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In the context of lung cancer, this dysregulation is marked by pronounced abnormalities in DNA methylation, typically characterized by a coexistence of genome-wide hypomethylation alongside specific hypermethylation of tumor suppressor gene promoters, including Death-associated protein kinase (DAPK), Ras association domain family member 1A (RASSF1A), and Retinoic acid receptor (RAR), among others (44, 45)

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Furthermore, some inflammatory markers, like tumor necrosis factor-alpha (TNF-), cyclooxygenase-2 (COX-2), and interleukins (IL), can induce the expression of antioxidant enzymes as part of the cellular response to inflammation [16]

Nothing is transmitted into the brain