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10.1074/mcp.M116.060350 http://scihub22266oqcxt.onion/10.1074/mcp.M116.060350 C5013317!5013317 !27412690     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27412690 &cmd=llinks): Failed to open stream: HTTP request failed! 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Human Leukocyte Antigen (HLA) Peptides Derived from Tumor Antigens Induced by Inhibition of DNA Methylation for Development of Drug-facilitated Immunotherapy |pdf=|usr=}}{{27412690 }} gab.com Text Human Leukocyte Antigen (HLA) Peptides Derived from Tumor Antigens Induced by Inhibition of DNA Methylation for Development of Drug-facilitated Immunotherapy JO: Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=27412690 #FOAvip Treatment of cancer cells with anticancer drugs often fails to achieve complete remission. Yet, such drug treatments may induce alteration in the tumor's gene expression patterns, including those of Cancer/Testis Antigens (CTA). The degradation products of such antigens can be presented as HLA peptides on the surface of the tumor cells and be developed into anticancer immunotherapeutics. For example, the DNA methyl transferase inhibitor, 5-aza-2'-deoxycytidine (Decitabine) has limited antitumor efficacy, yet it induces the expression of many genes, including CTAs that are normally silenced in the healthy adult tissues. In this study, the presentation of many new HLA peptides derived from CTAs and induced by Decitabine was demonstrated in three human Glioblastoma cell lines. Such presentation of CTA-derived HLA peptides can be exploited for development of new treatment modalities, combining drug treatment with anti-CTA targeted immunotherapy. The Decitabine-induced HLA peptidomes include many CTAs that are not normally detected in healthy tissues or in cancer cells, unless treated with the drug. In addition, the study included large-scale analyses of the simultaneous effects of Decitabine on the transcriptomes, proteomes and HLA peptidomes of the human Glioblastoma cells. It demonstrates the poor correlations between these three levels of gene expression, both in their total levels and in their response to the drug. The proteomics and HLA peptidomics data are available via ProteomeXchange with identifier PXD003790 and the transcriptomics data are available via GEO with identifier GSE80137. Twit Text FOAVip Human Leukocyte Antigen (HLA) Peptides Derived from Tumor Antigens Induced by Inhibition of DNA Methylation for Development of Drug-facilitated Immunotherapy ????Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=27412690 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27412690 #FOAvip English Wikipedia <ref>{{Cite pmid|27412690 }}</ref> Human Leukocyte Antigen (HLA) Peptides Derived from Tumor Antigens Induced by Inhibition of DNA Methylation for Development of Drug-facilitated Immunotherapy #MMPMID27412690 Shraibman B ; Kadosh DM ; Barnea E ; Admon A Mol Cell Proteomics 2016[Sep]; 15 (9 ): 3058-70 PMID27412690 show ga Treatment of cancer cells with anticancer drugs often fails to achieve complete remission. Yet, such drug treatments may induce alteration in the tumor's gene expression patterns, including those of Cancer/Testis Antigens (CTA). The degradation products of such antigens can be presented as HLA peptides on the surface of the tumor cells and be developed into anticancer immunotherapeutics. For example, the DNA methyl transferase inhibitor, 5-aza-2'-deoxycytidine (Decitabine) has limited antitumor efficacy, yet it induces the expression of many genes, including CTAs that are normally silenced in the healthy adult tissues. In this study, the presentation of many new HLA peptides derived from CTAs and induced by Decitabine was demonstrated in three human Glioblastoma cell lines. Such presentation of CTA-derived HLA peptides can be exploited for development of new treatment modalities, combining drug treatment with anti-CTA targeted immunotherapy. The Decitabine-induced HLA peptidomes include many CTAs that are not normally detected in healthy tissues or in cancer cells, unless treated with the drug. In addition, the study included large-scale analyses of the simultaneous effects of Decitabine on the transcriptomes, proteomes and HLA peptidomes of the human Glioblastoma cells. It demonstrates the poor correlations between these three levels of gene expression, both in their total levels and in their response to the drug. The proteomics and HLA peptidomics data are available via ProteomeXchange with identifier PXD003790 and the transcriptomics data are available via GEO with identifier GSE80137. |Antigens, Neoplasm/*chemistry [MESH] |Azacitidine/*analogs & derivatives/pharmacology [MESH] |Brain Neoplasms/drug therapy/*immunology [MESH] |Cell Line, Tumor [MESH] |DNA Methylation/drug effects [MESH] |Decitabine [MESH] |Gene Expression Profiling/methods [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Glioblastoma/drug therapy/*immunology [MESH] |HLA Antigens/*chemistry [MESH] |Humans [MESH] |Immunotherapy [MESH] |Peptides/*isolation & purification [MESH] |Proteomics/methods [MESH]Human Leukocyte Antigen (HLA) Peptides Derived from Tumor Antigens Ind(epmc).pdf DeepDyve Pubget Overpricing