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10.1002/mc.22026 http://scihub22266oqcxt.onion/10.1002/mc.22026 C4004705!4004705 !23681918     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23681918 &cmd=llinks): Failed to open stream: HTTP request failed! 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Triplex-forming oligonucleotides targeting c-MYC potentiate the anti-tumor activity of gemcitabine in a mouse model of human cancer |pdf=|usr=}}{{23681918 }} gab.com Text Triplex-forming oligonucleotides targeting c-MYC potentiate the anti-tumor activity of gemcitabine in a mouse model of human cancer JO: Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=23681918 #FOAvip Antimetabolite chemotherapy remains an essential cancer treatment modality, but often produces only marginal benefit due to the lack of tumor specificity, the development of drug resistance, and the refractoriness of slowly proliferating cells in solid tumors. Here, we report a novel strategy to circumvent the proliferation-dependence of traditional antimetabolite-based therapies. Triplex-forming oligonucleotides (TFOs) were used to target site-specific DNA damage to the human c-MYC oncogene, thereby inducing replication-independent, unscheduled DNA repair synthesis (UDS) preferentially in the TFO-targeted region. The TFO-directed UDS facilitated incorporation of the antimetabolite, gemcitabine (GEM), into the damaged oncogene, thereby potentiating the anti-tumor activity of GEM. Mice bearing COLO 320DM human colon cancer xenografts (containing amplified c-MYC) were treated with a TFO targeted to c-MYC in combination with GEM. Tumor growth inhibition produced by the combination was significantly greater than with either TFO or GEM alone. Specific TFO binding to the genomic c-MYC gene was demonstrated, and TFO-induced DNA damage was confirmed by NBS1 accumulation, supporting a mechanism of enhanced efficacy of GEM via TFO-targeted DNA damage-induced UDS. Thus, coupling antimetabolite chemotherapeutics with a strategy that facilitates selective targeting of cells containing amplification of cancer-relevant genes can improve their activity against solid tumors, while possibly minimizing host toxicity. Twit Text FOAVip Triplex-forming oligonucleotides targeting c-MYC potentiate the anti-tumor activity of gemcitabine in a mouse model of human cancer ????Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=23681918 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23681918 #FOAvip English Wikipedia <ref>{{Cite pmid|23681918 }}</ref> Triplex-forming oligonucleotides targeting c-MYC potentiate the anti-tumor activity of gemcitabine in a mouse model of human cancer #MMPMID23681918 Boulware SB ; Christensen LA ; Thames H ; Coghlan L ; Vasquez KM ; Finch RA Mol Carcinog 2014[Sep]; 53 (9 ): 744-52 PMID23681918 show ga Antimetabolite chemotherapy remains an essential cancer treatment modality, but often produces only marginal benefit due to the lack of tumor specificity, the development of drug resistance, and the refractoriness of slowly proliferating cells in solid tumors. Here, we report a novel strategy to circumvent the proliferation-dependence of traditional antimetabolite-based therapies. Triplex-forming oligonucleotides (TFOs) were used to target site-specific DNA damage to the human c-MYC oncogene, thereby inducing replication-independent, unscheduled DNA repair synthesis (UDS) preferentially in the TFO-targeted region. The TFO-directed UDS facilitated incorporation of the antimetabolite, gemcitabine (GEM), into the damaged oncogene, thereby potentiating the anti-tumor activity of GEM. Mice bearing COLO 320DM human colon cancer xenografts (containing amplified c-MYC) were treated with a TFO targeted to c-MYC in combination with GEM. Tumor growth inhibition produced by the combination was significantly greater than with either TFO or GEM alone. Specific TFO binding to the genomic c-MYC gene was demonstrated, and TFO-induced DNA damage was confirmed by NBS1 accumulation, supporting a mechanism of enhanced efficacy of GEM via TFO-targeted DNA damage-induced UDS. Thus, coupling antimetabolite chemotherapeutics with a strategy that facilitates selective targeting of cells containing amplification of cancer-relevant genes can improve their activity against solid tumors, while possibly minimizing host toxicity. |*Drug Synergism [MESH] |Animals [MESH] |Antimetabolites, Antineoplastic/*pharmacology [MESH] |Antineoplastic Combined Chemotherapy Protocols [MESH] |Chromatin Immunoprecipitation [MESH] |Colonic Neoplasms/genetics/pathology/*prevention & control [MESH] |DNA, Neoplasm/*genetics [MESH] |Deoxycytidine/*analogs & derivatives/pharmacology [MESH] |Female [MESH] |Gemcitabine [MESH] |Humans [MESH] |Mice [MESH] |Mice, Nude [MESH] |Oligonucleotides/*pharmacology [MESH] |Proto-Oncogene Proteins c-myc/*antagonists & inhibitors/genetics/metabolism [MESH] |Tumor Cells, Cultured [MESH]Triplex-forming oligonucleotides targeting c-MYC potentiate the anti-t(epmc).pdf DeepDyve Pubget Overpricing