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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

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