Abstract
Mirones et al. demonstrate that keratinocytes deficient in VEGF are capable of forming tumors but use a distinct form of aneuploidy and signaling to form tumors. This knowledge is important because inhibitors of VEGF, including bevacizumab (anti-VEGF antibodies) and sorafenib (Braf/VEGFR2 kinase inhibitor), have already entered the clinic. These agents may "remodel" tumor signaling.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Comment
MeSH terms
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Aneuploidy
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Animals
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal, Humanized
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Benzenesulfonates / pharmacology
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Bevacizumab
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Carcinoma, Squamous Cell / metabolism*
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Gene Expression Regulation, Neoplastic*
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Mice
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Mice, Transgenic
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Models, Biological
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Mutation
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Niacinamide / analogs & derivatives
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Phenotype
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Phenylurea Compounds
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Pyridines / pharmacology
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Signal Transduction
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Skin Neoplasms / metabolism*
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Sorafenib
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Vascular Endothelial Growth Factor A / antagonists & inhibitors
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Vascular Endothelial Growth Factor A / metabolism
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Vascular Endothelial Growth Factor A / physiology*
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Benzenesulfonates
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Phenylurea Compounds
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Pyridines
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Vascular Endothelial Growth Factor A
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Niacinamide
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Bevacizumab
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Sorafenib