<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(10)</volume><submitter>Geißler AL</submitter><pubmed_abstract>EGFR-targeted therapy is a key treatment approach in patients with RAS wildtype metastatic colorectal cancers (CRC). Still, also RAS wildtype CRC may be resistant to EGFR-targeted therapy, with few predictive markers available for improved stratification of patients. Here, we investigated response of 7 CRC cell lines (Caco-2, DLD1, HCT116, HT29, LS174T, RKO, SW480) to Cetuximab and correlated this to NGS-based mutation profiles, EGFR promoter methylation and EGFR expression status as well as to E-cadherin expression. Moreover, tissue specimens of primary and/or recurrent tumors as well as liver and/or lung metastases of 25 CRC patients having received Cetuximab and/or Panitumumab were examined for the same molecular markers. In vitro and in situ analyses showed that EGFR promoter methylati</pubmed_abstract><journal>Oncotarget</journal><pagination>17164-17190</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5370031</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>ATM mutations and E-cadherin expression define sensitivity to EGFR-targeted therapy in colorectal cancer.</pubmed_title><pmcid>PMC5370031</pmcid><pubmed_authors>Geißler AL</pubmed_authors><pubmed_authors>Fichter CD</pubmed_authors><pubmed_authors>Weddeling B</pubmed_authors><pubmed_authors>Makowiec F</pubmed_authors><pubmed_authors>Werner M</pubmed_authors><pubmed_authors>Lassmann S</pubmed_authors><pubmed_authors>Geißler M</pubmed_authors><pubmed_authors>Kottmann D</pubmed_authors><pubmed_authors>Lutz L</pubmed_authors><pubmed_authors>Fritsch R</pubmed_authors></additional><is_claimable>false</is_claimable><name>ATM mutations and E-cadherin expression define sensitivity to EGFR-targeted therapy in colorectal cancer.</name><description>EGFR-targeted therapy is a key treatment approach in patients with RAS wildtype metastatic colorectal cancers (CRC). Still, also RAS wildtype CRC may be resistant to EGFR-targeted therapy, with few predictive markers available for improved stratification of patients. Here, we investigated response of 7 CRC cell lines (Caco-2, DLD1, HCT116, HT29, LS174T, RKO, SW480) to Cetuximab and correlated this to NGS-based mutation profiles, EGFR promoter methylation and EGFR expression status as well as to E-cadherin expression. Moreover, tissue specimens of primary and/or recurrent tumors as well as liver and/or lung metastases of 25 CRC patients having received Cetuximab and/or Panitumumab were examined for the same molecular markers. In vitro and in situ analyses showed that EGFR promoter methylati</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Mar</publication><modification>2026-05-30T13:07:18.325Z</modification><creation>2019-03-27T02:39:47Z</creation></dates><accession>S-EPMC5370031</accession><cross_references><pubmed>28199979</pubmed><doi>10.18632/oncotarget.15211</doi></cross_references></HashMap>