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10.1016/j.semcdb.2016.02.009 http://scihub22266oqcxt.onion/10.1016/j.semcdb.2016.02.009 C4867234!4867234 !26860754     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26860754 &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       Semin+Cell+Dev+Biol 2016 ; 54 (?): 28-41 Nephropedia Template TP {{tp|p=26860754 |t=2016. STAT3 in the systemic inflammation of cancer cachexia |pdf=|usr=}}{{26860754 }} gab.com Text STAT3 in the systemic inflammation of cancer cachexia JO: Semin Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=26860754 #FOAvip Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients. Twit Text FOAVip STAT3 in the systemic inflammation of cancer cachexia ????Semin Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=26860754 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26860754 #FOAvip English Wikipedia <ref>{{Cite pmid|26860754 }}</ref> STAT3 in the systemic inflammation of cancer cachexia #MMPMID26860754 Zimmers TA ; Fishel ML ; Bonetto A Semin Cell Dev Biol 2016[Jun]; 54 (?): 28-41 PMID26860754 show ga Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients. |Animals [MESH] |Cachexia/*etiology/*metabolism [MESH] |Humans [MESH] |Inflammation/*pathology [MESH] |Muscle, Skeletal/metabolism/pathology [MESH] |Neoplasms/*complications [MESH] |Organ Specificity [MESH]STAT3 in the systemic inflammation of cancer cachexia (epmc).pdf DeepDyve Pubget Overpricing