<HashMap><database>biostudies-other</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Saintigny Pierre</submitter><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-ECPF-GEOD-31852</full_dataset_link><project>EurocanPlatform</project><abstract>EGFR-mutated non-small cell lung cancers bear hallmarks including sensitivity to EGFR inhibitors,  and low proliferation, and increased MET.  However, the biology of EGFR dependence is still poorly understood. Using a training cohort of chemo-naive lung adenocarcinomas, we have developed a 72-gene signature that predicts (i) EGFR mutation status in four independent datasets; (ii) sensitivity to erlotinib in vitro; and (iii) improved survival, even in the wild-type EGFR subgroup. The signature includes differences associated with enhanced receptor tyrosine kinase (RTK) signaling, such as increased expression of endocytosis-related genes, decreased phosphatase levels, decreased expression of proliferation-related genes, increased folate receptor-1 (FOLR1) (a determinant of pemetrexed respons</abstract><repository>biostudies-other</repository><experiment_type>transcription profiling by array</experiment_type><data_source>EurocanPlatform</data_source><pubmed_authors>Heymach John</pubmed_authors><pubmed_authors>Coombes Kevin</pubmed_authors><pubmed_authors>Kim Edward</pubmed_authors><pubmed_authors>Lee J</pubmed_authors><pubmed_authors>Wistuba Ignacio</pubmed_authors><pubmed_authors>Herbst Roy</pubmed_authors><pubmed_authors>Saintigny Pierre</pubmed_authors><pubmed_authors>Lippman Scott</pubmed_authors><pubmed_authors>Hong Waun</pubmed_authors><pubmed_authors>Mao Li</pubmed_authors></additional><is_claimable>false</is_claimable><name>An EGFR-mutation signature reveals features of the EGFR-dependent phenotype and identifies MACC1 as an EGFR-associated regulator of MET</name><description>EGFR-mutated non-small cell lung cancers bear hallmarks including sensitivity to EGFR inhibitors,  and low proliferation, and increased MET.  However, the biology of EGFR dependence is still poorly understood. Using a training cohort of chemo-naive lung adenocarcinomas, we have developed a 72-gene signature that predicts (i) EGFR mutation status in four independent datasets; (ii) sensitivity to erlotinib in vitro; and (iii) improved survival, even in the wild-type EGFR subgroup. The signature includes differences associated with enhanced receptor tyrosine kinase (RTK) signaling, such as increased expression of endocytosis-related genes, decreased phosphatase levels, decreased expression of proliferation-related genes, increased folate receptor-1 (FOLR1) (a determinant of pemetrexed respons</description><dates><release>2016-04-14T14:01:52Z</release><modification>2016-04-14T14:01:52Z</modification><creation>2016-04-14T14:01:52Z</creation></dates><accession>S-ECPF-GEOD-31852</accession><cross_references><GEO>GSE31852</GEO><ArrayExpress>E-GEOD-31852</ArrayExpress><EFO>EFO_0000635</EFO><EFO>EFO_0005288</EFO><ArrayExpress files>E-GEOD-31852</ArrayExpress files></cross_references></HashMap>