ReviewInvestigational new drugs2020
Veliparib in ovarian cancer: a new synthetically lethal therapeutic approach.
Review in Investigational new drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Efficacy and Safety of PARP Inhibitor Combination Therapy in Recurrent Ovarian Cancer: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Trial
- Comparative Assessment of Free Energy Computational Methods for Revealing the Interactions Driving PARP1 Selective Inhibition.Journal of chemical information and modeling · 2026Article
- Cooperative molecular interaction networks govern PARP1 inhibitor selectivity and binding affinity.PLoS computational biology · 2026Article
- Clinical application of PARP inhibitors and emerging strategies to overcome resistance: a pan-cancer perspective.Biomarker research · 2026Review
- Enhancing PARP inhibitor efficacy in ovarian cancer: targeting the PI3K/AKT/mTOR pathway.Journal of ovarian research · 2025Review
- Future of PARP inhibitors in cancer treatment: overcoming resistance and enhancing efficacy with combination therapies.Journal of Zhejiang University. Science. B · 2025Review
- Synthesis, biological evaluation, and docking analysis of novel benzimidazole-triazole hybrids as potential anticancer agents.RSC advances · 2025Article
- Benzimidazole scaffold as a potent anticancer agent with different mechanisms of action (2016-2023).Molecular diversity · 2025Review
- Hydrogen Sulfide Expression May Affect Ovarian Cancer Progression and Drug Resistance.International journal of women's health · 2025Article
- Niraparib for the treatment of metastatic ccRCC in a patient withFrontiers in pharmacology · 2024Article
- Mass spectrometry-based proteomics as an emerging tool in clinical laboratories.Clinical proteomics · 2023Review
- DNA repair pathways in breast cancer: from mechanisms to clinical applications.Breast cancer research and treatment · 2023Review
- Clinical Challenges in the Management of Malignant Ovarian Germ Cell Tumours.International journal of environmental research and public health · 2023Review
- Preclinical evaluation of a brain penetrant PARP PET imaging probe in rat glioblastoma and nonhuman primates.European journal of nuclear medicine and molecular imaging · 2023Article
- Aberrations of DNA Repair Pathways in Prostate Cancer-The State of the Art.International journal of molecular sciences · 2023Article
- CCNE1 is a potential target of Metformin for tumor suppression of ovarian high-grade serous carcinoma.Cell cycle (Georgetown, Tex.) · 2023Article
- Exosomal transfer of miR-548aq-3p confers cisplatin resistanceAmerican journal of cancer research · 2023Article
- DNA Damage Response in Cancer Therapy and Resistance: Challenges and Opportunities.International journal of molecular sciences · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) accounts for nearly 90% of all ovarian malignancies. The standard therapeutic strategy includes cytoreductive surgery and neo (adjuvant) platinum-based chemotherapy. Relapse of advanced high grade serous ovarian cancer (HGSOC) is related to the development of drug resistance. A defective DNA damage response is a defining hallmark of HGSOC. Poly (ADP-ribose) polymerase (PARP) inhibitors exploit this deficiency through synthetic lethality and have emerged as promising anticancer therapies, especially in breast cancer gene (BRCA1 or BRCA2) mutation carriers. Apart from inducing synthetic lethality, PARP inhibitors have also been shown to trap PARP1 and PARP2 on DNA, leading to PARP-DNA complexes. This "PARP trapping" potentiates synergism between PARP inhibition and both alkylating agents and platinum-based chemotherapy. However, there are remarkable differences in the ability of PARP inhibitors to trap PARP, based on the size and structure of each separate molecule. Since monotherapy with PARP inhibitors is unlikely to induce cancer cell death in BRCA-proficient tumors, the efficacy of PARP inhibitors could be potentially optimized when combined with DNA-damaging agents, or with molecular targeted agents that also impair mechanisms of DNA repair. Olaparib, rucaparib, and niraparib have all obtained US Food and Drug Administration (FDA) and/or European Medicines Agency (EMA) approval in ovarian cancer in different settings. Veliparib does not yet have an approved label; nevertheless, there are currently promising results available in preclinical and early clinical settings. This comprehensive review summarizes the mechanism of action of veliparib and provides an overview of its early and ongoing clinical investigations.
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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.