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• W4383302252 abstract "Muscle-invasive urothelial carcinoma of the bladder (MIBC) has been treated with cisplatin-based chemotherapy for over 30 years. With the advent of immune checkpoint inhibitors, antibody drug conjugates and FGFR3 inhibitors new therapeutic options have been approved for patients with urothelial carcinoma (UC) and are still under investigation regarding association between patients’ response and recently defined molecular subtypes. Unfortunately, similar to chemotherapy, only a fraction of UC patients responds to these new treatment approaches. Thus, either further new efficacious therapeutic options for treatment of individual subtypes or new approaches to overcome treatment resistance and to increase patients’ response to standard of care treatment are needed. EpigeneticEpigenetics modifications of DNA and chromatin are known to mediate cellular plasticity or treatment resistance, and the responsible epigeneticEpigenetics regulators are frequently mutated or aberrantly expressed in UC. Thus, these enzymes provide targets for novel drugDrugs combination therapies to “episensitize” toward approved standard therapies by epigenetic primingEpigenetic priming. In general, these epigeneticEpigenetics regulators comprise writers and erasers like DNA methyltransferases and DNA demethylases (for DNA methylation), histone methyltransferases and histone demethylases (for histone methylation), as well as acetyl transferases and histone deacetylases (for histone and nonhistone acetylation). Such modifications, e.g., acetyl groups, are recognized by further epigeneticEpigenetics reader proteins, e.g., like the bromodomain and extra-terminal domain (BET) family proteins that often interact in multi-protein complexes and finally regulate chromatin conformation and transcriptional activity. Concurringly, epigeneticEpigenetics regulators target a plethora of cellular functions. Their pharmaceutical inhibitorsInhibitors often inhibit enzymatic activity of more than one isoenzyme or may have further noncanonical cytotoxic effects. Thus, analysis of their functions in UC pathogenesis as well as of the antineoplastic capacity of corresponding inhibitorsInhibitors alone or in combination with other approved drugsDrugs should follow a multidimensional approach. Here, we present our standard approach to analyze cellular effects of new epigeneticEpigenetics inhibitorsInhibitors on UC cells alone to define their potency and to conclude on putative reasonable combination therapy partners. We further describe our approach to identify efficacious synergistic combination therapies (e.g., with cisplatinCisplatin or PARP inhibitorsPARP inhibitors (PARPi)) that may have reduced normal toxicity through dose reduction, which can then be further analyzed in animal experiments. This approach may also serve as prototype for the preclinical evaluation of other epigeneticEpigenetics treatment approaches." @default.
• W4383302252 created "2023-07-07" @default.
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• W4383302252 date "2023-01-01" @default.
• W4383302252 modified "2023-10-05" @default.
• W4383302252 title "Epigenetic Priming and Development of New Combination Therapy Approaches" @default.
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• W4383302252 doi "https://doi.org/10.1007/978-1-0716-3291-8_16" @default.
• W4383302252 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37410240" @default.
• W4383302252 hasPublicationYear "2023" @default.
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