The tumor microenvironment (TME) is crucial for the onset, development, and resistance to treatment of lung cancer. The tumor microenvironment consisting of a complex array of immune cells, fibroblasts, endothelial cells, extracellular matrix elements, and signaling molecules, facilitates tumor growth and spread while inhibiting the body’s antitumor immune response. In lung cancer, tumor-associated macrophages, cancer-associated fibroblasts, mast cells, and dendritic cells interact through cytokines, chemokines, growth factors, and matrix metalloproteinases to create an immunosuppressive and proangiogenic milieu. Hypoxic conditions within the TME further enhance cancer cell adaptability through hypoxia-inducible factors (HIFs), promoting epithelial–mesenchymal transition, immune evasion, and metastasis. Moreover, miRNAs have emerged as key regulators of gene expression within the TME, offering novel insights into tumor behavior and potential therapeutic targets. Targeting dynamic interactions within the TME, particularly through the modulation of immune responses, angiogenesis, and stromal remodeling, offers promising avenues for precision pharmacological approaches. This review covers the current understanding of the lung TME, highlighting its impact on cancer pathophysiology and treatment strategies. Understanding and therapeutically reprogramming the TME may pave the way for personalized and more effective interventions for lung cancer treatment.

The tumor microenvironment (TME) plays a pivotal role in the initiation, progression, and therapeutic resistance of lung cancer. Comprising a complex network of immune cells, fibroblasts, endothelial cells, extracellular matrix components, and signaling molecules, the TME supports tumor survival and metastasis while suppressing anti-tumor immunity. In lung cancer, tumor-associated macrophages, cancer-associated fibroblasts, mast cells, and dendritic cells interact through cytokines, chemokines, growth factors, and matrix metalloproteinases to shape an immunosuppressive and pro-angiogenic milieu. Hypoxic conditions within the TME further enhance cancer cell adaptability through hypoxia-inducible factors (HIFs), promoting epithelial-mesenchymal transition, immune evasion, and metastatic potential. Moreover, microRNAs have emerged as key regulators of gene expression within the TME, offering novel insights into tumor behavior and potential targets for therapy. Targeting the dynamic interactions within the TME—especially through modulation of immune responses, angiogenesis, and stromal remodeling—offers promising avenues for precision pharmacology. This review summarizes current knowledge of the lung TME, highlighting its impact on cancer patho-physiology and treatment strategies. Understanding and therapeutically reprogramming the TME may pave the way for personalized and more effective interventions in lung cancer management.

Single-cell RNA sequencing (scRNA-seq) has revolutionized neuroscience by enabling the analysis of cellular heterogeneity and dynamic molecular processes at single-cell resolution. In spinal cord research, scRNA-seq provides critical insights into cell type diversity, developmental trajectories, and pathological mechanisms. This review summarizes recent progress in applying scRNA-seq to spinal cord development, injury, and neurodegenerative diseases, and discusses current challenges and future directions. Relevant studies were retrieved from PubMed and Web of Science, focusing on key applications of scRNA-seq, including advances in spatial transcriptomics and mul-ti-omics integration. scRNA-seq has enabled the identification of distinct spinal cord cell populations and revealed gene regulatory networks driving development. In injury models, it has uncovered the temporal dynamics of immune and glial responses, alongside potential regenerative processes. In neurodegenerative conditions, scRNA-seq has highlighted cell-specific vulnerabilities and molecular changes. Inte-gration with spatial transcriptomics and computational tools, such as machine learning, has further improved the resolution of spinal cord biology. However, challenges remain in data complexity, sample acquisition, and clinical translation. Single-cell tran-scriptomics is a powerful approach to understanding spinal cord biology. Its integration with emerging technologies will advance both basic research and clinical applications, supporting personalized and regenerative therapies. Addressing technical and analyt-ical barriers is essential to fully realize the potential of scRNA-seq in spinal cord science.

Study Design: Retrospective cohort study. Objectives: Thoracic ossification of the posterior longitudinal ligament (OPLL) is traditionally considered progressive, raising concern that the ossified mass left after posterior decompression and instrumented fusion (PDF) may enlarge. We characterized long-term CT-based changes in focal OPLL thickness after PDF and assessed whether the residual mass continued to enlarge. Methods: We reviewed all consecutive adult patients who underwent PDF for thoracic OPLL (2009–2023) with ≥2 years of follow-up. Maximum OPLL thickness was measured on axial CT and tracked longitudinally; a predefined 2-mm threshold, prespecified as the minimal clinically important difference, classified change. Thoracic kyphosis (TK) and modified Japanese Orthopaedic Association (mJOA) scores were also assessed. Results: Twenty-six patients (mean age 49.5 ± 12.4 years; 15 men) were followed 5.4 ± 2.7 years (range 2–11). Mean axial OPLL thickness changed from 7.02 ± 1.58 to 6.90 ± 2.01 mm (Δ −0.12 ± 1.03 mm). By the 2-mm threshold, 92.3% were stable, 3.8% decreased, and 3.8% increased; directional decreases occurred in 69.2% and increased with longer follow-up (37.5%, 77.8%, 88.9%; p = 0.023). TK increased (+6.2°, p < 0.001) but was uncorrelated with thickness change (r = 0.250). mJOA improved from 7.3 to 8.7 (p = 0.0001; recovery rate 34.9%; excellent/good 53.8%). The mean change was equivalent to zero within ±2 mm (two one-sided tests p < 0.001). Conclusions: Focal thoracic OPLL thickness remained predominantly stable after PDF, with threshold-level progression infrequent and neurological improvement maintained. Focal radiographic stability, rather than continued enlargement of the residual mass, was the predominant postoperative course after PDF.