Abstract
Cancer rarely results from a single gene defect but emerges from disruptions in complex cellular networks. The Network Medicine perspective guides our investigation of cancer-driving interactions, particularly focusing on RAS signaling pathways that are key mediator for cancer development. We analyzed gene expression patterns in colon and lung cancers to identify stage-specific molecular drivers. Using computational modelling combined with patient tissue analysis, we discovered five key genes that are specifically altered in early-stage colon cancer: RAF1, PLCE1, RGL1, RIN1, and GRB7. These genes work as RAS effectors in signaling and can effectively distinguish between normal and cancerous colon tissue. Our approach combines network analysis with gene expression studies to understand how RAS signaling disruption contributes to colon cancer development. These findings suggest that targeting early-stage RAS-related changes could offer therapeutic opportunities before cancer becomes more complex and harder to treat.