Nras gene mutation might be one of the mechanisms of oncogenesis of lung adenocarcinoma.

lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1.

NRAS mutations define a distinct subset of lung cancers with potential sensitivity to MEK inhibitors.

Data suggest that Src kinases inhibitors may act with different mechanisms in non-small cell lung cancer (NSCLC) depending on EGF receptor (EGFR)/Ras protein (Ras) mutational profile.

Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS

Interleukin-8-related chemokines were identified as the tumor cell-secreted culprits for NRAS-dependent pulmonary metastatic propensity, signaling to lung endothelial and myeloid cells to facilitate pulmonary invasion.