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10.1093/jnci/djw030 http://scihub22266oqcxt.onion/10.1093/jnci/djw030 C5017954!5017954 !27059374     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27059374 &cmd=llinks): Failed to open stream: HTTP request failed! 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Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma |pdf=|usr=}}{{27059374 }} gab.com Text Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma JO: J Natl Cancer Inst http://www.kidney.de/pget.php?&tw=1&pmid=27059374 #FOAvip BACKGROUND: The anti-angiogenic Sorafenib is the only approved systemic therapy for advanced hepatocellular carcinoma (HCC). However, acquired resistance limits its efficacy. An emerging theory to explain intrinsic resistance to other anti-angiogenic drugs is 'vessel co-option,' ie, the ability of tumors to hijack the existing vasculature in organs such as the lungs or liver, thus limiting the need for sprouting angiogenesis. Vessel co-option has not been evaluated as a potential mechanism for acquired resistance to anti-angiogenic agents. METHODS: To study sorafenib resistance mechanisms, we used an orthotopic human HCC model (n?=?4-11 per group), where tumor cells are tagged with a secreted protein biomarker to monitor disease burden and response to therapy. Histopathology, vessel perfusion assessed by contrast-enhanced ultrasound, and miRNA sequencing and quantitative real-time polymerase chain reaction were used to monitor changes in tumor biology. RESULTS: While sorafenib initially inhibited angiogenesis and stabilized tumor growth, no angiogenic 'rebound' effect was observed during development of resistance unless therapy was stopped. Instead, resistant tumors became more locally infiltrative, which facilitated extensive incorporation of liver parenchyma and the co-option of liver-associated vessels. Up to 75% (±10.9%) of total vessels were provided by vessel co-option in resistant tumors relative to 23.3% (±10.3%) in untreated controls. miRNA sequencing implicated pro-invasive signaling and epithelial-to-mesenchymal-like transition during resistance development while functional imaging further supported a shift from angiogenesis to vessel co-option. CONCLUSIONS: This is the first documentation of vessel co-option as a mechanism of acquired resistance to anti-angiogenic therapy and could have important implications including the potential therapeutic benefits of targeting vessel co-option in conjunction with vascular endothelial growth factor receptor signaling. Twit Text FOAVip Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma ????J Natl Cancer Inst http://www.kidney.de/pget.php?&tw=1&pmid=27059374 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27059374 #FOAvip English Wikipedia <ref>{{Cite pmid|27059374 }}</ref> Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma #MMPMID27059374 Kuczynski EA ; Yin M ; Bar-Zion A ; Lee CR ; Butz H ; Man S ; Daley F ; Vermeulen PB ; Yousef GM ; Foster FS ; Reynolds AR ; Kerbel RS J Natl Cancer Inst 2016[Aug]; 108 (8 ): ä PMID27059374 show ga BACKGROUND: The anti-angiogenic Sorafenib is the only approved systemic therapy for advanced hepatocellular carcinoma (HCC). However, acquired resistance limits its efficacy. An emerging theory to explain intrinsic resistance to other anti-angiogenic drugs is 'vessel co-option,' ie, the ability of tumors to hijack the existing vasculature in organs such as the lungs or liver, thus limiting the need for sprouting angiogenesis. Vessel co-option has not been evaluated as a potential mechanism for acquired resistance to anti-angiogenic agents. METHODS: To study sorafenib resistance mechanisms, we used an orthotopic human HCC model (n?=?4-11 per group), where tumor cells are tagged with a secreted protein biomarker to monitor disease burden and response to therapy. Histopathology, vessel perfusion assessed by contrast-enhanced ultrasound, and miRNA sequencing and quantitative real-time polymerase chain reaction were used to monitor changes in tumor biology. RESULTS: While sorafenib initially inhibited angiogenesis and stabilized tumor growth, no angiogenic 'rebound' effect was observed during development of resistance unless therapy was stopped. Instead, resistant tumors became more locally infiltrative, which facilitated extensive incorporation of liver parenchyma and the co-option of liver-associated vessels. Up to 75% (±10.9%) of total vessels were provided by vessel co-option in resistant tumors relative to 23.3% (±10.3%) in untreated controls. miRNA sequencing implicated pro-invasive signaling and epithelial-to-mesenchymal-like transition during resistance development while functional imaging further supported a shift from angiogenesis to vessel co-option. CONCLUSIONS: This is the first documentation of vessel co-option as a mechanism of acquired resistance to anti-angiogenic therapy and could have important implications including the potential therapeutic benefits of targeting vessel co-option in conjunction with vascular endothelial growth factor receptor signaling. |*Drug Resistance, Neoplasm/genetics [MESH] |Actins/metabolism [MESH] |Animals [MESH] |Antigens, CD34/metabolism [MESH] |Antineoplastic Agents/*therapeutic use [MESH] |Blood Vessels/diagnostic imaging/pathology [MESH] |Carcinoma, Hepatocellular/*blood supply/drug therapy/genetics/pathology [MESH] |Contrast Media [MESH] |Disease Models, Animal [MESH] |Epithelial-Mesenchymal Transition/genetics [MESH] |Homeodomain Proteins/genetics [MESH] |Humans [MESH] |Liver Neoplasms/*blood supply/drug therapy/genetics/pathology [MESH] |Liver/*blood supply [MESH] |Male [MESH] |Mice [MESH] |Mice, SCID [MESH] |MicroRNAs/analysis [MESH] |Neoplasm Invasiveness [MESH] |Neoplasm Transplantation [MESH] |Neovascularization, Pathologic/diagnostic imaging/*metabolism/prevention & control [MESH] |Niacinamide/*analogs & derivatives/therapeutic use [MESH] |Osteopontin/blood [MESH] |Phenylurea Compounds/*therapeutic use [MESH] |Repressor Proteins/genetics [MESH] |Sequence Analysis, RNA [MESH] |Signal Transduction/genetics [MESH] |Sorafenib [MESH] |Ultrasonography [MESH] |Up-Regulation [MESH] |Vascular Endothelial Growth Factor A/blood [MESH] |Vimentin/genetics [MESH] |Zinc Finger E-box Binding Homeobox 2 [MESH]Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acqui(epmc).pdf DeepDyve Pubget Overpricing