Fiche publication
Date publication
février 2026
Journal
Frontiers in cell and developmental biology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr DEMIDOV Oleg
Tous les auteurs :
Lisitsa DA, Shindyapin VV, Nurislamov AR, Demidov ON, Bogdanova DA
Lien Pubmed
Résumé
Colorectal cancer (CRC) progression is influenced by genetic and epigenetic aberrations. Oncogenesis of CRC involves the accumulation of mutations in proteins involved in the regulation of cell proliferation, growth and death (Graphical abstract A). DNA methylation has been demonstrated to contribute to tumor initiation, progression, and modulation of therapeutic responses. In this particular landscape, the 9p21.3 locus has been observed to integrate various cellular processes, including cell cycle control ( and ANRIL), immune signaling (cluster of ), and metabolic regulation (). This creates relationships that may affect tumor intrinsic and extrinsic features, immunogenicity, and therapeutic sensitivity. The objective of our analysis is to provide a comprehensive overview of the role of the 9p21.3 locus in CRC, focusing on its potential implications for treatment decisions and prediction of treatment responses. Analyzing the 9p21.3 status would help stratify CRC patients into different groups and guide the choice of personalized therapy for CRC. It could also enhance current CRC treatment by pretreating patients with demethylating agents and using an immunotherapeutic approach in combination with senolytic drugs (Graphical abstract B).
Mots clés
9p21.3 locus, CDKN2A, CDKN2B, colorectal cancer (CRC), senescence, type I IFNs
Référence
Front Cell Dev Biol. 2026 02 11;14:1741704