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10.1016/j.it.2017.01.002 http://scihub22266oqcxt.onion/10.1016/j.it.2017.01.002 C5378645!5378645 !28233639     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28233639 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28233639 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Trends+Immunol 2017 ; 38 (4 ): 298-305 Nephropedia Template TP {{tp|p=28233639 |t=2017. MYC: Master Regulator of Immune Privilege |pdf=|usr=}}{{28233639 }} gab.com Text MYC: Master Regulator of Immune Privilege JO: Trends Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28233639 #FOAvip Cancers are often initiated by genetic events that activate proto-oncogenes or inactivate tumor-suppressor genes. These events are also crucial for sustained tumor cell proliferation and survival, a phenomenon described as oncogene addiction. In addition to this cell-intrinsic role, recent evidence indicates that oncogenes also directly regulate immune responses, leading to immunosuppression. Expression of many oncogenes or loss of tumor suppressors induces the expression of immune checkpoints that regulate the immune response, such as PD-L1. We discuss here how oncogenes, and in particular MYC, suppress immune surveillance, and how oncogene-targeted therapies may restore the immune response against tumors. Twit Text FOAVip MYC: Master Regulator of Immune Privilege ????Trends Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28233639 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28233639 #FOAvip English Wikipedia <ref>{{Cite pmid|28233639 }}</ref> MYC: Master Regulator of Immune Privilege #MMPMID28233639 Casey SC ; Baylot V ; Felsher DW Trends Immunol 2017[Apr]; 38 (4 ): 298-305 PMID28233639 show ga Cancers are often initiated by genetic events that activate proto-oncogenes or inactivate tumor-suppressor genes. These events are also crucial for sustained tumor cell proliferation and survival, a phenomenon described as oncogene addiction. In addition to this cell-intrinsic role, recent evidence indicates that oncogenes also directly regulate immune responses, leading to immunosuppression. Expression of many oncogenes or loss of tumor suppressors induces the expression of immune checkpoints that regulate the immune response, such as PD-L1. We discuss here how oncogenes, and in particular MYC, suppress immune surveillance, and how oncogene-targeted therapies may restore the immune response against tumors. |*Carcinogenesis/genetics [MESH] |*Immune Tolerance [MESH] |Animals [MESH] |B7-H1 Antigen/genetics/metabolism [MESH] |Cell Proliferation [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Immunologic Surveillance [MESH] |Immunomodulation [MESH] |Molecular Targeted Therapy [MESH] |Neoplasms/drug therapy/genetics/*metabolism [MESH] |Proto-Oncogene Proteins c-myc/*immunology [MESH] |Tumor Escape [MESH]MYC: Master Regulator of Immune Privilege (epmc).pdf DeepDyve Pubget Overpricing