Non-small cell lung cancer cell survival pathways

Non-small cell lung cancer (NSCLC) cell survival pathways represent a complex network of intracellular signaling cascades that are aberrantly activated to promote tumor growth, evasion of programmed cell death, and metabolic adaptation. Central to these networks are receptor tyrosine kinase (RTK) pathways, including the Epidermal Growth Factor Receptor (EGFR), Anaplastic Lymphoma Kinase (ALK), and ROS1, which trigger downstream effectors such as the PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways (Source: National Cancer Institute). These pathways collectively regulate critical cellular processes including protein synthesis, cell cycle progression, and the suppression of pro-apoptotic proteins (Source: Nature Reviews Cancer). In NSCLC, specific driver mutations or genomic rearrangements provide a selective survival advantage to malignant cells, making these pathways the primary focus of precision oncology. While targeted therapies like tyrosine kinase inhibitors (TKIs) have significantly improved patient outcomes, the inherent redundancy and crosstalk between these pathways often lead to the emergence of acquired resistance, necessitating the development of combination strategies or next-generation inhibitors (Source: Journal of Thoracic Oncology).

Other names

NSCLC signaling pathwaysLung cancer survival signalingOncogenic survival cascades in NSCLCNSCLC cell survival signaling network

Targeted inhibition of specific oncogenic drivers (e.g., EGFR, ALK, KRAS, ROS1) that constitutively activate downstream survival signaling cascades such as PI3K/AKT/mTOR and MAPK/ERK to induce apoptosis and inhibit tumor growth.