ArticleNature communications2017
Somatic chromosomal engineering identifies BCAN-NTRK1 as a potent glioma driver and therapeutic target.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 70 citations in OpenAlex.
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- Machine learning-based prognostic model of lactylation-related genes for predicting prognosis and immune infiltration in patients with lung adenocarcinoma.Cancer cell international · 2024Article
- NTRK fusion promotes tumor migration and invasion through epithelial-mesenchymal transition and closely interacts with ECM1 and NOVA1.BMC cancer · 2024Article
- Zurletrectinib is a next-generation TRK inhibitor with strong intracranial activity against NTRK fusion-positive tumours with on-target resistance to first-generation agents.British journal of cancer · 2024Article
- How CRISPR Is Revolutionizing the Generation of New Models for Cancer Research.Cold Spring Harbor perspectives in medicine · 2024Review
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- Advances in Making Cancer Mouse Models More Accessible and Informative through Non-Germline Genetic Engineering.Cold Spring Harbor perspectives in medicine · 2024Review
- Preclinical Modeling of Pathway-Targeted Therapy of Human Lung Cancer in the Mouse.Cold Spring Harbor perspectives in medicine · 2024Review
- The landscape of cancer-associated transcript fusions in adult brain tumors: a longitudinal assessment in 140 patients with cerebral gliomas and brain metastases.Frontiers in oncology · 2024Article
- Leveraging a cuproptosis-based signature to predict the prognosis and drug sensitivity of cutaneous melanoma.Journal of translational medicine · 2023Article
- Population-wide gene disruption in the murine lung epithelium via AAV-mediated delivery of CRISPR-Cas9 components.Molecular therapy. Methods & clinical development · 2022Article
- Application of CRISPR for In Vivo Mouse Cancer Studies.Cancers · 2022Review
- Rat and Mouse Brain Tumor Models for Experimental Neuro-Oncology Research.Journal of neuropathology and experimental neurology · 2022Review
- Review
- i-Modern: Integrated multi-omics network model identifies potential therapeutic targets in glioma by deep learning with interpretability.Computational and structural biotechnology journal · 2022Article
- Engineering chromosome rearrangements in cancer.Disease models & mechanisms · 2021Review
- NTRK Fusions Can Co-Occur With H3K27M Mutations and May Define Druggable Subclones Within Diffuse Midline Gliomas.Journal of neuropathology and experimental neurology · 2021Article
- Fusion Genes Altered in Adult Malignant Gliomas.Frontiers in neurology · 2021Review
- TRK xDFG Mutations Trigger a Sensitivity Switch from Type I to II Kinase Inhibitors.Cancer discovery · 2021Article
- Promising Molecular Targets for the Targeted Therapy of Biliary Tract Cancers: An Overview.OncoTargets and therapy · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The widespread application of high-throughput sequencing methods is resulting in the identification of a rapidly growing number of novel gene fusions caused by tumour-specific chromosomal rearrangements, whose oncogenic potential remains unknown. Here we describe a strategy that builds upon recent advances in genome editing and combines ex vivo and in vivo chromosomal engineering to rapidly and effectively interrogate the oncogenic potential of genomic rearrangements identified in human brain cancers. We show that one such rearrangement, an microdeletion resulting in a fusion between Brevican (BCAN) and Neurotrophic Receptor Tyrosine Kinase 1 (NTRK1), is a potent oncogenic driver of high-grade gliomas and confers sensitivity to the experimental TRK inhibitor entrectinib. This work demonstrates that BCAN-NTRK1 is a bona fide human glioma driver and describes a general strategy to define the oncogenic potential of novel glioma-associated genomic rearrangements and to generate accurate preclinical models of this lethal human cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.