Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Somatic BRCA1/2 Recovery as a Resistance Mechanism After Exceptional Response to Poly (ADP-ribose) Polymerase Inhibition.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology - 10 Apr 2017

Lheureux Stephanie, Bruce Jeff P, Burnier Julia V, Karakasis Katherine, Shaw Patricia A, Clarke Blaise A, Yang S Y Cindy, Quevedo Rene, Li Tiantian, Dowar Mark, Bowering Valerie, Pugh Trevor J, Oza Amit M

Abstract excerpt

Purpose Durable and long-term responses to the poly (ADP-ribose) polymerase inhibitor olaparib are observed in patients without BRCA1/2 mutations. However, beyond BRCA1/2 mutations, there are no approved biomarkers for olaparib in high-grade serous ovarian cancer (HGSOC). To determine mechanisms of durable response and resistance to olaparib therapy, we performed an analysis of HGSOC tumors from three patients...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Genes, BRCA1
Share to Genes, BRCA2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Neoplasm Grading

Share to Phthalazines

Share to Piperazines

Share to Poly(ADP-ribose) Polymerase Inhibitors

Share to Recombinational DNA Repair

Share to Sequence Analysis, RNA

Source

Identifiers

PMID: 28221868
DOI: 10.1200/JCO.2016.71.3677

Genes

BRCA1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Somatic BRCA1/2 Recovery as a Resistance Mechanism After Exceptional Response to Poly (ADP-ribose) Polymerase Inhibition.PMID 28221868Read ↗

Landscape of genomic alterations in high-grade serous ovarian cancer from exceptional long- and short-term survivorsSemantic proximity Read ↗

Biological and clinical evidence for somatic mutations in BRCA1 and BRCA2 as predictive markers for olaparib response in high-grade serous ovarian cancers in the maintenance setting.Semantic proximity Read ↗

Long-Term Responders on Olaparib Maintenance in High-Grade Serous Ovarian Cancer: Clinical and Molecular Characterization.Semantic proximity Read ↗

Mutation profiles in circulating cell-free DNA predict acquired resistance to olaparib in high-grade serous ovarian carcinoma.Semantic proximity Read ↗

Candidate Markers of Olaparib Response from Genomic Data Analyses of Human Cancer Cell LinesSemantic proximity Read ↗

PARP inhibitor resistance and TP53 mutations in patients treated with olaparib for BRCA-mutated cancer: Four case reportsSemantic proximity Read ↗

Mutation landscape of germline and somatic BRCA1/2 in patients with high-grade serous ovarian cancer.Semantic proximity Read ↗

Lessons learned from understanding chemotherapy resistance in epithelial tubo-ovarian carcinoma from BRCA1and BRCA2mutation carriers.Semantic proximity Read ↗

Genetic heterogeneity after first-line chemotherapy in high-grade serous ovarian cancer.Semantic proximity Read ↗

Platinum resistance induces diverse evolutionary trajectories in high grade serous ovarian cancerSemantic proximity Read ↗

Overall Survival With Maintenance Olaparib at a 7-Year Follow-Up in Patients With Newly Diagnosed Advanced Ovarian Cancer and a BRCA Mutation: The SOLO1/GOG 3004 Trial.Semantic proximity Read ↗

Olaparib-Resistant BRCA2MUT Ovarian Cancer Cells with Restored BRCA2 Abrogate Olaparib-Induced DNA Damage and G2/M Arrest Controlled by the ATR/CHK1 Pathway for SurvivalSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.