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In concordance, Abraxanes tumor uptake was antagonized by inhibition of caveolar-mediated endocytosis, and the knockdown of Cav-1, the structural component of caveolae, also attenuated Abraxanes anti-tumor properties in vivo ( 110)

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The early observation that rapidly growing tumors were heavily vascularized, while dormant ones were not, led Judah Folkman to propose that initiation of tumor angiogenesis was required for tumor progression [1]

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