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10.1158/1078-0432.CCR-16-0895 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-16-0895 C5433896!5433896!28137923     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28137923&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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Cancer+Res 2017 ; 23 (10): 2382-90 Nephropedia Template TP {{tp|p=28137923|t=2017. Molecular Pathways: Hypoxia-activated prodrugs in cancer therapy |pdf=|usr=}}{{28137923}} gab.com Text Molecular Pathways: Hypoxia-activated prodrugs in cancer therapy JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28137923 #FOAvip Hypoxia is a known feature of aggressive solid tumors as well as a critical hallmark of the niche in aggressive hematologic malignances. Hypoxia is associated with insufficient response to standard therapy, resulting in disease progression and curtailed patients? survival through maintenance of noncycling cancer stem-like cells. A better understanding of the mechanisms and signaling pathways induced by hypoxia is essential to overcoming these effects. Recent findings demonstrate that bone marrow in the setting of hematologic malignancies is highly hypoxic and that progression of the disease is associated with expansion of hypoxic niches and stabilization of the oncogenic hypoxia-inducible factor-1alpha (HIF-1?). Solid tumors have also been shown to harbor hypoxic areas, maintaining survival of cancer cells via the HIF-1? pathway. Developing new strategies for targeting hypoxia has become a crucial approach in modern cancer therapy. The number of preclinical and clinical trials targeting low-oxygen tumor compartments or the hypoxic bone marrow niche via hypoxia-activated prodrugs is increasing. This review discusses the development of the hypoxia-activated prodrugs and their applicability in treating both hematologic malignancies and solid tumors. Twit Text FOAVip Molecular Pathways: Hypoxia-activated prodrugs in cancer therapy ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28137923 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28137923 #FOAvip English Wikipedia <ref>{{Cite pmid|28137923}}</ref> Molecular Pathways: Hypoxia-activated prodrugs in cancer therapy #MMPMID28137923 Baran N; Konopleva M Clin Cancer Res 2017[May]; 23 (10): 2382-90 PMID28137923show ga Hypoxia is a known feature of aggressive solid tumors as well as a critical hallmark of the niche in aggressive hematologic malignances. Hypoxia is associated with insufficient response to standard therapy, resulting in disease progression and curtailed patients? survival through maintenance of noncycling cancer stem-like cells. A better understanding of the mechanisms and signaling pathways induced by hypoxia is essential to overcoming these effects. Recent findings demonstrate that bone marrow in the setting of hematologic malignancies is highly hypoxic and that progression of the disease is associated with expansion of hypoxic niches and stabilization of the oncogenic hypoxia-inducible factor-1alpha (HIF-1?). Solid tumors have also been shown to harbor hypoxic areas, maintaining survival of cancer cells via the HIF-1? pathway. Developing new strategies for targeting hypoxia has become a crucial approach in modern cancer therapy. The number of preclinical and clinical trials targeting low-oxygen tumor compartments or the hypoxic bone marrow niche via hypoxia-activated prodrugs is increasing. This review discusses the development of the hypoxia-activated prodrugs and their applicability in treating both hematologic malignancies and solid tumors. äMolecular Pathways: Hypoxia-activated prodrugs in cancer therapy (epmc).pdf DeepDyve Pubget Overpricing