ReviewDrugs2017
PARP Inhibitors in Reproductive System Cancers: Current Use and Developments.
Review in Drugs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed.
- Functional validation of somatic variability inCancer biology & therapy · 2025Article
- Article
- KPT330 promotes the sensitivity of glioblastoma to olaparib by retaining SQSTM1 in the nucleus and disrupting lysosomal function.Autophagy · 2024Article
- The Complex Network of ADP-Ribosylation and DNA Repair: Emerging Insights and Implications for Cancer Therapy.International journal of molecular sciences · 2023Review
- Effects of Dihydroartemisinin against Cystic EchinococcosisInfection and immunity · 2023Article
- A glance at the emerging diagnostic biomarkers in the most prevalent genitourinary cancers.Saudi journal of biological sciences · 2022Review
- Complex molecular profile of DNA repair genes in epithelial ovarian carcinoma patients with different sensitivity to platinum-based therapy.Frontiers in oncology · 2022Article
- PARP Inhibitor Applicability: Detailed Assays for Homologous Recombination Repair Pathway Components.OncoTargets and therapy · 2022Review
- Article
- Inferring Homologous Recombination Deficiency of Ovarian Cancer From the Landscape of Copy Number Variation at Subchromosomal and Genetic Resolutions.Frontiers in oncology · 2021Article
- Review
- Myc targeted CDK18 promotes ATR and homologous recombination to mediate PARP inhibitor resistance in glioblastoma.Nature communications · 2019Article
- Exploiting interconnected synthetic lethal interactions between PARP inhibition and cancer cell reversible senescence.Nature communications · 2019Article
- Drug resistance-related microRNAs in osteosarcoma: Translating basic evidence into therapeutic strategies.Journal of cellular and molecular medicine · 2019Review
- Prospect for Application of PARP Inhibitor in Patients with HER2 Negative Breast Cancer.International journal of biological sciences · 2019Review
- Nanoformulation of Talazoparib Delays Tumor Progression and Ascites Formation in a Late Stage Cancer Model.Frontiers in oncology · 2019Article
- Annual Congress of the European Society for Medical Oncology (ESMO): Munich, Germany, 19-23 October 2018.Targeted oncology · 2018Article
- Where Do We Stand on the Integration of PARP Inhibitors for the Treatment of Breast Cancer?Current oncology reports · 2018Review
- Candidate synthetic lethality partners to PARP inhibitors in the treatment of ovarian clear cell cancer.Biomedical reports · 2017Article
- Editorial: US Cancer Statistics of Survival: Achievements, Challenges, and Future Directions.Journal of the National Cancer Institute · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The repair of DNA damage is a critical cellular process governed by multiple biochemical pathways that are often found to be defective in cancer cells. The poly(ADP-ribose) polymerase (PARP) family of proteins controls response to single-strand DNA breaks by detecting these damaged sites and recruiting the proper factors for repair. Blocking this pathway forces cells to utilize complementary mechanisms to repair DNA damage. While PARP inhibition may not, in itself, be sufficient to cause tumor cell death, inhibition of DNA repair with PARP inhibitors is an effective cytotoxic strategy when it is used in patients who carry other defective DNA-repair mechanisms, such as mutations in the genes BRCA 1 and 2. This discovery has supported the development of PARP inhibitors (PARPi), agents that have proven effective against various types of tumors that carry BRCA mutations. With the application of next-generation sequencing of tumors, there is increased interest in looking beyond BRCA mutations to identify genetic and epigenetic aberrations that might lead to similar defects in DNA repair, conferring susceptibility to PARP inhibition. Identification of these genetic lesions and the development of screening assays for their detection may allow for the selection of patients most likely to respond to this class of anticancer agents. This article provides an overview of clinical trial results obtained with PARPi and describes the companion diagnostic assays being established for patient selection. In addition, we review known mechanisms for resistance to PARPi and potential strategies for combining these agents with other types of therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.