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10.18632/oncotarget.14338 http://scihub22266oqcxt.onion/10.18632/oncotarget.14338 C5352419!5352419!28052027     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (5): 8522-35 Nephropedia Template TP {{tp|p=28052027|t=2017. Estrogen receptor ? ligation inhibits Hodgkin lymphoma growth by inducing autophagy |pdf=|usr=}}{{28052027}} gab.com Text Estrogen receptor ligation inhibits Hodgkin lymphoma growth by inducing autophagy JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28052027 #FOAvip Although Hodgkin lymphoma (HL) is curable with current therapy, at least 20% of patients relapse or fail to make complete remission. In addition, patients who achieve long-term disease-free survival frequently undergo infertility, secondary malignancies, and cardiac failure, which are related to chemotherapeutic agents and radiation therapies. Hence, new therapeutic strategies able to counteract the HL disease in this important patient population are still a matter of study. Estrogens, in particular 17?-estradiol (E2), have been suggested to play a role in lymphoma cell homeostasis by estrogen receptors (ER) ? activation. On these bases, we investigated whether the ligation of ER? by a selective agonist, the 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), could impact HL tumor growth. We found that DPN-mediated ER? activation led to a reduction of in vitro cell proliferation and cell cycle progression by inducing autophagy. In nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice engrafted with HL cells, ER? activation by DPN was able to reduce lymphoma growth up to 60% and this associated with the induction of tumor cell autophagy. Molecular characterization of ER?-induced autophagy revealed an overexpression of damage-regulated autophagy modulator 2 (DRAM2) molecule, whose role in autophagy modulation is still debated. After ER? activation, both DRAM2 and protein 1 light chain 3 (LC3), a key actor in the autophagosome formation, strictly interacted each other and localized at mitochondrial level.Altogether these results suggest that targeting ER? with selective agonists might affect HL cell proliferation and tumor growth via a mechanism that brings into play DRAM2-dependent autophagic cascade. Twit Text FOAVip Estrogen receptor ligation inhibits Hodgkin lymphoma growth by inducing autophagy ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28052027 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28052027 #FOAvip English Wikipedia <ref>{{Cite pmid|28052027}}</ref> Estrogen receptor ? ligation inhibits Hodgkin lymphoma growth by inducing autophagy #MMPMID28052027 Pierdominici M; Maselli A; Locatelli SL; Ciarlo L; Careddu G; Patrizio M; Ascione B; Tinari A; Carlo-Stella C; Malorni W; Matarrese P; Ortona E Oncotarget 2017[Jan]; 8 (5): 8522-35 PMID28052027show ga Although Hodgkin lymphoma (HL) is curable with current therapy, at least 20% of patients relapse or fail to make complete remission. In addition, patients who achieve long-term disease-free survival frequently undergo infertility, secondary malignancies, and cardiac failure, which are related to chemotherapeutic agents and radiation therapies. Hence, new therapeutic strategies able to counteract the HL disease in this important patient population are still a matter of study. Estrogens, in particular 17?-estradiol (E2), have been suggested to play a role in lymphoma cell homeostasis by estrogen receptors (ER) ? activation. On these bases, we investigated whether the ligation of ER? by a selective agonist, the 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), could impact HL tumor growth. We found that DPN-mediated ER? activation led to a reduction of in vitro cell proliferation and cell cycle progression by inducing autophagy. In nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice engrafted with HL cells, ER? activation by DPN was able to reduce lymphoma growth up to 60% and this associated with the induction of tumor cell autophagy. Molecular characterization of ER?-induced autophagy revealed an overexpression of damage-regulated autophagy modulator 2 (DRAM2) molecule, whose role in autophagy modulation is still debated. After ER? activation, both DRAM2 and protein 1 light chain 3 (LC3), a key actor in the autophagosome formation, strictly interacted each other and localized at mitochondrial level.Altogether these results suggest that targeting ER? with selective agonists might affect HL cell proliferation and tumor growth via a mechanism that brings into play DRAM2-dependent autophagic cascade. äEstrogen receptor ? ligation inhibits Hodgkin lymphoma growth by induc(epmc).pdf DeepDyve Pubget Overpricing