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Amylin promotes satiety by signaling fullness to the brain through pathways distinct from GLP-1offering a complementary approach to appetite control

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Although advances in molecular typing and targeted therapies have improved the prognosis of patients with specific subtypes, the heterogeneity of AML, its driving mechanisms, and complex interactions between leukemia stem cells (LSCs) and the bone marrow microenvironment remain unclear (3)

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