Multiple cancer-related signaling pathways

Cancer is driven by intricate networks of altered signaling pathways that govern cell survival, proliferation, resistance to therapy, and metastasis. Well-studied pathways include PI3K/AKT/mTOR, Ras/MAPK, Notch, Wnt/β-catenin, TGF-β, and NF-κB, each consisting of multiple protein components and feedback loops[1][3][6]. These signaling axes mediate effects via receptor tyrosine kinases, transcription factors, and cytoplasmic effector proteins, and their dysregulation can confer tumorigenicity, therapy resistance, and complex interactions between cancer and the tumor microenvironment[2]. Therapeutics have been developed to target components within these pathways using small molecule inhibitors (e.g., kinase inhibitors) and monoclonal antibodies, often in combination approaches to overcome feedback and resistance[1][3][7]. However, "multiple cancer-related signaling pathways" is not a distinct molecular entity or receptor, and for structured annotation, only specific pathway members (such as AKT1 kinase, Notch receptor, or HER2) should be used. For structured data annotation, select precise, well-defined molecules (such as "Phosphatidylinositol 3-kinase catalytic subunit alpha" or "Epidermal growth factor receptor") rather than the umbrella category "multiple cancer-related signaling pathways"[1][3][4][6][8].

Other names

cancer signaling networksoncogenic signaling pathwayssignal transduction pathways in cancer