Overcoming acquired resistance to BIBW2992 in HCC827, a non-small cell lung cancer cell line by dasatinib

ABSTRACT: EGFR tyrosine kinase inhibitors (TKIs) have demonstrated tremendous clinical benefits in non-small cell lung cancer (NSCLC) patients. However, resistance emerges rapidly due to a variety of mechanisms including a secondary mutation of T790M in EGFR that abrogates the binding of the drugs. It has been postulated that EGFR TKIs, such as afatinib (BIBW2992), with activity against the T790M mutant EGFR kinase might overcome the drug resistance problem or, when used as the first-line treatment, delay or suppress the emergence of resistance in EGFR. In this study, we generated BIBW2992-resistant cells, HCC827-BR1 and HCC827-BR2, from the parental HCC827 cells. In HCC827-BR cells, EGFR, MET, and Erb2 were down-regulated and no secondary mutation was found to be present in the coding region of EGF

ORGANISM(S): Homo sapiens

SUBMITTER: Shih Sheng Jiang 

PROVIDER: E-GEOD-62504 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress