Telomere maintenance in interplay with DNA repair in pathogenesis and treatment of colorectal cancer.

摘要: Colorectal cancer (CRC) continues to be one of the leading malignancies and causes tumour-related deaths worldwide. Both impaired DNA repair mechanisms disrupted telomere length homeostasis represent key culprits in CRC initiation, progression prognosis. Mechanistically, altered results accumulation mutations genome and, ultimately, genomic instability. also determines response chemotherapeutics treatment, suggesting its utilisation prediction therapy individual approach patients. Telomere attrition resulting replicative senescence, simultaneously by-passing cell cycle checkpoints, is a hallmark malignant transformation cell. Telomerase almost ubiquitous advanced solid cancers, including CRC, expression fundamental immortalisation. Therefore, there persistent effort develop therapeutics, which are telomerase-specific gentle non-malignant tissues. However, practice, we still at level clinical trials. The current state knowledge route, research takes, gives us positive perspective that problem molecular models telomerase activation stabilisation will finally solved. We summarise literature herein, by pointing out crosstalk between proteins involved relation CRC.