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Several mechanisms have been proposed for anti-angiogenic therapy resistance, including direct effects of hypoxia such as induction of tumor invasion and metastasis, co-option of normal vessels in the surrounding tissue, vascular mimicry as well as the contribution of stromal cells including recruitment of TAMs, EPC and pro-angiogenic myeloid cells as well as the upregulation of alternative pro-angiogenic factors [297] [298]

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