Research has revealed that microRNA (miR)‑4500 is downregulated in non‑small cell lung cancer (NSCLC), and miR‑4500 suppresses tumor growth by targeting lin‑28 homolog B and NRAS proto‑oncogene, GTPase.
In total 50 plasma samples from patients newly diagnosed with advanced NSCLC or resistant to first-line tyrosine kinase inhibitors (TKIs) were subjected to deep sequencing on a seven-gene panel (BRAF, EGFR, ERBB2, KRAS, NRAS, PIK3CA, PTEN) incorporated with molecular barcodes to improve accuracy in variant detection.
In this study, we assessed 179 clinical cases of non-small cell lung carcinoma (NSCLC) that had been previously tested for EGFR, KRAS, NRAS, and BRAF mutations using a novel multiplexed analytic approach that reduces wild-type signal and allows for detection of low mutation load approaching 1%, iPLEX® HS panel for the MassARRAY® System (Agena Bioscience, San Diego, CA).
While 95% of patients were former or current smokers, smoking-related G:C>T:A transversions were significantly less frequent in NRAS-mutated lung tumors than KRAS-mutant non-small cell lung cancer [NSCLC; NRAS: 13% (4/30), KRAS: 66% (1772/2733), P < 0.00000001].
Alterations in 5 microsatellite loci were analyzed in tumors from 137 patients with primary non-small cell lung carcinomas that were also genotyped for the Hras1 variable number of tandem repeats (VNTR) locus.