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10.1016/j.oraloncology.2015.11.022 http://scihub22266oqcxt.onion/10.1016/j.oraloncology.2015.11.022 C5590227!5590227!26733183     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oral+Oncol 2016 ; 56 (ä): 84-92 Nephropedia Template TP {{tp|p=26733183|t=2016. The STAT3 pathway as a therapeutic target in head and neck cancer: Barriers and innovations |pdf=|usr=}}{{26733183}} gab.com Text The STAT3 pathway as a therapeutic target in head and neck cancer: Barriers and innovations JO: Oral Oncol http://www.kidney.de/pget.php?&tw=1&pmid=26733183 #FOAvip Proteins of the signal transducer and activator of transcription (STAT) family mediate cellular responses to cytokines and growth factors. Aberrant regulation of the STAT3 oncogene contributes to tumor formation and progression in many cancers, including head and neck squamous cell carcinoma (HNSCC), where hyperactivation of STAT3 is implicated in both treatment resistance and immune escape. There are no oncogenic gain-of-function mutations in HNSCC. Rather, aberrant STAT3 signaling is primarily driven by upstream growth factor receptors, such as Janus kinase (JAK) and epidermal growth factor receptor (EGFR). Moreover, genomic silencing of select protein tyrosine phosphatase receptors (PTPRs), tumor suppressors that dephosphorylate STAT3, may lead to prolonged phosphorylation and activation of STAT3. This review will summarize current knowledge of the STAT3 pathway and its contribution to HNSCC growth, survival, and resistance to standard therapies, and discuss STAT3-targeting agents in various phases of clinical development. Twit Text FOAVip The STAT3 pathway as a therapeutic target in head and neck cancer: Barriers and innovations ????Oral Oncol http://www.kidney.de/pget.php?&tw=1&pmid=26733183 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26733183 #FOAvip English Wikipedia <ref>{{Cite pmid|26733183}}</ref> The STAT3 pathway as a therapeutic target in head and neck cancer: Barriers and innovations #MMPMID26733183 Geiger JL; Grandis JR; Bauman JE Oral Oncol 2016[May]; 56 (ä): 84-92 PMID26733183show ga Proteins of the signal transducer and activator of transcription (STAT) family mediate cellular responses to cytokines and growth factors. Aberrant regulation of the STAT3 oncogene contributes to tumor formation and progression in many cancers, including head and neck squamous cell carcinoma (HNSCC), where hyperactivation of STAT3 is implicated in both treatment resistance and immune escape. There are no oncogenic gain-of-function mutations in HNSCC. Rather, aberrant STAT3 signaling is primarily driven by upstream growth factor receptors, such as Janus kinase (JAK) and epidermal growth factor receptor (EGFR). Moreover, genomic silencing of select protein tyrosine phosphatase receptors (PTPRs), tumor suppressors that dephosphorylate STAT3, may lead to prolonged phosphorylation and activation of STAT3. This review will summarize current knowledge of the STAT3 pathway and its contribution to HNSCC growth, survival, and resistance to standard therapies, and discuss STAT3-targeting agents in various phases of clinical development. äThe STAT3 pathway as a therapeutic target in head and neck cancer: Bar(epmc).pdf DeepDyve Pubget Overpricing