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Cell-free chromatin particles (cfChPs) are fragments of chromatin, consisting of DNA and histone proteins, that are released into the extracellular space and systemic circulation following cell death via apoptosis or necrosis [2, 4]. These particles act as potent endogenous stressors that can be internalized by healthy bystander cells, where they integrate into the host genome and induce double-strand DNA breaks, genomic instability, and chronic inflammation [4, 9]. This 'vicious cycle' of cell death and chromatin release is implicated in the progression of cancer, the development of sepsis, and the systemic toxicity associated with chemotherapy and radiotherapy [1, 3, 20]. Therapeutic interventions targeting cfChPs, such as the Resveratrol-Copper (R-Cu) combination or DNase I, aim to degrade or deactivate these particles to prevent their pathological integration and signaling [9, 18]. By neutralizing cfChPs, these treatments have shown potential in reducing inflammation, preventing metastasis, and mitigating the side effects of conventional cancer therapies [1, 5, 12].
Deactivation and degradation of extracellular chromatin particles to prevent genomic integration and subsequent DNA damage and inflammation.
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