Emergence and maintenance of actionable genetic drivers at medulloblastoma relapse.

doi:10.1093/neuonc/noab178

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

Community

Back to search

Article

Emergence and maintenance of actionable genetic drivers at medulloblastoma relapse.

Neuro-oncology - 5 Jan 2022

Richardson Stacey, Hill Rebecca M, Kui Christopher, Lindsey Janet C, Grabovksa Yura, Keeling Claire, Pease Louise, Bashton Matthew, Crosier Stephen, Vinci Maria, André Nicolas, Figarella-Branger Dominique, Hansford Jordan R, Lastowska Maria, Zakrzewski Krzysztof, Jorgensen Mette, Pickles Jessica C, Taylor Michael D, Pfister Stefan M, Wharton Stephen B, Pizer Barry, Michalski Antony, Joshi Abhijit, Jacques Thomas S, Hicks Debbie, Schwalbe Edward C, Williamson Daniel, Ramaswamy Vijay, Bailey Simon, Clifford Steven C

Abstract excerpt

BACKGROUND: Less than 5% of medulloblastoma (MB) patients survive following failure of contemporary radiation-based therapies. Understanding the molecular drivers of medulloblastoma relapse (rMB) will be essential to improve outcomes. Initial genome-wide investigations have suggested significant genetic divergence of the relapsed disease. METHODS: We undertook large-scale integrated characterization of the...

Read the complete abstract on PubMed

Topics

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

Share to Brain Metastases and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cerebellar Neoplasms

Share to DNA Copy Number Variations

Share to Glioma Diagnosis and Treatment

Share to Medulloblastoma

Share to Meningioma and schwannoma management

Share to Mutation

Share to Neoplasm Recurrence, Local

Source

Open in PubMed Open full text

Identifiers

PMID: 34272868
DOI: 10.1093/neuonc/noab178
PMCID: PMC8730763

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Emergence and maintenance of actionable genetic drivers at medulloblastoma relapse.PMID 34272868Read ↗

Clinical Outcomes and Patient-Matched Molecular Composition of Relapsed MedulloblastomaSemantic proximity Read ↗

Comparison of transcriptome profiles between medulloblastoma primary and recurrent tumors uncovers novel variance effects in relapses.Semantic proximity Read ↗

Mutational landscape and patterns of clonal evolution in relapsed pediatric acute lymphoblastic leukemia.Semantic proximity Read ↗

The molecular landscape and associated clinical experience in infant medulloblastoma: prognostic significance of second‐generation subtypesSemantic proximity Read ↗

Medulloblastoma biology in the post-genomic era.Semantic proximity Read ↗

Genetic and molecular alterations across medulloblastoma subgroups.Semantic proximity Read ↗

The whole-genome landscape of medulloblastoma subtypes.Semantic proximity Read ↗

Drivers Underlying Metastasis and Relapse in Medulloblastoma and Targeting StrategiesSemantic proximity Read ↗

Clonal Evolution of Pediatric Acute Myeloid Leukemia and Its Contribution to Disease RelapseSemantic proximity Read ↗

Adaptive Convergence of Methylomes Reveals Epigenetic Drivers and Boosters of Repeated Relapses in Patient-matched Childhood Ependymomas and Identifies Targets for Anti-Recurrence TherapiesSemantic proximity Read ↗

Single-cell DNA sequencing identifies risk-associated clonal complexity and evolutionary trajectories in childhood medulloblastoma development.Semantic proximity Read ↗

Rise and fall of subclones from diagnosis to relapse in pediatric B-acute lymphoblastic leukaemia.Semantic proximity Read ↗

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