Hedgehog‐EGFR cooperation response genes determine the oncogenic phenotype of basal cell carcinoma and tumour‐initiating pancreatic cancer cells
dc.contributor.author | Eberl, Markus | en_US |
dc.contributor.author | Klingler, Stefan | en_US |
dc.contributor.author | Mangelberger, Doris | en_US |
dc.contributor.author | Loipetzberger, Andrea | en_US |
dc.contributor.author | Damhofer, Helene | en_US |
dc.contributor.author | Zoidl, Kerstin | en_US |
dc.contributor.author | Schnidar, Harald | en_US |
dc.contributor.author | Hache, Hendrik | en_US |
dc.contributor.author | Bauer, Hans‐christian | en_US |
dc.contributor.author | Solca, Flavio | en_US |
dc.contributor.author | Hauser‐kronberger, Cornelia | en_US |
dc.contributor.author | Ermilov, Alexandre N. | en_US |
dc.contributor.author | Verhaegen, Monique E. | en_US |
dc.contributor.author | Bichakjian, Christopher K. | en_US |
dc.contributor.author | Dlugosz, Andrzej A. | en_US |
dc.contributor.author | Nietfeld, Wilfried | en_US |
dc.contributor.author | Sibilia, Maria | en_US |
dc.contributor.author | Lehrach, Hans | en_US |
dc.contributor.author | Wierling, Christoph | en_US |
dc.contributor.author | Aberger, Fritz | en_US |
dc.date.accessioned | 2012-04-04T18:44:20Z | |
dc.date.available | 2013-05-01T17:24:44Z | en_US |
dc.date.issued | 2012-03 | en_US |
dc.identifier.citation | Eberl, Markus; Klingler, Stefan; Mangelberger, Doris; Loipetzberger, Andrea; Damhofer, Helene; Zoidl, Kerstin; Schnidar, Harald; Hache, Hendrik; Bauer, Hans‐christian ; Solca, Flavio; Hauser‐kronberger, Cornelia ; Ermilov, Alexandre N.; Verhaegen, Monique E.; Bichakjian, Christopher K.; Dlugosz, Andrzej A.; Nietfeld, Wilfried; Sibilia, Maria; Lehrach, Hans; Wierling, Christoph; Aberger, Fritz (2012). "Hedgehogâ EGFR cooperation response genes determine the oncogenic phenotype of basal cell carcinoma and tumourâ initiating pancreatic cancer cells ." EMBO Molecular Medicine 4(3): 218-233. <http://hdl.handle.net/2027.42/90605> | en_US |
dc.identifier.issn | 1757-4676 | en_US |
dc.identifier.issn | 1757-4684 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/90605 | |
dc.description.abstract | Inhibition of Hedgehog (HH)/GLI signalling in cancer is a promising therapeutic approach. Interactions between HH/GLI and other oncogenic pathways affect the strength and tumourigenicity of HH/GLI. Cooperation of HH/GLI with epidermal growth factor receptor (EGFR) signalling promotes transformation and cancer cell proliferation in vitro . However, the in vivo relevance of HH‐EGFR signal integration and the critical downstream mediators are largely undefined. In this report we show that genetic and pharmacologic inhibition of EGFR signalling reduces tumour growth in mouse models of HH/GLI driven basal cell carcinoma (BCC). We describe HH‐EGFR cooperation response genes including SOX2, SOX9, JUN, CXCR4 and FGF19 that are synergistically activated by HH‐EGFR signal integration and required for in vivo growth of BCC cells and tumour‐initiating pancreatic cancer cells. The data validate EGFR signalling as drug target in HH/GLI driven cancers and shed light on the molecular processes controlled by HH‐EGFR signal cooperation, providing new therapeutic strategies based on combined targeting of HH‐EGFR signalling and selected downstream target genes. | en_US |
dc.publisher | WILEY‐VCH Verlag | en_US |
dc.subject.other | Epidermal Growth Factor Receptor | en_US |
dc.subject.other | Cancer | en_US |
dc.subject.other | Hedgehog Signalling | en_US |
dc.subject.other | Signal Transduction | en_US |
dc.title | Hedgehog‐EGFR cooperation response genes determine the oncogenic phenotype of basal cell carcinoma and tumour‐initiating pancreatic cancer cells | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Dermatology, University of Michigan, MI, USA | en_US |
dc.contributor.affiliationum | Departments of Dermatology and Cell & Developmental Biology, University of Michigan, MI, USA | en_US |
dc.contributor.affiliationother | Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria | en_US |
dc.contributor.affiliationother | Department of Organismic Biology, University of Salzburg, Salzburg, Austria | en_US |
dc.contributor.affiliationother | Department of Vertebrate Genomics, Max‐Planck Institute for Molecular Genetics, Berlin, Germany | en_US |
dc.contributor.affiliationother | Department of Molecular Biology, University of Salzburg, Salzburg, Austria | en_US |
dc.contributor.affiliationother | Tel: +43 662 8044 5792; Fax: +43 662 8044 183 | en_US |
dc.contributor.affiliationother | Cold Spring Harbor Laboratory, New York, NY, USA | en_US |
dc.contributor.affiliationother | Institute of Cancer Research, Medical University of Vienna, Vienna, Austria | en_US |
dc.contributor.affiliationother | Department of Pathology, Paracelsus Medical University Salzburg, Salzburg, Austria | en_US |
dc.identifier.pmid | 22294553 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/90605/1/218_ftp.pdf | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/90605/2/emmm_201100201_sm_suppdata.pdf | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/90605/3/emmm_201100201_sm_Review_Process_File.pdf | |
dc.identifier.doi | 10.1002/emmm.201100201 | en_US |
dc.identifier.source | EMBO Molecular Medicine | en_US |
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dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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