| http://purl.uniprot.org/citations/20531297 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20531297 | http://www.w3.org/2000/01/rdf-schema#comment | "Endocrine therapy is the main therapeutic option for patients with estrogen receptor (ERalpha)-positive breast cancer. Resistance to this treatment is often associated with estrogen-independent activation of ERalpha. In this study, we show that in ERalpha-positive breast cancer cells, activation of the receptor tyrosine kinase RET (REarranged during Transfection) by its ligand GDNF results in increased ERalpha phosphorylation on Ser118 and Ser167 and estrogen-independent activation of ERalpha transcriptional activity. Further, we identify mTOR as a key component in this downstream signaling pathway. In tamoxifen response experiments, RET downregulation resulted in 6.2-fold increase in sensitivity of MCF7 cells to antiproliferative effects of tamoxifen, whereas GDNF stimulation had a protective effect against the drug. In tamoxifen-resistant (TAM(R)-1) MCF7 cells, targeting RET restored tamoxifen sensitivity. Finally, examination of two independent tissue microarrays of primary human breast cancers revealed that expression of RET protein was significantly associated with ERalpha-positive tumors and that in primary tumors from patients who subsequently developed invasive recurrence after adjuvant tamoxifen treatment, there was a twofold increase in the number of RET-positive tumors. Together these findings identify RET as a potentially important therapeutic target in ERalpha-positive breast cancers and in particular in tamoxifen-resistant tumors."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.org/dc/terms/identifier | "doi:10.1038/onc.2010.209"xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Martin L.A."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Robertson D."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Dowsett M."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Isacke C.M."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Drury S."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Morandi A."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Plaza-Menacho I."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/author | "Pancholi S."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/pages | "4648-4657"xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/title | "Targeting the receptor tyrosine kinase RET sensitizes breast cancer cells to tamoxifen treatment and reveals a role for RET in endocrine resistance."xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://purl.uniprot.org/core/volume | "29"xsd:string |
| http://purl.uniprot.org/citations/20531297 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20531297 |
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| http://purl.uniprot.org/uniprot/#_M9Z0T2-mappedCitation-20531297 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20531297 |
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