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10.1038/cr.2015.56 http://scihub22266oqcxt.onion/10.1038/cr.2015.56 C4456623!4456623 !25952668     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25952668 &cmd=llinks): Failed to open stream: HTTP request failed! 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Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics |pdf=|usr=}}{{25952668 }} gab.com Text Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics JO: Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=25952668 #FOAvip Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is an essential part of the cellular machinery that executes "programmed" or "regulated" necrosis. Here we show that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy-induced cell death. However, we show that RIP3 expression is often silenced in cancer cells due to genomic methylation near its transcriptional start site, thus RIP3-dependent activation of MLKL and downstream programmed necrosis during chemotherapeutic death is largely repressed. Nevertheless, treatment with hypomethylating agents restores RIP3 expression, and thereby promotes sensitivity to chemotherapeutics in a RIP3-dependent manner. RIP3 expression is reduced in tumors compared to normal tissue in 85% of breast cancer patients, suggesting that RIP3 deficiency is positively selected during tumor growth/development. Since hypomethylating agents are reasonably well-tolerated in patients, we propose that RIP3-deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional chemotherapeutics. Twit Text FOAVip Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics ????Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=25952668 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25952668 #FOAvip English Wikipedia <ref>{{Cite pmid|25952668 }}</ref> Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics #MMPMID25952668 Koo GB ; Morgan MJ ; Lee DG ; Kim WJ ; Yoon JH ; Koo JS ; Kim SI ; Kim SJ ; Son MK ; Hong SS ; Levy JM ; Pollyea DA ; Jordan CT ; Yan P ; Frankhouser D ; Nicolet D ; Maharry K ; Marcucci G ; Choi KS ; Cho H ; Thorburn A ; Kim YS Cell Res 2015[Jun]; 25 (6 ): 707-25 PMID25952668 show ga Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is an essential part of the cellular machinery that executes "programmed" or "regulated" necrosis. Here we show that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy-induced cell death. However, we show that RIP3 expression is often silenced in cancer cells due to genomic methylation near its transcriptional start site, thus RIP3-dependent activation of MLKL and downstream programmed necrosis during chemotherapeutic death is largely repressed. Nevertheless, treatment with hypomethylating agents restores RIP3 expression, and thereby promotes sensitivity to chemotherapeutics in a RIP3-dependent manner. RIP3 expression is reduced in tumors compared to normal tissue in 85% of breast cancer patients, suggesting that RIP3 deficiency is positively selected during tumor growth/development. Since hypomethylating agents are reasonably well-tolerated in patients, we propose that RIP3-deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional chemotherapeutics. |*DNA Methylation/drug effects [MESH] |Animals [MESH] |Antineoplastic Combined Chemotherapy Protocols/*pharmacology [MESH] |Breast Neoplasms/*drug therapy/genetics/*pathology [MESH] |Cell Survival/drug effects [MESH] |Dose-Response Relationship, Drug [MESH] |Female [MESH] |Humans [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Nude [MESH] |Necrosis/*drug therapy/genetics/metabolism/*pathology [MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/deficiency/*genetics [MESH] |Structure-Activity Relationship [MESH] |Tumor Cells, Cultured [MESH]Methylation-dependent loss of RIP3 expression in cancer represses prog(epmc).pdf DeepDyve Pubget Overpricing