Telomere length promotes colorectal cancer through dual parallel pathways involving growth signaling and protein metabolism

Longer telomeres causally increase CRC risk through dual parallel pathways: enhanced cellular proliferation via IGF-1 signaling and compromised immune surveillance through protein metabolic dysfunction. These findings challenge conventional protective roles attributed to telomeres and suggest that individuals with genetically longer telomeres may benefit from enhanced screening protocols and targeted interventions addressing both growth factor signaling and protein metabolic homeostasis.