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10.1158/1078-0432.CCR-14-0901 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-14-0901 C4294581!4294581!24963050     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24963050.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Cancer+Res 2014 ; 20 (18): 4882-93 Nephropedia Template TP {{tp|p=24963050|t=2014. Demethylating Drugs as Novel Analgesics for Cancer Pain |pdf=|usr=}}{{24963050}} gab.com Text Demethylating Drugs as Novel Analgesics for Cancer Pain JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24963050 #FOAvip Purpose: In this study we evaluated the analgesic potential of demethylating drugs on oral cancer pain. While demethylating drugs could affect expression many genes, we focused on the mu-opioid receptor (OPRM1) gene pathway, because of its role in pain processing. We determined the antinociceptive effect of OPRM1 re-expression in a mouse oral cancer model. Experimental Design: Using a mouse oral cancer model we determined whether demethylating drugs produced antinociception through re-expression of OPRM1. We then re-expressed OPRM1 with adenoviral transduction and determined if, and by what mechanism, OPRM1 re-expression produced antinociception. To determine the clinical significance of OPRM1 on cancer pain, we quantified OPRM1 methylation in painful cancer tissues and non-painful contralateral normal tissues of oral cancer patients, and non-painful dysplastic tissues of oral dysplasia patients. Results: We demonstrated that OPRM1 was methylated in cancer tissue, but not normal tissue, of oral cancer patients, and not in dysplastic tissues from oral dysplasia patients. Treatment with demethylating drugs resulted in mechanical and thermal antinociception in the mouse cancer model. This behavioral change correlated with OPRM1 re-expression in the cancer and associated neurons. Similarly, adenoviral-mediated OPRM1 re-expression on cancer cells resulted in naloxone-reversible antinociception. OPRM1 re-expression on oral cancer cells in vitro increased beta-endorphin secretion from the cancer, and decreased activation of neurons that were treated with cancer supernatant. Conclusion: Our study establishes the regulatory role of methylation in cancer pain. OPRM1 re-expression in cancer cells produces antinociception through cancer-mediated endogenous opioid secretion. Demethylating drugs have an analgesic effect that involves OPRM1. Twit Text FOAVip Demethylating Drugs as Novel Analgesics for Cancer Pain ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24963050 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24963050 #FOAvip English Wikipedia <ref>{{Cite pmid|24963050}}</ref> Demethylating Drugs as Novel Analgesics for Cancer Pain #MMPMID24963050 Viet CT; Dang D; Ye Y; Ono K; Campbell RR; Schmidt BL Clin Cancer Res 2014[Sep]; 20 (18): 4882-93 PMID24963050show ga Purpose: In this study we evaluated the analgesic potential of demethylating drugs on oral cancer pain. While demethylating drugs could affect expression many genes, we focused on the mu-opioid receptor (OPRM1) gene pathway, because of its role in pain processing. We determined the antinociceptive effect of OPRM1 re-expression in a mouse oral cancer model. Experimental Design: Using a mouse oral cancer model we determined whether demethylating drugs produced antinociception through re-expression of OPRM1. We then re-expressed OPRM1 with adenoviral transduction and determined if, and by what mechanism, OPRM1 re-expression produced antinociception. To determine the clinical significance of OPRM1 on cancer pain, we quantified OPRM1 methylation in painful cancer tissues and non-painful contralateral normal tissues of oral cancer patients, and non-painful dysplastic tissues of oral dysplasia patients. Results: We demonstrated that OPRM1 was methylated in cancer tissue, but not normal tissue, of oral cancer patients, and not in dysplastic tissues from oral dysplasia patients. Treatment with demethylating drugs resulted in mechanical and thermal antinociception in the mouse cancer model. This behavioral change correlated with OPRM1 re-expression in the cancer and associated neurons. Similarly, adenoviral-mediated OPRM1 re-expression on cancer cells resulted in naloxone-reversible antinociception. OPRM1 re-expression on oral cancer cells in vitro increased beta-endorphin secretion from the cancer, and decreased activation of neurons that were treated with cancer supernatant. Conclusion: Our study establishes the regulatory role of methylation in cancer pain. OPRM1 re-expression in cancer cells produces antinociception through cancer-mediated endogenous opioid secretion. Demethylating drugs have an analgesic effect that involves OPRM1. äDemethylating Drugs as Novel Analgesics for Cancer Pain (epmc).pdf DeepDyve Pubget Overpricing