ArticleCancer drug resistance (Alhambra, Calif.)2023
New perspectives on epigenetic modifications and PARP inhibitor resistance in HR-deficient cancers.
Article in Cancer drug resistance (Alhambra, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Sensitizing Colorectal Cancer to PARP Inhibitors: Biomarkers, Mechanisms, and Combination Strategies.International journal of molecular sciences · 2026Review
- HRR gene promoter methylation-guided nomogram predicts PARP inhibitor efficacy and progression-free survival in high-grade serous ovarian cancer.Clinical epigenetics · 2026Article
- A Clinically Translatable Multimodal Deep Learning Model for HRD Detection from Histopathology Images.Diagnostics (Basel, Switzerland) · 2026Article
- Clinical approaches to overcome PARP inhibitor resistance.Molecular cancer · 2025Review
- SETD1A-dependent EME1 transcription drives PARPi sensitivity in HR deficient tumour cells.British journal of cancer · 2025Article
- E3 ligase MKRN2 destabilizes PPP2CA proteins to inactivate canonical Wnt pathway and mitigates tumorigenesis of clear cell renal cell carcinoma.International journal of biological sciences · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.