@prefix rdf: . @prefix ns1: . rdf:type ns1:RelevantPaper , ns1:ReferencePaper , ns1:CitationPaper . @prefix rdfs: . rdfs:seeAlso , , , . @prefix bibo: . bibo:cites , , , , , , , , , , , , , , , , , ; ns1:cocitationWith , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ; ns1:hasRelevantBibliographicResourceOf _:b631340961 , _:b631340962 , _:b631340963 , _:b631340964 , _:b631340965 , _:b631340966 , _:b631340967 , _:b631340952 , _:b631340953 , _:b631340954 , _:b631340955 , _:b631340956 , _:b631340957 , _:b631340958 , _:b631340959 , _:b631340944 , _:b631340945 , _:b631340946 , _:b631340947 , _:b631340948 , _:b631340949 , _:b631340950 , _:b631340951 , _:b631340936 , _:b631340937 , _:b631340938 , _:b631340939 , _:b631340940 , _:b631340941 , _:b631340942 , _:b631340943 , _:b631340928 , _:b631340929 , _:b631340930 , _:b631340931 , _:b631340932 , _:b631340933 , _:b631340934 , _:b631340935 , _:b631340920 , _:b631340921 , _:b631340922 , _:b631340923 , _:b631340924 , _:b631340925 , _:b631340926 , _:b631340927 , _:b631340915 , _:b631340916 , _:b631340917 , _:b631340918 , _:b631340919 , _:b631341016 , _:b631341017 , _:b631341008 , _:b631341009 , _:b631341010 , _:b631341011 , _:b631341012 , _:b631341013 , _:b631341014 , _:b631341015 , _:b631341000 , _:b631341001 , _:b631341002 , _:b631341003 , _:b631341004 , _:b631341005 , _:b631341006 , _:b631341007 , _:b631340992 , _:b631340993 , _:b631340994 , _:b631340995 , _:b631340996 , _:b631340997 , _:b631340998 , _:b631340999 , _:b631340984 , _:b631340985 , _:b631340986 , _:b631340987 , _:b631340988 , _:b631340989 , _:b631340990 , _:b631340991 , _:b631340976 , _:b631340977 , _:b631340978 , _:b631340979 , _:b631340980 , _:b631340981 , _:b631340982 , _:b631340983 , _:b631340968 , _:b631340969 , _:b631340970 , _:b631340971 , _:b631340972 , _:b631340973 , _:b631340974 , _:b631340975 , _:b631340960 ; ns1:pmcid "PMC0" ; bibo:doi "10.18632%2Fgenesandcancer.136" . @prefix ns4: . ns4:contains _:b65383998 , _:b65383988 , _:b65384002 . _:b65383988 rdf:type ns4:Section . @prefix dc: . _:b65383988 dc:title "introduction" ; ns4:contains _:b65383989 , _:b65383990 , _:b65383991 , _:b65383996 , _:b65383997 , _:b65383992 , _:b65383993 , _:b65383994 , _:b65383995 . _:b65383989 rdf:type ns1:Context ; rdf:value "Innon-small cell lung cancer (NSCLC), responsible for the highest death toll among cancers [>>1<<], targeted therapy has been a remarkable success. Both EGFR\u2212, ALK\u2212, ROS1 -directed therapies are approved, and about a fifth of all metastatic NSCLC patients may be offered such therapies with median responses of around a year [2])." ; ns1:mentions . _:b65383990 rdf:type ns1:Context ; rdf:value "However, progression due to acquired resistance is virtually inevitable, and a number of different resistance mechanisms are described [>>3<<]. In EGFR-mutated tumours treated with the first (erlotinib, gefitinib) or second (afatinib) generation EGFR tyrosine kinase inhibitors, the most frequent mechanism of resistance is a secondary mutation in exon 20 of the EGFR-gene; T790M" ; ns1:mentions . _:b65383991 rdf:type ns1:Context ; rdf:value "In EGFR-mutated tumours treated with the first (erlotinib, gefitinib) or second (afatinib) generation EGFR tyrosine kinase inhibitors, the most frequent mechanism of resistance is a secondary mutation in exon 20 of the EGFR-gene; T790M [>>4<<]. Recently a drug targeting T790M-positive tumours, osimertinib, was approved after studies showing prolongation of progression free survival in EGFR-pre-treated and progressed patients harbouring T790M [5]." ; ns1:mentions . _:b65383992 rdf:type ns1:Context ; rdf:value "Recently a drug targeting T790M-positive tumours, osimertinib, was approved after studies showing prolongation of progression free survival in EGFR-pre-treated and progressed patients harbouring T790M [>>5<<]. Still, a substantial fraction of tumours harbour other resistance mechanisms of which some, as AXL over-expression [6] and MET amplification [7, 8] are known, but others are still unknown and where no targeted therapies are available." ; ns1:mentions . _:b65383993 rdf:type ns1:Context ; rdf:value "Still, a substantial fraction of tumours harbour other resistance mechanisms of which some, as AXL over-expression [>>6<<] and MET amplification [7, 8] are known, but others are still unknown and where no targeted therapies are available." ; ns1:mentions . _:b65383994 rdf:type ns1:Context ; rdf:value "Still, a substantial fraction of tumours harbour other resistance mechanisms of which some, as AXL over-expression [6] and MET amplification [>>7<<, 8] are known, but others are still unknown and where no targeted therapies are available." ; ns1:mentions . _:b65383995 rdf:type ns1:Context ; rdf:value "Still, a substantial fraction of tumours harbour other resistance mechanisms of which some, as AXL over-expression [6] and MET amplification [7, >>8<<] are known, but others are still unknown and where no targeted therapies are available." ; ns1:mentions . _:b65383996 rdf:type ns1:Context ; rdf:value "Yes-associated protein (YAP) has been found to both regulate the expression of Axl [>>9<<] and also drive the required phenotypic changes to cause epithelial to mesenchymal cell transformation (EMT) after binding with its transcriptional co-activator TEAD [10]." ; ns1:mentions . _:b65383997 rdf:type ns1:Context ; rdf:value "YAP expression is associated with reduced survival and relapse trends in NSCLC patients [>>11<<] which further highlights this co-transcription factor as an interesting target for drug-resistance research." ; ns1:mentions . _:b65383998 rdf:type ns4:Section ; dc:title "materials and methods" ; ns4:contains _:b65383999 , _:b65384000 , _:b65384001 . _:b65383999 rdf:type ns1:Context ; rdf:value "HCC827/ER sub-lines were cultured to 3.5 \u03BCM Erlotinib and HCC827/GR sub-lines cultured to 2.5 \u03BCM Gefitinib; their Cmax concentrations are 2.5 \u03BCM erlotinib [>>20<<] and 0.3 \u03BCM gefitinib respectively [21]." ; ns1:mentions . _:b65384000 rdf:type ns1:Context ; rdf:value "HCC827/ER sub-lines were cultured to 3.5 \u03BCM Erlotinib and HCC827/GR sub-lines cultured to 2.5 \u03BCM Gefitinib; their Cmax concentrations are 2.5 \u03BCM erlotinib [20] and 0.3 \u03BCM gefitinib respectively [>>21<<]. H1975/OR sub-lines took much longer to establish due to the response to osimertinib. These cells were cultured to 2.5 \u03BCM osimertinib stepwise over several months. The Cmax value for osimertinib is between 2-3 \u03BCM [22] and thus sustaining" ; ns1:mentions . _:b65384001 rdf:type ns1:Context ; rdf:value "The Cmax value for osimertinib is between 2-3 \u03BCM [>>22<<] and thus sustaining the sub-line at 2.5 \u03BCM was deemed acceptable." ; ns1:mentions . _:b65384002 rdf:type ns4:Section ; dc:title "discussion" ; ns4:contains _:b65384008 , _:b65384009 , _:b65384010 , _:b65384004 , _:b65384005 , _:b65384006 , _:b65384007 , _:b65384003 . _:b65384003 rdf:type ns1:Context ; rdf:value "We exposed the HCC827 cell line to two first generation EGFR inhibitors, erlotinib and gefitinib, and H1975 to osimertinib (AZD9291) and found AXL, a known mechanism of EGFR-TKI-resistance [>>6<<] to be expressed in all sub-lines." ; ns1:mentions . _:b65384004 rdf:type ns1:Context ; rdf:value "This was an interesting observation as previous studies have shown that YAP may regulate AXL expression in lung adenocarcinomas [>>9<<] and in hepatocellular carcinoma by way of TEAD binding to the promoter region of the AXL gene [12]." ; ns1:mentions . _:b65384005 rdf:type ns1:Context ; rdf:value "This was an interesting observation as previous studies have shown that YAP may regulate AXL expression in lung adenocarcinomas [9] and in hepatocellular carcinoma by way of TEAD binding to the promoter region of the AXL gene [>>12<<]. Thus YAP expression and activation may be a reason for AXL induction in drug-resistant adenocarcinomas and some other cancer types; though we did not evaluate AXL expression following YAP knockdown, which would have been interesting." ; ns1:mentions . _:b65384006 rdf:type ns1:Context ; rdf:value "Sakuma et al observed the down-regulation of EGFR after generating gefitinib-resistant HCC4006 adenocarcinoma cells \u2013 also harbouring the exon 19 E746-A750 deletion \u2013 but not in the HCC827 gefitinib-resistant sub-line [>>13<<]. This was concluded to be due to autophagocytosis and may explain why we also see this in our results after acquiring resistance to erlotinib and gefitinib. If this is also observed in the clinic it would be interesting to determine if" ; ns1:mentions . _:b65384007 rdf:type ns1:Context ; rdf:value "Vimentin induces morphological changes and increases cell motility [>>15<<]. It is conceivable that osimertinib may have off targets effecting the transcription of vimentin." ; ns1:mentions . _:b65384008 rdf:type ns1:Context ; rdf:value "YAP is only active once it has sequestered to the nucleus where it binds to TEAD and begins transcription of cell survival genes and EMT capabilities [>>16<<]. We confirmed YAP expression via western blot and RT-qPCR and found YAP was distributed in both cytoplasm and cell nucleus in the HCC827/ER and GR sub-lines, but more localized to the nucleus in the H1975/OR sub-line (figure 3). We" ; ns1:mentions . _:b65384009 rdf:type ns1:Context ; rdf:value "Our results highlight YAP as a possible mechanism of drug resistance also for the third-generation EGFR-inhibitors, and thus confirm and extend the findings by Hsu et al [>>17<<] whose group showed HCC827 erlotinib-resistant and H1975 cells to become re-sensitized to erlotinib after YAP was silenced." ; ns1:mentions . _:b65384010 rdf:type ns1:Context ; rdf:value "The use of statins has been studied and shown to be a potent inhibitor of YAP sequestering to the nucleus in breast cancer cell lines [>>19<<]. This study showed potential in pre-existing drugs already approved for use in the clinic which can be revaluated into a new role speeding up the use in YAP-driven cancers. 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