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

The Mechanism by Which MYCN Amplification Confers an Enhanced Sensitivity to a PCNA-Derived Cell Permeable Peptide in Neuroblastoma Cells

10 Nov 2015

Abstract excerpt

Dysregulated expression of MYC family genes is a hallmark of many malignancies. Unfortunately, these proteins are not amenable to blockade by small molecules or protein-based therapeutic agents. Therefore, we must find alternative approaches to target MYC-driven cancers. Amplification of MYCN, a MYC family member, predicts high-risk neuroblastoma (NB) disease. We have shown that R9-caPep blocks the interaction of...

Read the complete abstract on PubMed

Topics

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

Share to Cancer, Hypoxia, and Metabolism
Share to DNA Repair Mechanisms
Share to Neuroblastoma Research and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26844271
DOI: 10.1016/j.ebiom.2015.11.016

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Mechanism by Which MYCN Amplification Confers an Enhanced Sensitivity to a PCNA-Derived Cell Permeable Peptide in Neuroblastoma CellsPMID 26844271Read ↗

Chromosome 11q loss and MYCN amplification demonstrate synthetic lethality with checkpoint kinase 1 inhibition in neuroblastomaSemantic proximity Read ↗

SUV39H1 epigenetically modulates the MCPIP1-AURKA signaling axis to enhance neuroblastoma tumorigenesisSemantic proximity Read ↗

Orally bioavailable CDK9/2 inhibitor shows mechanism-based therapeutic potential in MYCN-driven neuroblastomaSemantic proximity Read ↗

MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumorsSemantic proximity Read ↗

A combination of PARP and CHK1 inhibitors efficiently antagonizes MYCN-driven tumors.Semantic proximity Read ↗

Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastomaSemantic proximity Read ↗

MYCN acts as a direct co-regulator of p53 in MYCN amplified neuroblastomaSemantic proximity Read ↗

Strategies to target the cancer driver MYC in tumor cellsSemantic proximity Read ↗

Inhibition of mTOR-kinase destabilizes MYCN and is a potential therapy for MYCN-dependent tumorsSemantic proximity Read ↗

MYCN expression induces replication stress and sensitivity to PARP inhibition in neuroblastomaSemantic proximity Read ↗

Targeting of the MYCN Protein with Small Molecule c-MYC InhibitorsSemantic proximity Read ↗

Identification and Pharmacological Inactivation of the MYCN Gene Network as a Therapeutic Strategy for Neuroblastic Tumor CellsSemantic proximity Read ↗

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