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Notably, combination with anti-PD-1 checkpoint blockade yields synergy, significantly enhancing the ICB responsiveness of TNBC and producing improved therapeutic efficacy

Since the discovery of the genetic etiology of AS, extensive efforts have been devoted to the understanding of the underlying mechanisms of AS pathophysiology, mainly by utilizing the AS mouse model, which was shown to replicate multiple phenotypes of the human disorder [5, 6]

It enables the cellular movement necessary for wound healing while also being implicated in cancer cell metastasis when the pathway becomes dysregulated

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