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Neutrophils have been observed to preferentially migrate toward end-target chemoattractants, even in the presence of elevated concentration of intermediary signals, 446 implying that the end-target chemoattractant receptor may regulate a more prioritized signaling pathway compared to the intermediary chemoattractant receptor

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reported that SALL2 was significantly downregulated during tamoxifen therapy, this led to independent ER tumor growth and it conferred ER resistant phenotype in ER + cancer cells

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