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Moreover, the communication between MAMs and the coordination of Ca 2+ flux from the ER to mitochondria are pivotal for triggering oxidative metabolic stress, a ROS surge, and an ensuing pro-paraptotic Ca 2+ overload in breast cancer cells [153]

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Given BPC-157's apparent pro-angiogenic effects (VEGF upregulation), a theoretical concern about promotion of tumor vascularization exists and has not been ruled out by long-term animal studies

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