| http://purl.uniprot.org/citations/26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26208487 | http://www.w3.org/2000/01/rdf-schema#comment | "Breast cancer is a heterogeneous disease and new clinical markers are needed to individualise disease management and therapy further. Alterations in the PI3K/AKT pathway, mainly PIK3CA mutations, have been shown frequently especially in the luminal breast cancer subtypes, suggesting a cross-talk between ER and PI3K/AKT. Aberrant PI3K/AKT signalling has been connected to poor response to anti-oestrogen therapies. In vitro studies have shown protein tyrosine phosphatase, non-receptor type 2 (PTPN2) as a previously unknown negative regulator of the PI3K/AKT pathway. Here, we evaluate possible genomic alterations in the PTPN2 gene and its potential as a new prognostic and treatment predictive marker for endocrine therapy benefit in breast cancer. PTPN2 gene copy number was assessed by real-time PCR in 215 tumour samples from a treatment randomised study consisting of postmenopausal patients diagnosed with stage II breast cancer 1976-1990. Corresponding mRNA expression levels of PTPN2 were evaluated in 86 available samples by the same methodology. Gene copy loss of PTPN2 was detected in 16% (34/215) of the tumours and this was significantly correlated with lower levels of PTPN2 mRNA. PTPN2 gene loss and lower mRNA levels were associated with activation of AKT and a poor prognosis. Furthermore, PTPN2 gene loss was a significant predictive marker of poor benefit from tamoxifen treatment. In conclusion, genomic loss of PTPN2 may be a previously unknown mechanism of PI3K/AKT upregulation in breast cancer. PTPN2 status is a potential new clinical marker of endocrine treatment benefit which could guide further individualised therapies in breast cancer."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.org/dc/terms/identifier | "doi:10.1007/s10549-015-3516-y"xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Karlsson E."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Nordenskjold B."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Stal O."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Fornander T."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Perez-Tenorio G."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Dutta C."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Emin S."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/author | "Veenstra C."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/name | "Breast Cancer Res Treat"xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/pages | "31-40"xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/title | "Loss of protein tyrosine phosphatase, non-receptor type 2 is associated with activation of AKT and tamoxifen resistance in breast cancer."xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://purl.uniprot.org/core/volume | "153"xsd:string |
| http://purl.uniprot.org/citations/26208487 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26208487 |
| http://purl.uniprot.org/citations/26208487 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26208487 |
| http://purl.uniprot.org/uniprot/#_B3KVH4-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_A0A0S2Z3D6-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_A0A142IKA9-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_A8K3N4-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_B0LPE5-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_D3DUJ3-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |
| http://purl.uniprot.org/uniprot/#_K7EQG9-mappedCitation-26208487 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26208487 |