ReviewOncogene2025
Combination strategies with PARP inhibitors in BRCA-mutated triple-negative breast cancer: overcoming resistance mechanisms.
Review in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 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
55 citing papers in PubMed.
- Epigenetic Plasticity in Triple-Negative Breast Cancer: Mechanisms of Therapy Resistance, Biomarkers, and Therapeutic Vulnerabilities.Biomedicines · 2026Review
- Antibody-Drug Conjugates and Peptide-Drug Conjugates: Current Understandings and Future Perspectives.MedComm · 2026Review
- Structure-Based Design, Synthesis, and Biological Evaluation of Oxadiazole-Morpholine Hybrids as Potent PARP-1 Inhibitors Inducing Apoptosis in Breast Cancer Cells.Drug development research · 2026Article
- Overcoming Resistance in Triple-Negative Breast Cancer: A Translational Perspective on Next-Generation DNA Damage Response Inhibitors and Synthetic Lethality.Molecules (Basel, Switzerland) · 2026Review
- Identification of novel drug-specific PARP inhibitor resistance mechanisms in ovarian cancer-implications for clinical practice.British journal of cancer · 2026Article
- PET Imaging of New Target PARP in Prostate Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Article
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
- Review
- Kaiso modulates androgen receptor expression in triple-negative breast cancer.Breast cancer research : BCR · 2026Article
- Article
- Advancements in the manufacturing routes for the synthesis of marketed PARP inhibitors.RSC advances · 2026Review
- Molecular profile of residual triple-negative breast cancer: opportunities for post-neoadjuvant therapeutic interventions.NPJ breast cancer · 2026Article
- Exosomal lncRNAsInternational journal of molecular sciences · 2026Article
- Association of obstructive sleep apnea with postoperative outcomes after breast reconstruction.BMC women's health · 2026Article
- Breast cancer immunotherapy: mechanisms of immune evasion, biomarkers, and emerging therapeutic strategies.Molecular cancer · 2026Review
- Article
- Targeted Therapies for Each Subtype of Breast Cancer.MedComm · 2026Review
- Epacadostat and Olaparib Synergistically Inhibit the Growth of BRCA-Proficient Triple-Negative Breast Cancer by Suppressing the Expression of BRCA1 and RAD51.Molecules (Basel, Switzerland) · 2026Article
- Revolutionizing Breast Cancer Treatment: Harnessing Ehrlich Ascites Carcinoma Model, Cancer Metabolism, and Nanotechnology-Enhanced Chemotherapy for Improved Patient Outcomes.Cell biochemistry and biophysics · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is a particularly aggressive breast cancer subtype, characterised by a higher incidence in younger women, rapid metastasis, and a generally poor prognosis. Patients with TNBC and BRCA mutations face additional therapeutic challenges due to the cancer's intrinsic resistance to conventional therapies. Poly (ADP-ribose) polymerase inhibitors (PARPis) have emerged as a promising targeted treatment for BRCA-mutated TNBC, exploiting vulnerabilities in the homologous recombination repair (HRR) pathway. However, despite initial success, the efficacy of PARPis is often compromised by the development of resistance mechanisms, including HRR restoration, stabilisation of replication forks, reduced PARP1 trapping, and drug efflux. This review explores latest breakthroughs in overcoming PARPi resistance through combination therapies. These strategies include the integration of PARPis with chemotherapy, immunotherapy, antibody-drug conjugates, and PI3K/AKT pathway inhibitors. These combinations aim to enhance the therapeutic efficacy of PARPis by targeting multiple cancer progression pathways. The review also discusses the evolving role of PARPis within the broader treatment paradigm for BRCA-mutated TNBC, emphasising the need for ongoing research and clinical trials to optimise combination strategies. By tackling the challenges associated with PARPi resistance and exploring novel combination therapies, this review sheds light on the future possibilities for improving outcomes for patients with BRCA-mutated TNBC.
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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.