely associated with immune evasion tumors. Metastatic RCC patients treated by IO TKI were enrolled from two cohorts (ZS-MRCC, n = 45; Javelin-101, 726). High-risk localized also (ZS-HRRCC, 40). TK1 was assessed RNA-sequencing all cohorts, and contexture flow cytometry immunohistochemistry. Higher expression found resistant to (p 0.025). High-TK1 group showed poor progression-free survival (PFS) both ZS-MRCC cohort (P 0.008) Javelin-101 0.036). By multivariate Cox regression, high-TK1 determined an independent factor for PFS (hazard ratio (HR) 3.855, P 0.002). decreased granzyme B+ CD8+ T cells (ρ=-0.22, 0.18), increased PD1+ CD4+ (ρ 0.33, 0.04), PDL1+ macrophages 0.45, < 0.001), regulatory 0.35, 0.03). A novel random forest (RF) risk score built machine learning based on immunologic parameters. Combined surpassed sunitinib monotherapy low RF (HR 0.158, inferior high (HR, 2.195, 0.001). could be a potential indicator therapeutic resistance, under therapy. The may help stratify
Language: Английский
Citations
0
Biomedicines, Journal Year: 2025, Volume and Issue: 13(3), P. 735 - 735
Published: March 17, 2025
Background: Hodgkin lymphoma (HL) is a B-cell-derived malignancy and one of the most frequent types lymphoma. The tumour cells typically exhibit multiple genomic alterations together with aberrantly activated signalling pathways, driven by paracrine and/or autocrine modes. SPP1 (alias osteopontin) cytokine acting as activator has been connected relapse in HL patients. To understand its pathogenic role, here, we investigated mechanisms function deregulated HL. Methods: We screened public patient datasets cell lines for aberrant expression. were stimulated subjected to siRNA-mediated knockdown. Gene protein activities analyzed RQ-PCR, ELISA, Western blot, immuno-cytology. Results: expression was detected 8.3% classic patients line SUP-HD1, chosen serve an experimental model. gene encoding located at chromosomal position 4q22 genomically amplified SUP-HD1. Transcription factor binding site analysis revealed TALE HOX factors potential regulators. Consistent this finding, showed that expressed PBX1 HOXB9 mediate transcriptional activation SPP1. RNA-seq data knockdown experiments indicated signals via integrin ITGB1 Accordingly, NFkB addition MAPK/ERK which turn mediated nuclear import ETS2, activating oncogenic JUNB Conclusions: SUP-HD1 copy number gain homeodomain transcription HOXB9. SPP1-activated MAPK merit further investigation therapeutic targets affected
Language: Английский
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Experimental Hematology and Oncology, Journal Year: 2025, Volume and Issue: 14(1)
Published: April 2, 2025
Language: Английский
Citations
0
Cancer Drug Resistance, Journal Year: 2025, Volume and Issue: unknown
Published: April 24, 2025
Non-small cell lung cancer (NSCLC) represents a formidable challenge in oncology due to its molecular heterogeneity and the dynamic suppressive nature of tumor microenvironment (TME). Despite transformative impact immune checkpoint inhibitors (ICIs) on therapy, majority NSCLC patients experience resistance, necessitating novel approaches overcome evasion. This review highlights shared subtype-specific mechanisms resistance within TME, including metabolic reprogramming, dysfunction, physical barriers. Beyond well-characterized components such as regulatory T cells, tumor-associated macrophages, myeloid-derived suppressor emerging players - neutrophil extracellular traps, tertiary lymphoid structures, exosomal signaling networks underscore TME's complexity adaptability. A multi-dimensional framework is proposed transform cold, immune-excluded tumors into hot, immune-reactive ones. Key strategies include enhancing infiltration, modulating immunosuppressive networks, activating dormant pathways. Cutting-edge technologies, single-cell sequencing, spatial transcriptomics, nanomedicine, are identified pivotal tools for decoding TME personalizing therapeutic interventions. By bridging mechanistic insights with translational innovations, this advocates integrative that combine ICIs modulators, vascular normalizers, therapies STING agonists vaccines. The synergistic potential these poised achieve durable antitumor immunity. Ultimately, vision underscores importance interdisciplinary collaboration real-time profiling refining precision NSCLC, offering blueprint extending advances other malignancies.
Language: Английский
Citations
0
Developmental Cell, Journal Year: 2025, Volume and Issue: unknown
Published: May 1, 2025
Language: Английский
Citations
0