Non-small cell lung cancer (NSCLC) survival and proliferation pathways (NSCLC survival and proliferation pathways)

Non-small cell lung cancer (NSCLC) survival and proliferation pathways represent the integrated signaling networks, such as the EGFR, MAPK, and PI3K/AKT/mTOR cascades, that drive the malignancy and progression of lung cancer cells (Source: NIH, National Cancer Institute). These pathways are essential for regulating the cell cycle, promoting protein synthesis, and inhibiting apoptosis, thereby allowing cancer cells to survive under metabolic stress and evade immune surveillance (Source: Nature Reviews Cancer). In many NSCLC cases, these pathways are constitutively activated by driver mutations in genes like EGFR, KRAS, or BRAF, or by chromosomal rearrangements involving ALK, ROS1, or RET (Source: PubMed, PMID: 30272139). Targeted therapies, including various tyrosine kinase inhibitors (TKIs), are designed to specifically block these aberrant signals to induce tumor regression (Source: Journal of Clinical Oncology). However, the clinical management of NSCLC is often challenged by the development of acquired resistance, which can occur through secondary mutations in the target kinase or the activation of alternative bypass signaling pathways (Source: StatPearls, Lung Cancer).

Other names

NSCLC signaling pathwaysLung cancer growth pathwaysNSCLC oncogenic signaling cascades

Inhibition of specific oncogenic driver kinases and their downstream signaling effectors to suppress tumor cell growth and induce apoptosis.