The role of laminins in cancer pathobiology: a comprehensive review.

Laminins (LMs) are a family of heterotrimeric glycoproteins that form the structural foundation of basement membranes (BM). By acting as molecular bridges between cells and the extracellular matrix (ECM) through integrins and other surface receptors, they regulate key cellular signals that influence cell behavior and tissue architecture. Despite their physiological importance, our understanding of the role of LMs in cancer pathobiology remains fragmented.

Biomechanical properties of laminins and their impact on cancer progression.

Laminins (LMs) constitute a family of heterotrimeric glycoproteins essential for the formation of basement membranes (BM). They act as molecular bridges between cells and the extracellular matrix (ECM), thereby transmitting signals influencing cell behavior and tissue organization. In the realm of cancer pathobiology, LMs regulate key processes such as migration, differentiation, or fibrosis.

Utilizing a Novel AI Tool to Detect the Posterior Superior Alveolar Artery's Location's Impact on Maxillary Sinus Mucosal Thickening in the Presence of Periapical Lesions.

Periapical lesions have been implicated in sinus-related complications, but the precise influence of anatomical variations in the posterior superior alveolar artery (PSAA) on mucosal thickening remains an uncharted aspect. The new AI tool employed in this research utilizes advanced image processing algorithms to enhance image visualization. : This study examines the accuracy of a new cone beam computed tomography (CBCT) software (eVol DXS, version 1.

Superoxide Dismutase-3 Downregulates Laminin α5 Expression in Tumor Endothelial Cells via the Inhibition of Nuclear Factor Kappa B Signaling.

The balance between laminin isoforms containing the α5 or the α4 chain in the endothelial basement membrane determines the site of leukocyte diapedesis under inflammatory conditions. Extracellular superoxide dismutase (SOD3) induces laminin α4 expression in tumor blood vessels, which is associated with enhanced intratumor T cell infiltration in primary human cancers. We show now that SOD3 overexpression in neoplastic and endothelial cells (ECs) reduces laminin α5 in tumor blood vessels.