ArticleMolecular oncology2014
BRCA2 inhibition enhances cisplatin-mediated alterations in tumor cell proliferation, metabolism, and metastasis.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- PARP inhibitors target cellular energy metabolism: Mechanisms of action and clinical implications.Translational oncology · 2026Review
- Review
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- Inducing mismatch repair deficiency sensitizes immune-cold neuroblastoma to anti-CTLA4 and generates broad anti-tumor immune memory.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Low level of BRCA2 in peripheral blood lymphocytes is associated with an increased risk for head and neck squamous cell carcinoma (HNSCC) in a population of North-East India: a case-control study.Ecancermedicalscience · 2023Article
- Crosstalk between CaInternational journal of molecular sciences · 2022Review
- Reply to: Reconciling differences in impact of molecular subtyping on response to cisplatin-based chemotherapy.Nature communications · 2021Article
- Crosstalk between autophagy and DNA repair systems.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- DNA polymerase beta modulates cancer progression via enhancing CDH13 expression by promoter demethylation.Oncogene · 2020Article
- Targeting Nuclear NADCancers · 2020Article
- Fanconi anemia pathway as a prospective target for cancer intervention.Cell & bioscience · 2020Review
- Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.The Journal of clinical investigation · 2019Article
- Correlation of BRCA2 gene mutation and prognosis as well as variant genes in invasive urothelial carcinoma of the bladder.Cancer biomarkers : section A of Disease markers · 2019Article
- DNA Damage, Repair, and Cancer Metabolism.Frontiers in oncology · 2018Review
- CD10Cell death & disease · 2017Article
- Catching moving targets: cancer stem cell hierarchies, therapy-resistance & considerations for clinical intervention.Molecular cancer · 2017Review
- Quantification of cancer cell extravasation in vivo.Nature protocols · 2016Article
- Reciprocal positive selection for weakness - preventing olaparib resistance by inhibiting BRCA2.Oncotarget · 2016Article
- Midline2 is overexpressed and a prognostic indicator in human breast cancer and promotes breast cancer cell proliferation in vitro and in vivo.Frontiers of medicine · 2016Article
- Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.BMC cancer · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor cells have unstable genomes relative to non-tumor cells. Decreased DNA integrity resulting from tumor cell instability is important in generating favorable therapeutic indices, and intact DNA repair mediates resistance to therapy. Targeting DNA repair to promote the action of anti-cancer agents is therefore an attractive therapeutic strategy. BRCA2 is involved in homologous recombination repair. BRCA2 defects increase cancer risk but, paradoxically, cancer patients with BRCA2 mutations have better survival rates. We queried TCGA data and found that BRCA2 alterations led to increased survival in patients with ovarian and endometrial cancer. We developed a BRCA2-targeting second-generation antisense oligonucleotide (ASO), which sensitized human lung, ovarian, and breast cancer cells to cisplatin by as much as 60%. BRCA2 ASO treatment overcame acquired cisplatin resistance in head and neck cancer cells, but induced minimal cisplatin sensitivity in non-tumor cells. BRCA2 ASO plus cisplatin reduced respiration as an early event preceding cell death, concurrent with increased glucose uptake without a difference in glycolysis. BRCA2 ASO and cisplatin decreased metastatic frequency in vivo by 77%. These results implicate BRCA2 as a regulator of metastatic frequency and cellular metabolic response following cisplatin treatment. BRCA2 ASO, in combination with cisplatin, is a potential therapeutic anti-cancer agent.
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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.