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Metastases are the main cause of cancer-related deaths. The chain of events leading to their development is called "the metastatic cascade". The biological and biochemical aspects of this process have been well studied but the importance of biomechanical parameters only recently became a focus in the field. Studies have shown the biological fluids (blood, lymph and interstitial fluid) to play a key role in the metastatic cascade. These fluids participate in the transport of circulating tumor cells (CTCs) as well as the factors that they secrete, while at the same time influencing the events of the metastatic cascade through the forces that they generate. The hemodynamic properties and topological constraints of the vascular architecture control the formation of metastatic niches and the metastatic potential of tumor cells. In this review, we discuss the importance of these mechanical forces and highlight the novel questions and research avenues that they open.
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http://dx.doi.org/10.1051/medsci/2020158 | DOI Listing |
Neuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFMater Today Bio
October 2025
Yunnan Key Laboratory of Breast Cancer Precision Medicine, Institute of Biomedical Engineering, Kunming Medical University, Kunming, 650500, Yunnan, China.
Achieving precise intratumoral accumulation and coordinated activation remains a major challenge in nanomedicine. Photothermal therapy (PTT) provides spatiotemporal control, yet its efficacy is hindered by heterogeneous distribution of PTT agents and limited synergy with other modalities. Here, we develop a dual-activation nanoplatform (IrO-P) that integrates exogenous photothermal stimulation with endogenous tumor microenvironment (TME)-responsive catalysis for synergistic chemodynamic therapy (CDT) and ferroptosis induction.
View Article and Find Full Text PDFCancer Pathog Ther
September 2025
Department of Biotechnology, Motilal Nehru National Institute of Technology, Allahabad 211004, India.
Background: Colorectal cancer (CRC) is a complex, heterogeneous disease characterized by frequent relapses and metastasis. Previous studies have reported that the invasion and progression of CRC in several cases can be controlled by targeting fusion genes. This study aimed to screen for potent fusion transcripts as potential molecular biomarkers and therapeutic targets for metastatic CRC (mCRC) using an approach.
View Article and Find Full Text PDFInt J Cancer
September 2025
Department of Biomedical Engineering, Virginia Commonwealth University, Richmond, Virginia, USA.
This study examined the effects of 24R,25-dihydroxyvitamin D (24R,25(OH)D) in estrogen-responsive laryngeal cancer tumorigenesis in vivo, the mechanisms involved, and whether the ability of the tumor cells to produce 24R,25(OH)D locally is estrogen-dependent. Estrogen receptor alpha-66 positive (ER+) UM-SCC-12 cells and ER- UM-SCC-11A cells responded differently to 24R,25(OH)D in vivo; 24R,25(OH)D enhanced tumorigenesis in ER+ tumors but inhibited tumorigenesis in ER- tumors. Treatment with 17β-estradiol (E) for 24 h reduced levels of CYP24A1 protein but increased 24R,25(OH)D production in ER+ cells; treatment with E for 9 min reduced CYP24A1 at 24 h and reduced 24R,25(OH)D production in ER- cells.
View Article and Find Full Text PDFFront Immunol
September 2025
College of Physical Education, Yangzhou University, Yangzhou, Jiangsu, China.
Traumatic spinal cord injury (TSCI) is a devastating neurological condition with limited therapeutic options and a high likelihood of permanent disability. Among the multifaceted secondary injury mechanisms triggered by TSCI, pyroptosis-an inflammatory form of programmed cell death-has emerged as a key pathological process. In particular, microglial pyroptosis plays a pivotal role in exacerbating neuroinflammation and disrupting tissue homeostasis, thereby amplifying the secondary injury cascade.
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