In the multi-cause and multi-step diseases we globally refer to as cancer, often the same or redundant biochemical circuits are disrupted or uncoupled by the cumulative action of diverse mutation events. Anticancer agents have been extensively designed and selected by their ability to specifically interact with malignant cells by the targeting of proteins, mRNAs or DNA sequences involved in the production of a transformed phenotype. In the post-genomic age, the amount of available information concerning DNA increases the interest of the genome and associated proteins as drug targets. The SELEX (Systematic Evolution of Ligands by EXponential enrichment) technique and Anti-gene strategy are both based on the production of high affinity ligands targeted to protein or nucleic acid counterparts, respectively. The different rational backgrounds of SELEX and Anti-gene approaches might be the basis for a complementary action in anticancer therapy.
Keywords: aptamer, selex, anti-gene, triplex-forming molecules, cancer, epigenome targeting
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