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Cellular DNA and RNA can be targeted by certain chemotherapeutic agents through **alkylation** or **cross-linking** mechanisms. These processes involve the covalent modification of nucleic acids—either by adding alkyl groups to nucleotide bases (*alkylation*) or forming covalent bonds between two nucleotides on the same strand (*intrastrand crosslink*) or opposite strands (*interstrand crosslink*), as well as between nucleic acids and proteins. Such modifications disrupt essential cellular processes like replication and transcription, ultimately leading to cell cycle arrest and cell death if not repaired. This mechanism is exploited in cancer therapy using drugs such as nitrogen mustards, platinum compounds, mitomycin C, and psoralens. While these approaches are effective against rapidly dividing cells such as cancer cells, they also pose significant risks including bone marrow suppression, organ toxicity, mutagenesis leading to secondary cancers, and other off-target effects. The term \"Cellular DNA/RNA via alkylation/cross-linking mechanisms\" does not refer to a single molecular entity but rather describes a class of therapeutic strategies targeting fundamental genetic material; thus it is not a canonical molecular target but rather a mechanistic category.
Alkylation of nucleobases in DNA or RNA leading to mispairing or strand breaks\nCross-link formation within or between strands of DNA/RNA, blocking replication and transcription
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