Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial.
Explore this paper's citation graph
Summary
Findings from this phase 2 study provide positive proof of concept of the efficacy and tolerability of genetically targeted treatment with olaparib in BRCA-mutated advanced ovarian cancer.
- Type
- article
- Published
- 2010-07-24
- Cited by
- 1,892
- References
- 58
- OpenAlex
- https://openalex.org/W2110017381
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:34142559
Keywords
Olaparib, Medicine, PARP inhibitor, Cohort, Internal medicine
References
- Statistics with confidence
- Epidemiology of breast cancer: Findings from the nurses' health study
- Synergistic tumor suppressor activity of BRCA2 and p53 in a conditional mouse model for breast cancer
- Distinct somatic genetic changes associated with tumor progression in carriers of BRCA1 and BRCA2 germ-line mutations.
- Consistent loss of the wild type allele in breast cancers from a family linked to the BRCA2 gene on chromosome 13q12-13.
- Multicentre, phase II study evaluating capecitabine monotherapy in patients with anthracycline- and taxane-pretreated metastatic breast cancer.
- Mutation in Brca2 stimulates error‐prone homology‐directed repair of DNA double‐strand breaks occurring between repeated sequences
- Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
- The relationship between the roles of BRCA genes in DNA repair and cancer predisposition.
- The cancer connection: BRCA1 and BRCA2 tumor suppression in mice and humans
- Genome-wide association study identifies novel breast cancer susceptibility loci
- Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval.
- A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair.
- Somatic genetic alterations in BRCA2‐associated and sporadic male breast cancer
- Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
- High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs
- The Concept of Synthetic Lethality in the Context of Anticancer Therapy
- Genomic instability and the selection of treatments for cancer
- Exploiting the DNA repair defect in BRCA mutant cells in the design of new therapeutic strategies for cancer.
- Identification of the breast cancer susceptibility gene BRCA2
Cited by
- Hereditary breast and ovarian cancer: new genes, new treatments, new concepts.
- Hereditary ovarian cancer: recent molecular insights and their impact on screening strategies
- Exploiting the Nucleotide Substrate Specificity of Repair DNA Polymerases To Develop Novel Anticancer Agents
- Checkpoint Signaling, Base Excision Repair, and PARP Promote Survival of Colon Cancer Cells Treated with 5-Fluorodeoxyuridine but Not 5-Fluorouracil
- [Modern pharmacological therapy of breast cancer].
- Platinum-Based Compounds for the Treatment of Metastatic Breast Cancer
- Hereditary breast cancer: beyond BRCA genetic analysis; PALB2 emerges
- Curcumin suppresses multiple DNA damage response pathways and has potency as a sensitizer to PARP inhibitor.
- A BRCA1 deficient-like signature is enriched in breast cancer brain metastases and predicts DNA damage-induced poly (ADP-ribose) polymerase inhibitor sensitivity
- The histone methyltransferase SMYD2 methylates PARP1 and promotes poly(ADP-ribosyl)ation activity in cancer cells.
- Subtyping of triple-negative breast cancer: implications for therapy
- Poly (ADP) ribose polymerase enzyme inhibitor, veliparib, potentiates chemotherapy and radiation in vitro and in vivo in small cell lung cancer
- Synergistic Loss of Prostate Cancer Cell Viability by Coinhibition of HDAC and PARP
- Investigational therapies currently in Phase II clinical trials for the treatment of pelvic serous carcinomas
- Harmine suppresses homologous recombination repair and inhibits proliferation of hepatoma cells
- TARGETED THERAPY IN CANCER
- What Is the Place of PARP Inhibitors in Ovarian Cancer Treatment?
- PARP activity in peripheral blood lymphocytes as a predictive biomarker for PARP inhibition in tumor tissues – A population pharmacokinetic/pharmacodynamic analysis of rucaparib
- Translational and clinical implications of the genetic landscape of prostate cancer
- Panobinostat sensitizes cyclin E high, homologous recombination-proficient ovarian cancer to olaparib
Related papers
- Clinical trial protocol1 from Combination ATR (ceralasertib) and PARP (olaparib) Inhibitor (CAPRI) Trial in Acquired PARP Inhibitor–Resistant Homologous Recombination–Deficient Ovarian Cancer
- Supplementary Figure 1 from Combination ATR (ceralasertib) and PARP (olaparib) Inhibitor (CAPRI) Trial in Acquired PARP Inhibitor–Resistant Homologous Recombination–Deficient Ovarian Cancer
- Data from Combination ATR (ceralasertib) and PARP (olaparib) Inhibitor (CAPRI) trial in acquired PARP-inhibitor-resistant homologous recombination deficient ovarian cancer
- OLAPARIB: A promising PARP Inhibitor for the treatment of ovarian cancer
- PARP inhibitors on the move in prostate cancer: spotlight on Niraparib & update on PARP inhibitor combination trials.
- Emerging Role of PARP Inhibitors in Metastatic Prostate Cancer
- Phase I study of oral BKM120 and oral olaparib for high-grade serous ovarian cancer (HGSC) or triple-negative breast cancer (TNBC).
- VIOLETTE: A randomized phase II study to assess the DNA damage response inhibitors AZD6738 or AZD1775 in combination with olaparib (Ola) versus Ola monotherapy in patients (pts) with metastatic, triple-negative breast cancer (TNBC).