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Cancer cell proliferation and survival pathways represent the collective signaling networks, such as the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK cascades, that drive the uncontrolled growth and resistance to apoptosis characteristic of malignancy (Hanahan and Weinberg, 2011). These pathways are frequently hyperactivated in tumors due to mutations in oncogenes or loss of tumor suppressor genes, leading to sustained proliferative signaling and evasion of growth suppressors (NIH, 2023). In a clinical context, these pathways are the primary focus of targeted cancer therapies, which aim to block specific enzymes or receptors that act as critical nodes within the network (StatPearls, 2023). However, because these pathways are also essential for the function of normal, healthy cells—particularly those that divide rapidly—targeting them can lead to significant systemic toxicities (PubMed, 2022). Furthermore, the inherent plasticity of cancer cells often allows them to bypass inhibited nodes through alternative signaling routes, necessitating the use of combination therapies to achieve durable responses (Nature Reviews Cancer, 2020).
Inhibition of intracellular signaling cascades (e.g., PI3K/AKT/mTOR, MAPK/ERK, JAK/STAT) to arrest cell cycle progression and induce programmed cell death.
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