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The aim of this study was to determine the expression of seven growth factor receptors in CC cell lines and to assess the effect of blocking the EGFR receptor <jats:italic>in vitro<\/jats:italic>.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Expression of EGFR (epithelial growth factor receptor), HGFR (hepatocyte growth factor receptor) IGF1R (insulin-like growth factor 1 receptor), IGF2R (insulin-like growth factor 2 receptor) and VEGFR1-3 (vascular endothelial growth factor receptor 1-3) were examined in four human CC cell lines (EGI-1, HuH28, OZ and TFK-1). The effect of the anti-EGFR-antibody cetuximab on cell growth and apoptosis was studied and cell lines were examined for <jats:italic>KRAS<\/jats:italic> mutations.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>EGFR, HGFR and IGFR1 were present in all four cell lines tested. IGFR2 expression was confirmed in EGI-1 and TFK-1. No growth-inhibitory effect was found in EGI-1 cells after incubation with cetuximab. Cetuximab dose-dependently inhibited growth in TFK-1. Increased apoptosis was only seen in TFK-1 cells at the highest cetuximab dose tested (1 mg\/ml), with no dose-response-relationship at lower concentrations. In EGI-1 a heterozygous <jats:italic>KRAS<\/jats:italic> mutation was found in codon 12 (c.35G&gt;A; p.G12D). HuH28, OZ and TFK-1 lacked <jats:italic>KRAS<\/jats:italic> mutation.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>CC cell lines express a pattern of different growth receptors <jats:italic>in vitro<\/jats:italic>. Growth factor inhibitor treatment could be affected from the <jats:italic>KRAS<\/jats:italic> genotype in CC. The expression of EGFR itself does not allow prognoses on growth inhibition by cetuximab.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2407-10-302","type":"journal-article","created":{"date-parts":[[2010,7,6]],"date-time":"2010-07-06T06:15:36Z","timestamp":1278396936000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Expression of growth factor receptors and targeting of EGFR in cholangiocarcinoma cell lines"],"prefix":"10.1186","volume":"10","author":[{"given":"Ling","family":"Xu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Hausmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Dietmaier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvia","family":"Kellermeier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa","family":"Pesch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuela","family":"Stieber-Gunckel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabeth","family":"Lippert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Klebl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard","family":"Rogler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,6,18]]},"reference":[{"issue":"3","key":"2101_CR1","doi-asserted-by":"publisher","first-page":"259","DOI":"10.1016\/j.critrevonc.2008.09.008","volume":"69","author":"S Mosconi","year":"2009","unstructured":"Mosconi S, Beretta GD, Labianca R, Zampino MG, Gatta G, Heinemann V: Cholangiocarcinoma. 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