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Kindlin-1 loss disrupts vascular and extracellular matrix organisation to sustain hypoxia in cutaneous squamous cell carcinoma
Kindlin-1, encoded by FERMT1, is an essential integrin co-activator that regulates cell extracellular matrix (ECM) adhesion, tissue architecture, and microenvironment signalling. Loss-of-function mutations in FERMT1 cause Kindler epidermolysis bullosa, which is strongly associated with aggressive cutaneous squamous cell carcinoma (cSCC). Although Kindlin-1 deficiency promotes hypoxia and invasion, the impacts on ECM-vascular organisation and oxygen homeostasis are not known.
High resolution spatial transcriptomics decodes the microenvironmental determinants of response to Nr-CWS therapy in cervical precancerous lesions
Immunotherapy with Nocardia rubra cell wall skeleton (Nr-CWS) can clear human papillomavirus (HPV) and induce regression of cervical precancerous lesions, yet many patients do not respond. The cellular and molecular basis for this heterogeneous clinical outcome remains unknown. Using high-resolution spatial transcriptomics, we profiled squamous intraepithelial lesions (SIL) from patients stratified by their subsequent response to Nr-CWS therapy.