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The oxygen supply fails to meet the metabolic requirements of tumor cells, which subsequently aggravates hypoxia along with tumor growth, resulting in the intratumoral microenvironment presenting a notable hypoxic phenotype (Verwilst et al., 2017
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Research data suggest that APOE4 leads to the pathogenesis of AD through various processes such as accelerated beta-amyloid aggregations that raised neurofibrillary tangle formation, cerebrovascular diseases, aggravated neuroinflammation, and synaptic loss
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