The Method of Viral Mimicry in Oncology and Prospects for its Improvement

Malignant neoplasms cells are characterized by clonal evolution that is resistant to the applied antitumor drug and evasion from effects of immune system. Therefore, a promising direction in modern oncology stimulation response against neoplasms. This method can be used combination with other anticancer drugs alone. Tumor produce CTLA4 (CTLA4 — cytotoxic T-lymphocyte protein 4) PD-1 (programmed cell death) checkpoints inhibit activity T-lymphocytes their production cytokines. The clinic uses antibodies CTLA4, PD-L1, monotherapy which increases effectiveness chemotherapy used, but significantly aggravates development adverse reactions, limits use. Monotherapy anti-PD/PD-L1 showed low efficacy also high risk pulmonary, hepatic, thyroid complications. In this regard, it necessary develop new methods tumor immunotherapy. most regard viral mimicry, when double-stranded RNA formed transcripts retroelements serve as trigger for interferon activation T-killers. For artificial retroelements, inhibitors DNA methyltransferases, deacetylases, histone methyltransferases used. Since located gene introns, mimicry spliceosomal targeted therapy. Transposons drivers carcinogenesis, therefore, addition activation, silencing using reverse transcriptase inhibitors. use non-specific demethylases lead suppression expression genes, possible side effects. technique guides direct modification enzymes loci location retroelement genes genome. Guides activate significant exclude elements involved initiation maintenance carcinogenesis. MicroRNAs, long non-coding RNAs, antisense oligonucleotides guides.