ReviewMolecular medicine (Cambridge, Mass.)2011
Poly(ADP-ribose) polymerase-1 inhibition: preclinical and clinical development of synthetic lethality.
Review in Molecular medicine (Cambridge, Mass.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 58 citations in OpenAlex.
- Development and evaluation of aEJNMMI radiopharmacy and chemistry · 2025Article
- Developments in Genetics: Better Management of Ovarian Cancer Patients.International journal of molecular sciences · 2023Review
- PET imaging of PARP expression usingEuropean journal of nuclear medicine and molecular imaging · 2023Article
- Review
- Nutlin-3a suppresses poly (ADP-ribose) polymerase 1 by mechanisms different from conventional PARP1 suppressors in a human breast cancer cell line.Oncotarget · 2020Article
- Rapamycin sensitizes cancer cells to growth inhibition by the PARP inhibitor olaparib.Oncotarget · 2017Article
- Trial watch - inhibiting PARP enzymes for anticancer therapy.Molecular & cellular oncology · 2016Review
- Molecular pathways: targeting the dependence of mutant RAS cancers on the DNA damage response.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).Pharmaceutical research · 2015Article
- Clinical next generation sequencing of pediatric-type malignancies in adult patients identifies novel somatic aberrations.Oncoscience · 2015Article
- Structural basis for the inhibition of poly(ADP-ribose) polymerases 1 and 2 by BMN 673, a potent inhibitor derived from dihydropyridophthalazinone.Acta crystallographica. Section F, Structural biology communications · 2014Article
- Niraparib (MK-4827), a novel poly(ADP-Ribose) polymerase inhibitor, radiosensitizes human lung and breast cancer cells.Oncotarget · 2014Article
- Targeting DNA repair pathways for cancer treatment: what's new?Future oncology (London, England) · 2014Review
- Autophagy and genomic integrity.Cell death and differentiation · 2013Review
- p53 regulates a non-apoptotic death induced by ROS.Cell death and differentiation · 2013Article
- Loss of BRCA1 expression leads to worse survival in patients with gastric carcinoma.World journal of gastroenterology · 2013Article
- Higher cytoplasmic and nuclear poly(ADP-ribose) polymerase expression in familial than in sporadic breast cancer.Virchows Archiv : an international journal of pathology · 2012Article
- Deficient expression of DNA repair enzymes in early progression to sporadic colon cancer.Genome integrity · 2012Article
- Oncogenic activation of ERG: A predominant mechanism in prostate cancer.Journal of carcinogenesis · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The hereditary forms of breast cancer identified by BRCA1 and BRCA2 genes have a defect in homologous DNA repair and demonstrate a dependence on alternate DNA repair processes by base excision repair, which requires poly(ADP-ribose) polymerase 1 (PARP-1). siRNA and deletion mutations demonstrate that interference with PARP-1 function results in enhanced cell death when the malignancy has a defect in homologous recombination. These findings resulted in a plethora of agents in clinical trials that interfere with DNA repair, and these agents offer the potential of being more selective in their effects than classic chemotherapeutic drugs. An electronic search of the National Library of Medicine for published articles written in English used the terms "PARP inhibitors" and "breast cancer" to find prospective, retrospective and review articles. Additional searches were done for articles dealing with mechanism of action. A total of 152 articles dealing with breast cancer and PARP inhibition were identified. PARP inhibition not only affects nonhomologous repair, but also has several other nongenomic functions. Mutational resistance to these agents was seen in preclinical studies. To date, PARP-1 inhibitors were shown to enhance cytotoxic effects of some chemotherapy agents. This new class of agents may offer more therapeutic specificity by exploiting a DNA repair defect seen in some human tumors with initial clinical trials demonstrating antitumor activity. Although PARP inhibitors may offer a therapeutic option for selected malignancies, the long-term effects of these agents have not yet been defined.
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.