sub:provenance {
  sub:assertion dcterms:description "[Epidermal growth factor receptor (EGFR) inhibitors are highly effective in treating non-small cell lung cancers (NSCLC) expressing activated EGFR, particularly those harboring EGFR mutations.� However, most patients who benefit from EGFR inhibitors achieve only partial responses or stable disease, facilitating the emergence of resistance.� Thus, progression-free survival advantages in responding patients are modest.� Combination therapy, preferably using agents with synergistic activity, could both improve responses and reduce acquired resistance rates.�� We hypothesized that combining MEK inhibitors with EGFR inhibitors could result in such a benefit.� The MAPK pathway lies downstream of EGFR and transduces both proliferative and survival signals in a variety of cancer types.� Inhibitors of this pathway are currently in clinical trials, but little evidence exists supporting the use of these agents as monotherapy in EGFR-dependent non-small cell lung cancer.�� In this study, we find EGFR-dependent NSCLC cell lines are moderately sensitive to loss of ERK1/2 activity, either by small molecule inhibition or by siRNA knockdown.� The consequence of inhibition is dependent upon the trophic content of the culture media, primarily anti-proliferative in serum-rich conditions and pro-apoptotic in serum-poor conditions.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ;
    wi:evidence dgn-void:source_evidence_literature ;
    sio:SIO_000772 miriam-pubmed:19305165 ;
    prov:wasDerivedFrom dgn-void:BEFREE ;
    prov:wasGeneratedBy eco:ECO_0000203 .
  dgn-void:BEFREE pav:importedOn "2017-02-19"^^xsd:date .
  dgn-void:source_evidence_literature a eco:ECO_0000212 ;
    rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en ;
    rdfs:label "DisGeNET evidence - LITERATURE"@en .
}