Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha

Abstract excerpt

CYLD cutaneous syndrome (CCS) skin tumors develop from puberty onwards, can number in the hundreds and progressively grow over time. CCS patients lack medical therapies and require repeated surgery to control tumor burden. CYLD loss of heterozygosity (LOH) drives tumor growth, and CCS tumors have previously been shown to demonstrate increased canonical NF-κB and Wnt signalling. Here, we demonstrate evidence of no...

Topics

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• Bone Neoplasms
• Cancer and Skin Lesions
• Catalytic Domain
• Cell Movement
• Deubiquitinating Enzyme CYLD
• Ear and Head Tumors
• NF-κB Signaling Pathways
• NF-kappa B

Identifiers and source

Literature Corpus work

05f2bc1e-479a-50c2-8c07-f6a258e177da

DOI

10.1101/2025.01.31.635629