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10.3389/fendo.2017.00031 http://scihub22266oqcxt.onion/10.3389/fendo.2017.00031 C5319972!5319972!28275367     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       Front+Endocrinol+(Lausanne) 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28275367|t=2017. PPAR-? Agonists As Antineoplastic Agents in Cancers with Dysregulated IGF Axis |pdf=|usr=}}{{28275367}} gab.com Text PPAR- Agonists As Antineoplastic Agents in Cancers with Dysregulated IGF Axis JO: Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=28275367 #FOAvip It is now widely accepted that insulin resistance and compensatory hyperinsulinemia are associated to increased cancer incidence and mortality. Moreover, cancer development and progression as well as cancer resistance to traditional anticancer therapies are often linked to a deregulation/overactivation of the insulin-like growth factor (IGF) axis, which involves the autocrine/paracrine production of IGFs (IGF-I and IGF-II) and overexpression of their cognate receptors [IGF-I receptor, IGF-insulin receptor (IR), and IR]. Recently, new drugs targeting various IGF axis components have been developed. However, these drugs have several limitations including the occurrence of insulin resistance and compensatory hyperinsulinemia, which, in turn, may affect cancer cell growth and survival. Therefore, new therapeutic approaches are needed. In this regard, the pleiotropic effects of peroxisome proliferator activated receptor (PPAR)-? agonists may have promising applications in cancer prevention and therapy. Indeed, activation of PPAR-? by thiazolidinediones (TZDs) or other agonists may inhibit cell growth and proliferation by lowering circulating insulin and affecting key pathways of the Insulin/IGF axis, such as PI3K/mTOR, MAPK, and GSK3-?/Wnt/?-catenin cascades, which regulate cancer cell survival, cell reprogramming, and differentiation. In light of these evidences, TZDs and other PPAR-? agonists may be exploited as potential preventive and therapeutic agents in tumors addicted to the activation of IGF axis or occurring in hyperinsulinemic patients. Unfortunately, clinical trials using PPAR-? agonists as antineoplastic agents have reached conflicting results, possibly because they have not selected tumors with overactivated insulin/IGF-I axis or occurring in hyperinsulinemic patients. In conclusion, the use of PPAR-? agonists in combined therapies of IGF-driven malignancies looks promising but requires future developments. Twit Text FOAVip PPAR- Agonists As Antineoplastic Agents in Cancers with Dysregulated IGF Axis ????Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=28275367 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28275367 #FOAvip English Wikipedia <ref>{{Cite pmid|28275367}}</ref> PPAR-? Agonists As Antineoplastic Agents in Cancers with Dysregulated IGF Axis #MMPMID28275367 Vella V; Nicolosi ML; Giuliano S; Bellomo M; Belfiore A; Malaguarnera R Front Endocrinol (Lausanne) 2017[]; 8 (ä): ä PMID28275367show ga It is now widely accepted that insulin resistance and compensatory hyperinsulinemia are associated to increased cancer incidence and mortality. Moreover, cancer development and progression as well as cancer resistance to traditional anticancer therapies are often linked to a deregulation/overactivation of the insulin-like growth factor (IGF) axis, which involves the autocrine/paracrine production of IGFs (IGF-I and IGF-II) and overexpression of their cognate receptors [IGF-I receptor, IGF-insulin receptor (IR), and IR]. Recently, new drugs targeting various IGF axis components have been developed. However, these drugs have several limitations including the occurrence of insulin resistance and compensatory hyperinsulinemia, which, in turn, may affect cancer cell growth and survival. Therefore, new therapeutic approaches are needed. In this regard, the pleiotropic effects of peroxisome proliferator activated receptor (PPAR)-? agonists may have promising applications in cancer prevention and therapy. Indeed, activation of PPAR-? by thiazolidinediones (TZDs) or other agonists may inhibit cell growth and proliferation by lowering circulating insulin and affecting key pathways of the Insulin/IGF axis, such as PI3K/mTOR, MAPK, and GSK3-?/Wnt/?-catenin cascades, which regulate cancer cell survival, cell reprogramming, and differentiation. In light of these evidences, TZDs and other PPAR-? agonists may be exploited as potential preventive and therapeutic agents in tumors addicted to the activation of IGF axis or occurring in hyperinsulinemic patients. Unfortunately, clinical trials using PPAR-? agonists as antineoplastic agents have reached conflicting results, possibly because they have not selected tumors with overactivated insulin/IGF-I axis or occurring in hyperinsulinemic patients. In conclusion, the use of PPAR-? agonists in combined therapies of IGF-driven malignancies looks promising but requires future developments. äPPAR-? Agonists As Antineoplastic Agents in Cancers with Dysregulated (epmc).pdf DeepDyve Pubget Overpricing