ReviewCancer science2022
Reconsidering the mechanisms of action of PARP inhibitors based on clinical outcomes.
Review in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Sensitizing Colorectal Cancer to PARP Inhibitors: Biomarkers, Mechanisms, and Combination Strategies.International journal of molecular sciences · 2026Review
- Dynamic changes in homologous recombination status before and after chemotherapy in advanced ovarian, fallopian tube, and primary peritoneal cancers.Journal of ovarian research · 2026Article
- Integrative proteomics reveals MSH6 to modulate PARP inhibitor sensitivity in BRCA1/2-proficient ovarian cancer.PloS one · 2026Article
- Poly (ADP-Ribose) Polymerase 1 and 2 in B-Cell Lymphoma: Pathogenic Roles and Therapeutic Implications.The American journal of pathology · 2025Review
- PARP Inhibitors in Genitourinary Cancer: A New Paradigm Beyond Prostate Cancer.International journal of urology : official journal of the Japanese Urological Association · 2025Review
- Phenotypic screening converges on CDK9 inhibition as a therapeutic strategy in translocation renal cell carcinoma.bioRxiv : the preprint server for biology · 2025Article
- SLFN11-mediated ribosome biogenesis impairment induces TP53-independent apoptosis.Molecular cell · 2025Article
- DNA damage response mutations enhance the antitumor efficacy of ATR and PARP inhibitors in cholangiocarcinoma cell lines.Oncology letters · 2025Article
- Exploration of organoids in ovarian cancer: From basic research to clinical translation.Translational oncology · 2024Review
- HMGB1 promotes chemoresistance in small cell lung cancer by inducing PARP1-related nucleophagy.Journal of advanced research · 2024Article
- Establish TIIC signature score based the machine learning fusion in bladder cancer.Discover oncology · 2024Article
- Leveraging PARP-1/2 to Target Distant Metastasis.International journal of molecular sciences · 2024Review
- Article
- The function and regulation of ADP-ribosylation in the DNA damage response.Biochemical Society transactions · 2023Article
- Temporal recruitment of base excision DNA repair factors in living cells in response to different micro-irradiation DNA damage protocols.DNA repair · 2023Article
- Roles of DNA damage repair and precise targeted therapy in renal cancer (Review).Oncology reports · 2022Article
- Reconsidering the mechanisms of action of PARP inhibitors based on clinical outcomes.Cancer science · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
PARP inhibitors (PARPis) were initially developed as DNA repair inhibitors that inhibit the catalytic activity of PARP1 and PARP2 and are expected to induce synthetic lethality in BRCA- or homologous recombination (HR)-deficient tumors. However, the clinical indications for PARPis are not necessarily limited to BRCA mutations or HR deficiency; BRCA wild-type and HR-proficient cancers can also derive some benefit from PARPis. These facts are interpretable by an additional primary antitumor mechanism of PARPis named PARP trapping, resulting from the stabilization of PARP-DNA complexes. Favorable response to platinum derivatives (cisplatin and carboplatin) in preceding treatment is used as a clinical biomarker for some PARPis, implying that sensitivity factors for platinum derivatives and PARPis are mainly common. Such common sensitivity factors include not only HR defects (HRD) but also additional factors. One of them is Schlafen 11 (SLFN11), a putative DNA/RNA helicase, that sensitizes cancer cells to a broad type of DNA-damaging agents, including platinum and topoisomerase inhibitors. Mechanistically, SLFN11 induces a lethal replication block in response to replication stress (ie, DNA damage). As SLFN11 acts upon replication stress, trapping PARPis can activate SLFN11. Preclinical models show the importance of SLFN11 in PARPi sensitivity. However, the relevance of SLFN11 in PARPi response is less evident in clinical data compared with the significance of SLFN11 for platinum sensitivity. In this review, we consider the reasons for variable indications of PARPis resulting from clinical outcomes and review the mechanisms of action for PARPis as anticancer agents.
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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.