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Thereby, our findings define ferroptosis as a basis for additive therapy in combination with ibrutinib in DLBCL and reveal a previously unrecognized role for ibrutinib in directly modulating anti-oxidant defense.

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Studies in experimental models of pulmonary fibrosis have demonstrated significant metabolic dysregulation, further highlighting its relevance in disease development

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Therapeutic strategies, including ROS amplification, inhibition of the antioxidant system, and induction of ferroptosis, are discussed as promising approaches for selectively targeting cancer cells