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

Loss of 53BP1 causes PARP inhibitor resistance in Brca1-mutated mouse mammary tumors.

Cancer discovery - 1 Jan 2013

Jaspers Janneke E, Kersbergen Ariena, Boon Ute, Sol Wendy, van Deemter Liesbeth, Zander Serge A, Drost Rinske, Wientjens Ellen, Ji Jiuping, Aly Amal, Doroshow James H, Cranston Aaron, Martin Niall M B, Lau Alan, O'Connor Mark J, Ganesan Shridar, Borst Piet, Jonkers Jos, Rottenberg Sven

Abstract excerpt

UNLABELLED: Inhibition of PARP is a promising therapeutic strategy for homologous recombination-deficient tumors, such as BRCA1-associated cancers. We previously reported that BRCA1-deficient mouse mammary tumors may acquire resistance to the clinical PARP inhibitor (PARPi) olaparib through activation of the P-glycoprotein drug efflux transporter. Here, we show that tumor-specific genetic inactivation of...

Read the complete abstract on PubMed

Topics

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

Share to ATP Binding Cassette Transporter, Subfamily B, Member 1
Share to Chromosomal Proteins, Non-Histone

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Mammary Neoplasms, Animal

Share to Phthalazines

Share to Piperazines

Share to Piperidines

Share to Poly(ADP-ribose) Polymerase Inhibitors

Share to Tumor Suppressor p53-Binding Protein 1

Source

Open in PubMed Open full text

Identifiers

PMID: 23103855
DOI: 10.1158/2159-8290.CD-12-0049
PMCID: PMC7518105

Genes

BRCA1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of 53BP1 causes PARP inhibitor resistance in Brca1-mutated mouse mammary tumors.PMID 23103855Read ↗

Selective resistance to the PARP inhibitor olaparib in a mouse model for BRCA1-deficient metaplastic breast cancerSemantic proximity Read ↗

Sensitivity and Acquired Resistance of BRCA1;p53-Deficient Mouse Mammary Tumors to the Topoisomerase I Inhibitor TopotecanSemantic proximity Read ↗

Molecular Pathways: How Can BRCA-Mutated Tumors Become Resistant to PARP Inhibitors?Semantic proximity Read ↗

Mechanisms of Therapy Resistance in Patient-Derived Xenograft Models of BRCA1-Deficient Breast Cancer.Semantic proximity Read ↗

BRCA2-Deficient Sarcomatoid Mammary Tumors Exhibit Multidrug ResistanceSemantic proximity Read ↗

Poly(ADP-ribose) polymerase-1 inhibitor treatment regresses autochthonous Brca2/p53-mutant mammary tumors in vivo and delays tumor relapse in combination with carboplatin.Semantic proximity Read ↗

Modulation of Early Mitotic Inhibitor 1 (EMI1) depletion on the sensitivity of PARP inhibitors in BRCA1 mutated triple-negative breast cancer cellsSemantic proximity Read ↗

Rapid activation of epithelial-mesenchymal transition drives PARP inhibitor resistance in Brca2-mutant mammary tumoursSemantic proximity Read ↗

53BP1 depletion causes PARP inhibitor resistance in ATM-deficient breast cancer cellsSemantic proximity Read ↗

Evaluation of candidate biomarkers to predict cancer cell sensitivity or resistance to PARP-1 inhibitor treatmentSemantic proximity Read ↗

Modulation of Early Mitotic Inhibitor 1 (EMI1) Depletion on the Sensitivity of PARP Inhibitors in BRCA1 Mutated Triple-Negative Breast Cancer CellsSemantic proximity Read ↗

Haploinsufficiency of Parp1 accelerates Brca1-associated centrosome amplification, telomere shortening, genetic instability, apoptosis, and embryonic lethality.Semantic proximity Read ↗

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