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10.1126/scitranslmed.aag0945 http://scihub22266oqcxt.onion/10.1126/scitranslmed.aag0945 C5936748!5936748 !29540614     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29540614 &cmd=llinks): Failed to open stream: HTTP request failed! 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Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2 |pdf=|usr=}}{{29540614 }} gab.com Text Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2 JO: Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=29540614 #FOAvip Anti-vascular endothelial growth factor (VEGF) therapy has failed to improve survival in patients with breast cancer (BC). Potential mechanisms of resistance to anti-VEGF therapy include the up-regulation of alternative angiogenic and proinflammatory factors. Obesity is associated with hypoxic adipose tissues, including those in the breast, resulting in increased production of some of the aforementioned factors. Hence, we hypothesized that obesity could contribute to anti-VEGF therapy's lack of efficacy. We found that BC patients with obesity harbored increased systemic concentrations of interleukin-6 (IL-6) and/or fibroblast growth factor 2 (FGF-2), and their tumor vasculature was less sensitive to anti-VEGF treatment. Mouse models revealed that obesity impairs the effects of anti-VEGF on angiogenesis, tumor growth, and metastasis. In one murine BC model, obesity was associated with increased IL-6 production from adipocytes and myeloid cells within tumors. IL-6 blockade abrogated the obesity-induced resistance to anti-VEGF therapy in primary and metastatic sites by directly affecting tumor cell proliferation, normalizing tumor vasculature, alleviating hypoxia, and reducing immunosuppression. Similarly, in a second mouse model, where obesity was associated with increased FGF-2, normalization of FGF-2 expression by metformin or specific FGF receptor inhibition decreased vessel density and restored tumor sensitivity to anti-VEGF therapy in obese mice. Collectively, our data indicate that obesity fuels BC resistance to anti-VEGF therapy via the production of inflammatory and angiogenic factors. Twit Text FOAVip Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2 ????Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=29540614 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29540614 #FOAvip English Wikipedia <ref>{{Cite pmid|29540614 }}</ref> Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2 #MMPMID29540614 Incio J ; Ligibel JA ; McManus DT ; Suboj P ; Jung K ; Kawaguchi K ; Pinter M ; Babykutty S ; Chin SM ; Vardam TD ; Huang Y ; Rahbari NN ; Roberge S ; Wang D ; Gomes-Santos IL ; Puchner SB ; Schlett CL ; Hoffmman U ; Ancukiewicz M ; Tolaney SM ; Krop IE ; Duda DG ; Boucher Y ; Fukumura D ; Jain RK Sci Transl Med 2018[Mar]; 10 (432 ): ä PMID29540614 show ga Anti-vascular endothelial growth factor (VEGF) therapy has failed to improve survival in patients with breast cancer (BC). Potential mechanisms of resistance to anti-VEGF therapy include the up-regulation of alternative angiogenic and proinflammatory factors. Obesity is associated with hypoxic adipose tissues, including those in the breast, resulting in increased production of some of the aforementioned factors. Hence, we hypothesized that obesity could contribute to anti-VEGF therapy's lack of efficacy. We found that BC patients with obesity harbored increased systemic concentrations of interleukin-6 (IL-6) and/or fibroblast growth factor 2 (FGF-2), and their tumor vasculature was less sensitive to anti-VEGF treatment. Mouse models revealed that obesity impairs the effects of anti-VEGF on angiogenesis, tumor growth, and metastasis. In one murine BC model, obesity was associated with increased IL-6 production from adipocytes and myeloid cells within tumors. IL-6 blockade abrogated the obesity-induced resistance to anti-VEGF therapy in primary and metastatic sites by directly affecting tumor cell proliferation, normalizing tumor vasculature, alleviating hypoxia, and reducing immunosuppression. Similarly, in a second mouse model, where obesity was associated with increased FGF-2, normalization of FGF-2 expression by metformin or specific FGF receptor inhibition decreased vessel density and restored tumor sensitivity to anti-VEGF therapy in obese mice. Collectively, our data indicate that obesity fuels BC resistance to anti-VEGF therapy via the production of inflammatory and angiogenic factors. |Animals [MESH] |Antineoplastic Agents/therapeutic use [MESH] |Breast Neoplasms/*drug therapy [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Female [MESH] |Fibroblast Growth Factor 2/*metabolism [MESH] |Humans [MESH] |Interleukin-6/*metabolism [MESH] |Metformin/therapeutic use [MESH] |Mice [MESH] |Obesity/*complications [MESH]Obesity promotes resistance to anti-VEGF therapy in breast cancer by (epmc).pdf DeepDyve Pubget Overpricing