| pubmed-article:20822910 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C0021083 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C0079427 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C0017636 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C0694888 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C1325410 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C2610891 | lld:lifeskim |
| pubmed-article:20822910 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:20822910 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:20822910 | pubmed:dateCreated | 2010-11-1 | lld:pubmed |
| pubmed-article:20822910 | pubmed:abstractText | The ability of glioma cells to escape the immune system remains a significant barrier to successful immunotherapy. Here we demonstrate that loss of the PTEN tumor suppressor gene, with associated activation of the PI3K/Akt/mTOR pathway, leads to a human glioma phenotype that induces autologous T-cell apoptosis upon contact. The PTEN status of pathologically confirmed glioblastoma specimens was defined, and primary cultures established after surgical resection of tumor from 26 patients. Autologous T-cells were isolated from these patients, and after T-cell activation was induced, these cells were co-cultured with matched autologous glioma cells, either alone, or after treatment with one of three inhibitors of the PI3K/Akt/mTOR pathway. When co-cultured with autologous T-cells, PTEN wild-type tumor cells induced apoptosis in a minimal number of activated T-cells (6-12% of T-cells), whereas tumors with PTEN loss induced much more profound levels of T-cell apoptosis (42-56% of T-cells). Prior treatment of PTEN-deficient tumor cells with specific inhibitors of the PI3K/Akt/mTOR pathway diminished T-cell apoptosis to levels seen after co-culture with wild-type PTEN tumor cells, suggesting that PTEN loss confers this immunoresistant phenotype through the PI3K/Akt/mTOR pathway. These results suggest that PTEN-deficient glioblastoma patients are suboptimal candidates for immunotherapy. In addition, our results raise the possibility of combining T-cell based immunotherapy protocols with clinical inhibitors of the PI3K/Akt/mTOR pathway. | lld:pubmed |
| pubmed-article:20822910 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20822910 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20822910 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20822910 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:20822910 | pubmed:issn | 1532-2653 | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:ParsaAndrew... | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:TihanTarikT | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:YangIsaacI | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:PieperRussell... | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:SughrueMichae... | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:WaldronJames... | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:HanSeungguS | lld:pubmed |
| pubmed-article:20822910 | pubmed:author | pubmed-author:MillsSteven... | lld:pubmed |
| pubmed-article:20822910 | pubmed:copyrightInfo | Copyright © 2010 Elsevier Ltd. All rights reserved. | lld:pubmed |
| pubmed-article:20822910 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20822910 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:20822910 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20822910 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20822910 | pubmed:pagination | 1543-7 | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:meshHeading | pubmed-meshheading:20822910... | lld:pubmed |
| pubmed-article:20822910 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20822910 | pubmed:articleTitle | Implications for immunotherapy of tumor-mediated T-cell apoptosis associated with loss of the tumor suppressor PTEN in glioblastoma. | lld:pubmed |
| pubmed-article:20822910 | pubmed:affiliation | Department of Neurological Surgery, University of California at San Francisco, San Francisco, California 94123, USA. | lld:pubmed |
| pubmed-article:20822910 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20822910 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20822910 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:5728 | entrezgene:pubmed | pubmed-article:20822910 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20822910 | lld:entrezgene |
