AI Article Synopsis
- PARP inhibitors have transformed the treatment of tumors with defective DNA repair, but their effectiveness is often reduced due to drug resistance.
- Recent research from our group has identified the lysine methyltransferase SETD1A as a new factor that contributes to this resistance.
- We explore the role of epigenetic changes and H3K4 methylation in this process, discussing how this knowledge could enhance the use of PARP inhibitors in clinical settings and offer potential strategies to overcome resistance in cancers.
Article Abstract
The clinical treatment of DNA-repair defective tumours has been revolutionised by the use of poly(ADP) ribose polymerase (PARP) inhibitors. However, the efficacy of these compounds is hampered by resistance, which is attributed to numerous mechanisms including rewiring of the DNA damage response to favour pathways that repair PARP inhibitor-mediated damage. Here, we comment on recent findings by our group identifying the lysine methyltransferase SETD1A as a novel factor that conveys PARPi resistance. We discuss the implications, with a particular focus on epigenetic modifications and H3K4 methylation. We also deliberate on the mechanisms responsible, the consequences for the refinement of PARP inhibitor use in the clinic, and future possibilities to circumvent drug resistance in DNA-repair deficient cancers.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10099596 | PMC |
| http://dx.doi.org/10.20517/cdr.2022.73 | DOI Listing |
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