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dc.creatorBarszczewska-Pietraszek, Gabriela
dc.creatorDrzewiecka, Małgorzata
dc.creatorCzarny, Piotr
dc.creatorSkorski, Tomasz
dc.creatorŚliwiński, Tomasz
dc.identifier.citationBarszczewska-Pietraszek, G.; Drzewiecka, M.; Czarny, P.; Skorski, T.; Śliwiński, T. Polθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours. Int. J. Mol. Sci. 2023, 24, 319.
dc.description.abstractDNA polymerase theta (Polθ)-mediated end joining (TMEJ) is, along with homologous recombination (HR) and non-homologous end-joining (NHEJ), one of the most important mechanisms repairing potentially lethal DNA double-strand breaks (DSBs). Polθ is becoming a new target in cancer research because it demonstrates numerous synthetically lethal interactions with other DNA repair mechanisms, e.g., those involving PARP1, BRCA1/2, DNA-PK, ATR. Inhibition of Polθ could be achieved with different methods, such as RNA interference (RNAi), CRISPR/Cas9 technology, or using small molecule inhibitors. In the context of this topic, RNAi and CRISPR/Cas9 are still more often applied in the research itself rather than clinical usage, different than small molecule inhibitors. Several Polθ inhibitors have been already generated, and two of them, novobiocin (NVB) and ART812 derivative, are being tested in clinical trials against HR-deficient tumors. In this review, we describe the significance of Polθ and the Polθ-mediated TMEJ pathway. In addition, we summarize the current state of knowledge about Polθ inhibitors and emphasize the promising role of Polθ as a therapeutic target.
dc.format.extent16 pages
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartInternational Journal of Molecular Sciences, Vol. 24, Iss. 1
dc.rightsAttribution CC BY
dc.subjectPolθ inhibitors
dc.subjectAnticancer treatment
dc.subjectDNA double-strand break repair
dc.subjectDNA repair enzyme
dc.titlePolθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours
dc.type.genreJournal article
dc.contributor.groupFels Cancer Institute for Personalized Medicine (Temple University)
dc.description.departmentCancer and Cellular Biology
dc.description.departmentMicrobiology, Immunology and Inflammation
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact
dc.description.schoolcollegeLewis Katz School of Medicine
dc.temple.creatorSkorski, Tomasz

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