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Tumors employ multiple compensatory pro-angiogenic factors and signaling pathways in anti-VEGF environment In a broader sense, the multiple compensatory angiogenic factors/signaling pathways that tumors employ during anti-VEGF stress (Figures 1 and 2,) can be conveniently categorized as VEGF-dependent pathways, VEGF-independent signaling, mechnisms involving myeloid/stromal/tumor cell interactions and angiogenesis-independent vascular remodeling processes such as vessel cooption, intussusceptions and vascular mimicry

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