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This study observed that patients with CYLD mutations frequently experienced severe, painful tumors beyond the head and neck, impacting their quality of life, with hormonal factors possibly contributing to tumor development.

This study found that transgenic mice expressing a mutant CYLD protein lacking deubiquitinase function showed signs of premature aging and spontaneous tumor development, likely due to over-activation of specific molecular pathways and chronic inflammation.

In this study, researchers identified CENPV as a new CYLD interacting partner that localizes to primary cilia and regulates acetylated tubulin levels, offering insights into the pathogenesis of skin appendage tumors.

In this study, researchers found that inhibiting IKKα in patient-derived CCS tumour models reduces tumour viability, supporting the potential for topical IKKα inhibitors as a treatment for CCS.

The researchers reported increased ubiquitination of proteins such as the insulin receptor in CYLD cutaneous syndrome skin tumors, suggesting that CYLD dysfunction may affect protein secretion and signaling processes.