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10.1158/1078-0432.CCR-16-1317 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-16-1317 C5381521!5381521 !27797972     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27797972 &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       Clin+Cancer+Res 2017 ; 23 (7 ): 1771-1784 Nephropedia Template TP {{tp|p=27797972 |t=2017. Inhibition of STAT3 with the Generation 2 5 Antisense Oligonucleotide, AZD9150, Decreases Neuroblastoma Tumorigenicity and Increases Chemosensitivity |pdf=|usr=}}{{27797972 }} gab.com Text Inhibition of STAT3 with the Generation 2 5 Antisense Oligonucleotide, AZD9150, Decreases Neuroblastoma Tumorigenicity and Increases Chemosensitivity JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27797972 #FOAvip Purpose: Neuroblastoma is a pediatric tumor of peripheral sympathoadrenal neuroblasts. The long-term event-free survival of children with high-risk neuroblastoma is still poor despite the improvements with current multimodality treatment protocols. Activated JAK/STAT3 pathway plays an important role in many human cancers, suggesting that targeting STAT3 is a promising strategy for treating high-risk neuroblastoma.Experimental Design: To evaluate the biologic consequences of specific targeting of STAT3 in neuroblastoma, we assessed the effect of tetracycline (Tet)-inducible STAT3 shRNA and the generation 2.5 antisense oligonucleotide AZD9150 which targets STAT3 in three representative neuroblastoma cell line models (AS, NGP, and IMR32).Results: Our data indicated that Tet-inducible STAT3 shRNA and AZD9150 inhibited endogenous STAT3 and STAT3 target genes. Tet-inducible STAT3 shRNA and AZD9150 decreased cell growth and tumorigenicity. In vivo, STAT3 inhibition by Tet-inducible STAT3 shRNA or AZD9150 alone had little effect on growth of established tumors. However, when treated xenograft tumor cells were reimplanted into mice, there was a significant decrease in secondary tumors in the mice receiving AZD9150-treated tumor cells compared with the mice receiving ntASO-treated tumor cells. This indicates that inhibition of STAT3 decreases the tumor-initiating potential of neuroblastoma cells. Furthermore, inhibition of STAT3 significantly increased neuroblastoma cell sensitivity to cisplatin and decreased tumor growth and increased the survival of tumor-bearing mice in vivoConclusions: Our study supports the development of strategies targeting STAT3 inhibition in combination with conventional chemotherapy for patients with high-risk neuroblastoma. Clin Cancer Res; 23(7); 1771-84. ©2016 AACR. Twit Text FOAVip Inhibition of STAT3 with the Generation 2 5 Antisense Oligonucleotide, AZD9150, Decreases Neuroblastoma Tumorigenicity and Increases Chemosensitivity ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27797972 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27797972 #FOAvip English Wikipedia <ref>{{Cite pmid|27797972 }}</ref> Inhibition of STAT3 with the Generation 2 5 Antisense Oligonucleotide, AZD9150, Decreases Neuroblastoma Tumorigenicity and Increases Chemosensitivity #MMPMID27797972 Odate S ; Veschi V ; Yan S ; Lam N ; Woessner R ; Thiele CJ Clin Cancer Res 2017[Apr]; 23 (7 ): 1771-1784 PMID27797972 show ga Purpose: Neuroblastoma is a pediatric tumor of peripheral sympathoadrenal neuroblasts. The long-term event-free survival of children with high-risk neuroblastoma is still poor despite the improvements with current multimodality treatment protocols. Activated JAK/STAT3 pathway plays an important role in many human cancers, suggesting that targeting STAT3 is a promising strategy for treating high-risk neuroblastoma.Experimental Design: To evaluate the biologic consequences of specific targeting of STAT3 in neuroblastoma, we assessed the effect of tetracycline (Tet)-inducible STAT3 shRNA and the generation 2.5 antisense oligonucleotide AZD9150 which targets STAT3 in three representative neuroblastoma cell line models (AS, NGP, and IMR32).Results: Our data indicated that Tet-inducible STAT3 shRNA and AZD9150 inhibited endogenous STAT3 and STAT3 target genes. Tet-inducible STAT3 shRNA and AZD9150 decreased cell growth and tumorigenicity. In vivo, STAT3 inhibition by Tet-inducible STAT3 shRNA or AZD9150 alone had little effect on growth of established tumors. However, when treated xenograft tumor cells were reimplanted into mice, there was a significant decrease in secondary tumors in the mice receiving AZD9150-treated tumor cells compared with the mice receiving ntASO-treated tumor cells. This indicates that inhibition of STAT3 decreases the tumor-initiating potential of neuroblastoma cells. Furthermore, inhibition of STAT3 significantly increased neuroblastoma cell sensitivity to cisplatin and decreased tumor growth and increased the survival of tumor-bearing mice in vivoConclusions: Our study supports the development of strategies targeting STAT3 inhibition in combination with conventional chemotherapy for patients with high-risk neuroblastoma. Clin Cancer Res; 23(7); 1771-84. ©2016 AACR. |Animals [MESH] |Antineoplastic Combined Chemotherapy Protocols [MESH] |Apoptosis/drug effects [MESH] |Carcinogenesis/drug effects [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cisplatin/administration & dosage [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Humans [MESH] |Mice [MESH] |Neuroblastoma/*drug therapy/genetics/pathology [MESH] |Oligonucleotides, Antisense/*administration & dosage [MESH] |Oligonucleotides/*administration & dosage [MESH] |STAT3 Transcription Factor/*genetics [MESH]Inhibition of STAT3 with the Generation 2 5 Antisense Oligonucleotide,(epmc).pdf DeepDyve Pubget Overpricing