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CD38 in adenosinergic pathways and metabolic re-programming in human multiple myeloma cells: In-tandem insights from basic science to therapy

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Future therapeutic strategies should pivot from mere receptor blockade to targeting the core upstream drivers of checkpoint expression, such as epigenetic reprogramming, key cytokine signaling, or metabolic dysregulation, to fundamentally reverse the T-cell exhaustion program

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This dysfunction cascade further compromises cellular integrity and energy-dependent physiological functions such as ion channel activity and synaptic transmission [54, 55]

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